Numbers for ENDO exam 2 Flashcards
prediabetes A1C
above 5.6 to 6.4
hypoglycemia
less than 60 to 70
how o
how often to screen for DM and who
when -
all adults 35 years old or more.
if screen -, repeat every 3 years
if positive, retest annually
who -
at 24 weeks for preg
or 1st prenatal visit for risk factors
any age with risk of gestational DM, pancreatitis, prediabetes, are overweight, and have 1+ DM risk factor
HIV + (ART makes them more susceptible to DM)
ADA Risk test
Screening tests for DM
Fasting BG
2Hr plasma glucose during oral glucose tolerance test OGTT - 75 mg
HgbA1c (not for DM1)
random plasma glucose
BGTT is using 75 g standarized form and 2 hrs later. a 2 hr postprandial is unstandardized 2 hours after a meal.
Metabolic syndrome criteria
Waist circumference: > 40in (M) or > 35in (F) Fasting TGs: > 150 OR on meds for it Metabolic Syndrome HDL cholesterol: < 40 (M) or < 50 (F) OR on meds (MetS)
BP: > 130 systolic or > 85 diastolic, or on meds Fasting plasma glucose: ≥ 100 OR on meds
3 +
being on meds for it counts
Risk factors type II DM
- WARM family BAG
Weight
Activity
Race- blacks, latinos, asisans, hawii, native americans
Metabolic syndrome -ANY aspects of metabolic syndrome - (clinical presentation part of it)
Family
B irthweight over 9 lbs (increases the moms risk of gestational DM)
Age
G lucose high - or A1C over 5.6% (prediabetes)
Clinical presentation of metabolic syn
increased waist circumference
HTN
acanthosis nigricans - velvety darkening of skin folds assoc w insulin resistant
Hepatic enlargement - if fatty liver present
hyperuricemia - gouty arthritis
PCOS - menstrual irreg, obese, hirutism, infertile
OSA -obesity and HTN
fasting plasma glucose, 2 hr plasma glucose, hemoglobin A1c in a normal person
70 to 99, less than 140, 4.0 to 5.6%
fasting plasma glucose, 2 hr plasma glucose, hemoglobin A1c in a diabetic
126, 200, 6.5%+
interfering factors glucose
increased
pregnancy elevates it - sometimes get gestastional diabetes.
HCT < 40%
interfering factors glucose - decreased
acetaminophen can make you hypoglycemic
uric acid level high
HCT > 50%
Uric acid causes insulin resistance
Hgb1Ac interfering decreased
decreased-
RBCs have to be around for a while to accumulate Aba1c - if you lose blood, create new fresh blood, and kill blood cells, it lowers it.
Hemoglobinopathies - HbF for example. if you have F you dont have enough H
Hgb1Ac interfering increased
splenectomy (spleen isnt around to kill/phagocytize old blood cells)
- prolonged stress increases your blood sugar, so if it goes on long enough your HgbA1c will pick it up and be increased
high blood glucose reasons
pancreatitis - if its inflamed then it won’t be making enough insulin
chronic renal failure - insulin resistance. it can also make glucose high or low
pancreatitis = sticky glucose pancakes
How much of Hgb is HbA1
HbgA is 7% of HgbA
proportion of hemoglobin A1 that has been glycosylated
8 to 12 weeks measure
Glucose Tolerance Testing -
75 mg in 300mL
30 m, 1 hr, 2, 3, 4 hr in AM
avoid physical activity b/c phys act increases insulin sensitivity
smoking is bad
C peptide and C peptide insulin ratio
eval of insulinomas, identify causes of hypoglycemia
C peptide is more stable and has a longer HL
C peptide - interfering factors - elevated
-renal failure because its renally excreted so it accumulates
-pancreas transplant: more pancreas more insulin
-sulfonylureas: zaps the insulin to make more
Ketones - test & interfering factors
eval presence of ketosis (blood or urine)
greater than 3 is concerning
during exercise, or ill, or cold, the body goes through its sugar supplies and starts using gluconeogeneisis
Vitamen C can interfere, valporic acid, levodopa, phenazopyridine (acids)
DM goals for non pregnant adults pts w DM
HgbA1c check every 3 to 6 mo <7%
fasting GH 80 to 130
post prand glucose 1-2h after - <180
contin. glucose monitors CGM - be in target range 70% of time
How many times do you check T1DM a day
3+/d
how many times a day do you check T2DM
1-2/d
Who is high protein diets NOT for (if they go on a low carb keto diet)
diabetic neuropathy
DM mangement besides pharm?
