Im: Endocrine 1

Front 1

type 1 DM is characerized by ABSOLUTE insulin DEFICIENCY

Back 1

rather than insulin resistance

Front 2

how common is T1DM?

Back 2

not very. it's only 10% of DM cases

Front 3

what is type IA vs. type IB diabetes?

Back 3

Ia is associated with anti-islet cell antibody and anti-glutamic acid decarboxylase

also antibody to the tyrosine phosphatase IA-2

Front 4

what about IB?

Back 4

it is NOT assocaited with any antibodies really

Front 5

what about a woman who presents with recurrent vaginal candidiasis?

Back 5

get a fingerstick BS because she likely has diabetes

Front 6

how does type I present?

Back 6

DKA or just with really notable symptoms like polyuria, dipsia, weight loss, dehydration etc.

Front 7

dx criteria for diabetes

Back 7

fasting blood glucose over 126

glycosuria- an osmotic diuresis that leads to dehydration

HbA1c = a measure of glucose control over the past 3 months. if over 6.5% ever then it's diagnostic

Front 8

any use for oral agents for T1DM?

Back 8

no

Front 9

2 fast-acting insulins

Back 9

lispro and aspart

Front 10

short-acting insulins

Back 10

regular insulin- 2 to 4 hours after admin

Front 11

main intermediate-acting insulin

Back 11

NPH

Front 12

long-acting insulins

Back 12

detemir and glargine

Front 13

biggest risk factor for developing foot ulcers

Back 13

diabetic neuropathy

Front 14

what is it called when a patient returns with high fingerstick values in the AM and weird nightmares after starting insulin?

Back 14

the Somogyi effect

Front 15

Why does this happen?

Back 15

because they're on too short-acting of an insulin at night and around 3 am they get hypoglycemic

hyperglycemia that occurs is due to a rebound effect

Front 16

what insulin is used for DKA tx

Back 16

the reg

Front 17

how do you divide the dose of insulin

Back 17

2/3 morning
1/3 later

Front 18

what does a T1DM patient do when they're fasting?

Back 18

they still need to take insulin, but maybe a lower dose

Front 19

what is the Dawn phenomenon?

Back 19

it's the observation that glucose tends to rise jst before breakfast because there is a big GH secretion that occurs at that time

Front 20

the reason why you get a Somogyi effect is that the intermediate-acting insulin tends to peak around midnight in these cases

Back 20

ok

Front 21

age of dx for T2DM

Back 21

depends but mostly after age 30

Front 22

what is the concordance rate among twins for T2DM

Back 22

over 90%

Front 23

what is the next step if you suspect a Somogyi effect?

Back 23

to dx this you have to check a 3AM glucose level and find them hypoglycemic

Front 24

what causes the hyperglycemia of T2DM?

Back 24

a combination of insulin resistance and deficiency

there is also impaired inhibition of hepatic gluconeogenesis

Front 25

what is metabolic syndrome

Back 25

the syndrome marked by a combination of obesity, diabetes, hyperlipidemia and CAD

Front 26

and what is the problem with hyperglycemia in th elong run?

Back 26

it can induce insulin resistance by just being there by itself

Front 27

how often should people measure fingerstick blood sugars?

Back 27

5x per day

Front 28

how long after a meal is considered post prandial?

Back 28

2 hrs

Front 29

so if a patient has low sugar readings each morning, what do you do?

Back 29

you decrease bedtime NPH even if their bedtime levels are high

Front 30

why is neuropathy such a big risk for ulcers?

Back 30

because even with really large foot wounds they don't feel any pain from them

Front 31

what type of infection are diabetics at high risk for?

Back 31

recurrent fungal infections

Front 32

why are fungi such a problem?

Back 32

cell-mediated immunity is impaired by acute hyperglycemia

Front 33

why would a T2dm patient present with DKA?

Back 33

if they have atypical T2 aka "ketosis-prone" T2DM

Front 34

how common is non-ketotic hyperglycemic hyperosmolar state?