Medical Nutrition Therapy
routine vaccinations (they are considered ICP)
regular exercise, 150/min/wk of moderate aerobic exercise divded over 3+ days. no more than 2 d without exercise. no more than 90 min in a sedentary position.
Diabetes BP HTN goal
<130/80
1st line is ACE or ARB if elevated.
CCB or thiazide if they don’t have CAD or albuminuria
How often should diabetics get their HLD checked
HLD checked yearly. usually on moderate to high intensity statin (above age 40)
Antiplatelets Tx for diabetics
75-162 mg ASA for DM who have ASCVD or if their risk of developing it is calc to be more than 10%
& NO increased bleeding risk
Diabetics CVD screening and HF screening
NO ROUTINE SCREENING for CAD unless s/s
HF - screen all DM adult.
screen HF with a BNP. echo is abnormal.
Diabetes Peripheral vascular dz screening -
ankle brachial index IF -
50 y/o, or had DM for 10 years.
or have end organ damage from DM
or foot complications.
DM - nephropathy check in who?
- In every DM1 after 5 years of treatment - then check annual
- In all DM with HTN
- In DM2 at the time they are diagnosed
- protien intake should be 0.8
- ACE/ARB is pref. for proteinuria
- SerCreatine K+ BMP periodically
DM retinopathy
dialated and comprehensive eye exam first
DM1 - w/i 5 years for T1 of onset
DM2 - immediately
After first exam, do a dialated exam every year
can be every 2 years if you didn’t find anything in the first exam
Liver Disease in DM
70% of T2DM has non alcoholic fatty liver disease
Screen with** FIB-4 score:**
Obesity
CVD
Insulin Resist
50+
AST or ALT elevated > 6 mo
if moderate to high risk then rx GLP-1R agonist (semaglutide mimics incretins which reduces appetite)
predict to not need to know criteria but more need to know FIB -4 and se
DM Prediabetes - how to manage?
definition - Presence of impaired fasting glucose, impaired glucose tolerane, Alc 5.6-6.4%
tell patient to achieve 7% body wt loss and increase physical activity
Metformin - reduces risk of DM esp if are morbidly obese (BMI 35), if they are young (less than 60), or have had gestational diabetes in the past
Treat and screen for CVD (obese, HTN, HLD)
a greater life expectancy makes more sense to treat chronic issues
DM neuropathy -
- diabetic foot exam is yearly in T1Dm pts with at least 5 years of dx
- T2DM from onset
- screen by monofilament, and 1+ neuro test - pinprick, vibe, reflex)
- foot care edu
IF they have loss of foot sensation, deformities, PAD, or foot ulcer history, or amputee, always examine their feet at each visit
Type 1 diabetic treatment is what
Insulin tx
When would we give insulin to DM2
its last line
Insulin formula
0.5U/kg
50% basal
50% bolus to cover meals throughout the day
most units are 100
if i weigh 50 kg, then i need 25 U of insulin for the whole day. 50% (12.5 for basal) and 12.5 for bolus. I take 12.5 and divide that by three for breakfast lunch and dinner.
insulin pens are adjustable so that you can get exactly how much you want.
Insulin pumps are used for
it automatically injects insulin in you so that you dont have to manually inject yourself. high risk of hypoglycemia because you might not eat enough that day…
What is the starting guideline for carb counting before fine tuning it to each person
45 g/meal, 15g/snack for women
60g/meal, 30g/snack for men
Somogyi means what
-so much insulin. need to bring insulin down lower at bedtime.
-their body is countering the exogenous insulin so you want to lower the insulin.
AM rebound hyperglucemia - dip super low and go back up
Dawn phenomenon
-down insulin
increase the bedtime insulin dose but only if certain
AM hyperglycemia - naturally process, their sugar dips but not as low
Dosing regimen for basal bolus
3-4 times a day w meals
dosing regimen for mixed
dosed 2-3 /d and check 2-3 / d
dosing regimen for long acting
once a day
is analog insulin better than human insulin?
yes. its effect is more consistent and predictable. human insulin has more variation, absorption, and peak. analogs are more consistent . this is true for both basal and bolus dosing.
Biguanides are
metformin
thiazolidinediones are
Pioglitazone
sulfonylureas are
Glimepride
Glipizide
Glyburide
Meglinitides are
Repaglinide
Nateglinide
Risk of hypoglycemia
Sulfoynureas
meglinitides
pramlintides
insulin
Guidelines for non preg patients DM
HBa1c checked every 3-6 mo. <7%.
fast BG 80-130
PPBG less than 180
CGM 70% of the time
when to change target A1C
Hypoglycemia is more dangerous than hyper and we dont want to over-correct. if they have a severe hypoglycemic history then its fine to shoot for a higher A1C.
and if they are going to die next tuesday its ok if they have a lolipop.
<6% or <8% depending on the decision.
DM1 pharm plan
insulin pump or
DM2 pharm plan
- 1st line metformin + diet/ex
- if not impr, when they come back in 3 mo, add any other one except for bile acid sequestrants
- do it again for next time
- if still not improved then INSULIN + the rest
In what case do you give insulin at ONSET for DM2?
9% or more A1C
or significant hyperglycemia s/s (911?)
Alternative first line to metformin - when do you give alt treatments for DM2? What comorbidities?
ASCVD: GLP-1 tides or SGLT2
HF: SGLT2
CKD: SGLT2 or GLP-1
keep tides away from HF
SGLT2 is the kidney people
GLP-1 is the tide people
HTN and DM
130/80 on ACE or ARB esp if 1- year ascvd is >15%
Obesity and DM screening
- at EACH visit.
- calc BMI, mortality, poor DM outcomes
- assess patients readiness and motivation to pursue further weight loss
Obesity and DM diet - short term duration
<800 calories per day for < 3 months
Obesity and DM diet - long term duration
200 to 300 minutes a week exercise
reduce caloric intake
When would you talk about bariatric surgery with DM
when BMI is 30 or over
OR
poorly controlled diabetes
DM and wt loss medications
BMI 27
Tobacco and DM
increases incidence of what?
screen when?
it increases incidence of CV events
screening
EVERY visit- trying to convince them to quit smoking using 5 A’s
can use tobacco cessation meds
DKA vs HHS
- DKA - 250-600 glucose, HHS 600-1200
- DKA is less dehydrated. Osmol is 300 -320 for DKA.
- Osmol is 330 to 380 for HHS.
- pH 6.8-7.3 DKA , >7.3 in HHS
- DKA potassium elevated slightly
B-hydroxybutryate is…
manufactured 3x higher than other keyones in DKA
DKA management
- fluid replace -
4-5 L deficiet but only give them 1L/hr NS 0.9% for 1 hour
If they get salty, give them a dilute saline. 0.45%
- Insulin IV - 0.1U/kg, –>continutous IV. incr in 2-4 h if not better
- check FSBG Q1, electrlytes Q4, for 24 hours
- take vitals every 1 to 4 hours
- You have to watch for the cells once they get out of the acidotic state. the potassium will fly back into the cells, creating low potassium. no insulin until potassium is corrected. we dont want to create an emergency hypokalemia.
- K min 3.3
- Once their glucose is down to 200, you want to start adding sugar at that point to keep their sugar between 150 and 250.
- wait for resolution of ketosis and acidosis
9.
HHS management - what do you do different
6-10 L def. at first give them 1L 0.9% NS over 1 hr. change to 0.45%NS once stable. decr. rate of inf as vol status improves.
Insulin - IV bolus 0.1 U/kg.
serum glu reaches 250, change IV fluids to dextrose
serum glucose 250-300 mg/dL. reduces risk of cerebral
dextrose is sugar IV if you dont know
Diabetic Neuropathy - present, labs
or is it diabetic nephropathy?
intiitially, proteinuria. only the following can detect it:
SPOT urine albumin => x2
microalbumin above 30
macroalbumin above 300
Most accurate is the 24 h urine collection.