Back 34

it's still rare but it's more common in type 2

Front 35

dx criteria for diabetes

Back 35

random blood sugar over 200 + symptoms

asymptomatic patients require a fasting glucose over 126 on two separate occasions

if a pt has a fasting glucose level over 100 and under 126 then you need to do an OGTT

Front 36

so what is considered a positive OGTT?

Back 36

if the test shows a level over 200 two hours after ingestion of 75 g of glucose

Front 37

principles in initial mgmt of diabetes

Back 37

education is key
diet and exercise

Front 38

why educate

Back 38

because it increases compliance and success for the patient essentially

Front 39

so what if you check back with them and they still have poor sugar control with diet and exercise?

Back 39

then you need to start oral anti-hypoglycemic

Front 40

firstline drug for diabetes

Back 40

metformin

Front 41

what to add next after metformin

Back 41

usually a secretagogue e.g. glipizide or glyburide

Front 42

What new type of med is becoming more and more popular though?

Back 42

DPP-4 inhibitor

Front 43

what are some advantages of sulfonylureas?

Back 43

they're cheap, and we know a lot about them. they also work fairly well

Front 44

downsides of sulfonylureas

Back 44

hypoglycemia can occur
weight gain

you also have to have at least a small amount of pancreatic function to use them

Front 45

mechanism of sulfonylureas

Back 45

stimulate insulin secretion by closing the K+ channels in Beta cells

Front 46

what type of drug is metformin?

Back 46

a biguanide

Front 47

mechanism of metformin

Back 47

decreases liver production of glucose and also slightly increases glucose uptake at the muscles

Front 48

big benefits of metformin

Back 48

no hypoglycemia or weight gain

Front 49

major side effect of metformin

Back 49

GI upset

Front 50

most serious side effect of metformin

Back 50

lactic acidosis

Front 51

one big contraindication to metformin

Back 51

contrast dye in the past 48 hours

Front 52

other contraindications to metformin

Back 52

liver and renal disease
CHF
excessive alcohol intake

Front 53

MOA for TZDs

Back 53

insulin sensitization

Front 54

big benefits of TZDs

Back 54

no hypoglycemia and they can actually affect your lipids positively too

Front 55

side effects of TZDs

Back 55

weight gain

may increase risk of cardiovascular disease

Front 56

what are acarbose and miglitol?

Back 56

they are alpha glucosidase inhibitors which bascially block the digestion of sugars

Front 57

benefits of acarbose

Back 57

no weight gain
no hypoglycemia

Front 58

side effects of acarbose

Back 58

diarrhea- this is the main reason they're not used very often

Front 59

example of a DPP4 inhibitor

Back 59

Januvia- sitagliptin

Front 60

MOA for sitagliptin

Back 60

increases insulin production and decreases liver glucose production so it's a double whammy

Front 61

big reason we don't use them

Back 61

they have very limited side effects but are veyr new and expensive

Front 62

some infections that diabetics are at high risk for

Back 62

Mucor/Rhizopus
Pseudomonas
Actinomyces
Aspergillosis
Renal abscess

so just remember FUnGAL infections are a big problem

Front 63

What patients CANNOT take metformin?

Back 63

heart failure advanced stages

liver failure, renal failure

Front 64

Why did we make up metabolic syndrome?

Back 64

to remember a constellation of findings that point to a high risk of cardiovascular disease, MI, stroke nd death

Front 65

dx definition of metabolic syndrome

Back 65

fasting plasma glucose over 100
abdominal obesity
serum triglycerides over 150
HDL under 40 for men
HDL under 50 in women
BP over 130/85

Front 66

What is exenatide?

Back 66

it's a GLP-1 analog. It enhances insulin secretion in the pancreas, suppresses appetite, and decreases liver's gluocse output

Front 67

benefits of exenatide

Back 67

weight loss
N/V
hypoglycemia when combined with glipizide

Front 68

What is pramlintide?

Back 68

it's an analog of amylin that gets cosecreted with insulin by the pancreas.

this a last-line agent used in patients with poor sugar control despite a lot of insulin therapy and metformin

Front 69

benefit of pramlintide w

Back 69

weight loss

Front 70

What is the most common acute complication of diabetes?