sugar damages the nervous tissue in the kidney
DM w/ CV conditions prevlaence of what is increased
30 x more chance of gangrene to your feet if you have CV with diabetes
3X CVA
5X CAD, PAD, MI, CHF
when can fingerstick glucose r/o hypoglycemia
venous is 65+ and fingerstick is 80+
Functions of cortisol
Actions of cortisol: Promotion of hepatic gluconeogenesis Inhibits peripheral tissue utilization of glucose by ↓ expression of GLUT (esp GLUT-4)
HHS classic presentation (not labs)
- Classic - elderly T2DM pt w/ several days of polyuria, polydipsia, weakness, ↓ oral intake,
- wt loss culminating in lethargy AMS or coma
- Hyperglycemia - polyuria, +/- polydipsia
- Leads to glycosuria, dehydration, and volume depletion
- May have hx of ↓ PO intake d/t lack of thrist, N, inaccessibility of fluids
- Hypotension, tachy d/t vol depletion
*
HHS/DKA pt edu
when your sugar gets past 300, check your ketones (OTC)
check it During illness or when ↓ oral intake is present: Freq capillary BG monitoring
Adeq fluid intake and appropriate insulin dosing
What percentage and what type of DM is retinopathy most common
DM2
60% after 16 years
what type gets diabetic nephropathy more
T1DM
but 30% of all DM patients
which skin complication of diabetes is treatable
Necrobiosis lipoidca diabeticorum - treat with topical steriods and imp BG control
Eruptive Cutaneous xanthomas - severe TG, control the TG
Candida - azole
Endogenous apo vs exogenous apo
Endogenous is apo-B100 (at liver round trip)
Exogenous is apo-B48 (at SI) and apo E to go back to the liver
in the blood they make a pit stop to reach peripheral tissues. to pass through blood they both use apo E and apo C. at peripheral they drop off some TG
what does the liver do with the TG?
it uses various proteins to break TG into FFA, and then create cholesterol –> bile
what % of the LDL is removed by the liver
70%. the rest is donated to the peripheral tissues
How much IDL is taken up by the liver?
40-60%.
The rest is broken down into hepatic lipase.
How does an HDL mature
HDL has apoA ticket. it uses it to pick up an LDL from a macrophage. when it does that, HDL matures.
HDL matures again by picking up cholesterol.
The cholesterol is deposited into the liver.
MCC dyslipidemia?
excessive hepatic secretion of VLDL
red triceratops, red dump trunk (HDL)
Where are eruptive xanthomas MC
butt
due to high TGs (chylomicrons) or VLDL
lipemia retinalis
high TGs
milky serum
high TGs
tendinous Xanthomas
high LDL
LDL monster
Who do we screen for Dyslipidemia
All adults 20+
Children 2+ if they have:
+ fmhx of early cvd or
+ fmhx of primary hypercholesterolemia
What do we order INITIALLY for dyslipidemia to SCREEN
Order total cholesterol (TC) and HDL - pref initial testing but usually order a full panel
Fasting vs. non-fasting → confirm abn results w/ fasting sample
Ind for a full panel: Total Cholesterol 250+, HDL less than 40
Non-fasting may result in falsely ↑ TG’s
Fasting Lipid FULL panel & numbers
TC less than 200
LDL less than 100
HDL betwen 40 and 60
TGs less than 150
must be 9 to 12 hr fast
What messes up a fasting lipid panel
exercise (increases HDL, lower TG and LDL)
OCPs (raise TG and total chol)
High stress (lowers HDL)
H for H igh stress
How often do you screen for Dyslipidemia for avg adult
5 years.
3 borderline.
Annually for those on treatment.
cease screening around 75 years old
Who always gets a statin?
190 LDL
When does pharmaceutical primary prevention start for ASCVD
ASCVD risk of 7.5%
What increases your risk of developing ASCVD
tobacco, DM, HTN, Obesity BMI 30+, FMHx premature heart dz (55M&65F), CAD, non coronary atherosclerosis, AAA, peripheral artery dz, carotid artery stenosis
anything that might make your blood vessels more narrow
these people do not yet have ASCVD
Clinical ASCVD diagnostic criteria
To 100% diagnose ASCVD
- acute coronary syndromes (MI or angina)
- Coronary arterial revascularization
- ischemic CVA (stroke)
- TIA
- PAD
Block, build, PAD
Determining Risk - general guideline
how dangerous is your 100% diagnosed CVD. we need to know the level to treat it in order to prevent it at the level you need
very high risk is 2 major ASCVD events OR 1 event and 2 high risk conditions
Major ASCVD events
how dangerous is your CVD? part1
ACS w/i past 12 months (MI, angina)
Had MI or ischemic stroke in the past
Symptomatic PAD
High risk conditions:
how dangerous is your ASCVD part 2
65 + y/o
CKD (CGF less than 60)
Coronary bypass
current smoker
DM
HTN
Hereditary familial hyperlipidemia
Hx of HF
LDL-C 100+ despite max tolerated statin + ezetimibe
65,CCCDHHHL
You have 100% ASCVD diagnosed.
How should we treat you?
First goal. Either choose a high intensity statin or a moderate intensity statin.
Second goal. High intensity = still time to live life (less than 75 y/o), OR very high risk ASCVD.
Moderate intensity = diagnosed with ASCVD and they don’t meet the above criteria
What is the goal of ASCVD lipid mangement?
The first goal is a 50% reduction in LDL-C
reassess in 1-3 months and then every 3-12 months.
The second goal is to reduce LDL so low that it stops the increasing risk of CVD events every year. This is determined as either 70mg or 55mg.
you will need to be at 55 mg goal if you have a family history with the baseline LDL at 190. OR you will need to be at 55 mg if you are a very high risk.
everyone else is 70 mg goal.
Primary HLD management
If anyone’s LDL is greater than 190, start a high intensity statin. reassess 1-3 mo then 3-12 mo. goal is 50% reduction then LDL less than 100.
Diabetes lipid management
calc 10 year risk via ASCVD online calculator and THEN look at diabetes specific factors to come up with a choice between two:
1) 10 yr risk > 7.5 OR + DM risk factors = high intensity statin
2) 10 yr risk < 7.5 AND - DM risk factors = moderate intensity statin
What are the Diabetes Specific High Risk Factors?
used to make a tx determination for prevention of ascvd on a diabetes patient
- had DM2 for 10 years
- had DM1 for 20 years
- albumin is greater than 30
- eGFR less than 60
- retinopathy
- neuropathy
- ankle brachial index <0.9
What are the diabetes specific goals for ASCVD prevention tx?
If on high intensity statins, they need a 50% reduction in LDL and an LDL less than 70
If on moderate intensity statins, need a 30-49% reduction in LDL and LDL less than 100
When do you give statins preventatively (when they dont have ASCVD)
To anyone at least 190 LDL, high intensity
If they have DM they automatically get at least moderate intensity
When they are under the age of 20 and have a family history
If under 40 and family history + LDL is 160+
If they are between 40 and 75 with LDL between 70 and 190:
- Perform ASCVD risk calculator online
- If between 7.5% and 20% risk, assess for risk enhancers
- if 20%+, they get a statin
5-7.5% risk for people between the ages of 40 to 75
and chol is less than 190 but greater than 70
Put on a moderate intensity statin if the Risk Enhancers are present
What about 7.5 to 20% - dx/tx plan?
If they are between a 7.5% and 20% risk,
look for risk enhancers. if present, put them on a moderate intensity statin.
If still uncertain, (no risk enhancers), order a CAC (coronary artery calcium scan). it measures the plaque in the heart.
What is CAC and what are the qualifiers
for people between 40 and 75, and LDL is between 70 and190
1) ASCVD risk btw 7.5 and 20%, and risk factor no present or uncertain.
2) the following:
* CAC more than 100 = add statin
* CAC 1 to 99 = add a statin after 55 y/o
* CAC 0 = no statin & Reassess CAC in 5 to 10 years
Risk Enhancing Factors for people b/w the ages of 40 to 75 with a LDL between 70 and 190
Fx of premature ASCVD
primary hypercholesterolemia
metabolic syndrome
CKD
chronic inflammation
Hx premature menopause or pre-clampsia
For people between the ages of 40 and 75, with a LDL between 70 and 190, what are the treatment goals (of prevention) from 7.5% to 20%
b/c they don’t have ascvd so we treat to prevent clinical ascvd
If between 7.5% and 20%, goal of moderate intensity statin is to reduce the LDL by 30% and LDL under 100
For people between the ages of 40 and 75, with a LDL between 70 and 190, what are the treatment goals (of prevention) of beyond 20% calculated risk
reduce 50% reduction of LDL
lower LDL under 70
(we don’t want to make their risk of CVD events higher because its already so high)
High intensity statins rx
atorvastatin 40 mg
rosuvastatin 20 mg
if can’t tolerate the statin you give
try another statin such as fluvastatin or pravastatin
Hypertriglyceridemia screen/tx
Screen for 20 y/o and up
defintion is above 150 TG
* severe TG is 1000 alone - tx with pharm
* 40-75 y/o above 500 TG and ASCVD of 7.5% - tx with pharm
* everyone else lifestyle changes
What is severe hypertriglyceridemia caused by?
pancreatitis
MEN1 screening
2+ MEN1 assoc endo tumors
1st degree relatives w MEN1 mutation carrier even if asymptomatic
perform DNA genetic test
prognosis is 50% death by age 50 yr old
MEN2 screening
All patients with MTC even if family history doesn’t have it
d/t de novo germline RET mutation
patients with bilateral pheo or unilateral pheo as well esp with increased calcitonin levels