Back 70

hyper and hypoglycemic emergencies

Front 71

What is the pathophys of DKA?

Back 71

the body is so insulin-deficient, that it switches to metabolizing its own lipids instead of circulating carbs

Front 72

what are some risk factors for developing DKA?

Back 72

lapse in insulin treatments
infections
major stressors or trauma

Front 73

what ethnicity can often present with DKA even with T2DM?

Back 73

African Americans

Front 74

Why do they get so severely dehydrated in DKA

Back 74

because they induce an osmotic diuresis with such high blood sugar.

Front 75

Where do the ketones come from?

Back 75

beta oxidation in the liver because it thinks there is no carbohydrate available

Front 76

What acid base disturbances do you see?

Back 76

high gap acidosis and Kussmaul breathing to compensate

Front 77

other exam findings

Back 77

acetone on the breath
pseudohyponatremia

Front 78

What is pseudohyponatremia?

Back 78

it's the finding that there is falsely low sodium secondary to osmotic shifts. the blood is super hyperosmolar in DKA so the Na is pushed into the cells

Front 79

symptoms of DKA

Back 79

polyuria
polydipsia
N/V
abdominal pain
lethargy and fatigue later

hypotension
tachycardia

Front 80

kussmaul breathing

Back 80

rapid deep breaths

Front 81

labs show

Back 81

high sugar
hyperketonemia
pH under 7.3
low bicarb

Front 82

Is the K+ high or low?

Back 82

it's high in the serum because of acidosis and insulin deficiency

it drops with insulin administration

Front 83

what is the big goal of tx for DKA?

Back 83

correcting the acidosis

Front 84

how do you follow their progress as you tx them?

Back 84

with their anion gap, it should close

Front 85

so why do this instead of follow glucose levels?

Back 85

because the glucose levels will fall to normal, but if they are still acidotic you have not fully corrected their metabolic disease yet

Front 86

do you give bicarb to a DKA patient?

Back 86

still controversial right now

can give it with severe acidosis

Front 87

tx for DKA

Back 87

IV insulin drip
K+
Aggressive IVNS administration
give D5W when their sugar level is normal to prevent a huge hypoglycemic episode

Front 88

what are bad prognostic indicators for a DKA patient?

Back 88

coma, lethargy
hypotension

Front 89

What else do you have to do

Back 89

treat their infection if that's what caused it

Front 90

major causes of death in DKA

Back 90

circulatory failure
hypokalemia
infection

Front 91

How does HHS differ?

Back 91

it can show even high blood sugars (over 600) and shows plasma osmolality over 320 mOsm/L

t shows no acidosis and no ketosis

Front 92

what type of patient will present with HHS?

Back 92

T2DM patient

the classic picture is a known diabetic that comes in with confusion, lethargy and dehydration but no ketones

Front 93

What is the biggest complication of HHS?

Back 93

extreme dehydration

Front 94

what usually precedes HHS episodes?

Back 94

hyperglycemic symptoms

Front 95

Why elderly?

Back 95

because they have a decreased thirst response in the first place so are at high risk for HHS

Front 96

what drugs can lead to HHS?

Back 96

steroids

Front 97

labs for HHS

Back 97

glucose usually over 1000
osmolarity usually over 385
BUN/Cr levels hugely elevated from dehydration

Front 98

first goal of treatment of HHS

Back 98

stabilizing their vital signs with aggressive IVF resuscitation

Front 99

Do you use normal saline 0.9%?

Back 99

yes- your first priority is to replete their volume

Front 100

then what?

Back 100

you switch to D5-1/2 NS and watch their serum K+

Front 101

So when do you give insulin to HHS?

Back 101

you wait until after their volume status is restored.

Front 102

Why wait on insulin?

Back 102

because it will just drive glucose back into the cells and exacerbate their volum depletion

Front 103

what can happen if you correct their osmolarity too quickly however?

Back 103

cerebral edema can develop

Front 104

at what glucose level do you start adding glucose to the insulin infusion?

Back 104

at 250 mg/dl