Endocrine Exam 2

Front 1

3 Macronutrients and percentage they should make up in the diet

Back 1

Carbs 50-60%
Fats 20-30%
Protein 15-20%

Front 2

This macronutrient increases TG stores by increasing adipose tissue uptake of glucose.

Back 2

Carbs

Front 3

This macronutreint does growth and tissue maintenance, is the 2ndary energy source, and may need to be limited in renal disease.

Back 3

protein

Front 4

_____ fats increase cholesterol.

Back 4

saturated

Front 5

Type 2 diabetics should restrict Na to what level.

Back 5

<2 grams/day

Front 6

Type 2 diabetic's CHO meal restriction? (women; men)

Back 6

women:45-60 grams/ meal

Hint 6

male: 60-75 gm/meal

Front 7

Type 2 diabetic's CHO snack restrictions.

Back 7

15-30 grams/snack

Front 8

ICU patient's goal blood glucose

Back 8

140-180 mg/dL

Front 9

non-ICU patients' goal blood glucose (pre-meals, random)

Back 9

<140 mg/dL

Hint 9

<180 mg/dL

Front 10

Dangerous blood glucose level for ICU patient?

Back 10

<110 mg/dL

Front 11

What form of insulin should ICU patients get? What about non-ICU patients?

Back 11

IV

Hint 11

Subcutaneous

Front 12

What 2 reasons allow a "diabetic" inpatient to get oral agents?

Back 12

1. clinically stable non-ICU patient
2. consumes meals at regular intervals

Front 13

This sulfonylurea has active metabolites; is 50% renally excreted and not recommend at all for inpatient care.

Back 13

Glyburide

Front 14

What organ should be continually watched while a patient is on a sulfonylurea? Why?

Back 14

Kidneys

Hint 14

bc sulfonylureas promote insulin secretion, which is eliminated by the kidneys

Front 15

Onset, peak and duration of Regular (short acting) insulin?

Back 15

onset: 30-60 min
peak: 2-4 hours
duration: 6-10 hours

Front 16

Onset, peak and duration of rapid acting insulin?

Back 16

onset: < or = to 15 min
peak: 1-2 hours
duration: 3-5 hours

Front 17

Onset, peak and duration of Lantus (long-acting)?

Back 17

onset: 1 hour
peak: NO PEAK!!!
duration: 24 hours

Front 18

Onset, peak and duration of NPH (intermediate acting)?

Back 18

onset: 1-4 hours
peak: 6-10 hours
duration: 12+ hours

Front 19

ADA's pre-prandial glucose levels?

Back 19

90-130 before meals

Hint 19

<180 (about 2 hours after meals)

Front 20

During exercise, insulin sensitivity increases or decrease?

Back 20

increases; so don't need as much insulin as before (rm: DM type 2 patients are insulin insensitive)

Front 21

For intensive insulin therapy, basal daily dose is _____ % of total and ____ % is a bolus.

Back 21

50-70% (basal - before bk, lunch, and dinner)

Hint 21

30-50% (bolus - before bedtime)

Front 22

70/30 Humulin/Novolin is what combo? When can you eat once inject?

Back 22

70% NPH
30% regular

Hint 22

must wait 30 minutes

Front 23

70/30 Novolog mix is what combo? When can you eat once inject?

Back 23

70% aspartate protamine
30% aspartate

Hint 23

immediately

Front 24

Which insulin dosage is more often to cause nocturnal hypoglycemia?

Back 24

conventional method (BID)
not good for type 1

Front 25

For conventional insulin dosing, ___ is given in the AM and ___ is given in the PM.

Back 25

2/3
(of which 70% is NPH and 30% is regular)

Hint 25

1/3
(of which 70% NPH and 30% regular)

Front 26

In the Correctional insulin regimen the denominator tells what?

Back 26

how insulin sensitive the person is
(the lower the number the more insensitive the person is; so the bigger the person = more insulin insensitive)

Front 27

Weight gain of conventional insulin dosing?

Back 27

4-8 lbs for every 1% point decrease in A1C

Front 28

Unless there our CI's a diabetic patients should be on ____ and ____.

Back 28

lifestyle modifications
metformin

Front 29

Does Pioglitazone cause hypoglycemia? Do GLP-1 agonist?

Back 29

no

Hint 29

no

Front 30

Basal insulin and sulfonylureas cause what two adverse effects?

Back 30

weight gain
hypoglycemia

Front 31

Once FBG is at goal, what is the next target?

Back 31

pre-meal blood glucose levels; as well as bedtime

Front 32

Starting dose of insulin (Lantus at bedtime or NPH at bedtime or in AM)?

Back 32

10 units
(or 0.2 units per kg)
titrate up unitl FBG < 100

Front 33

What 3 drug interactions are there with metformin?

Back 33

cimetidine
fluoroquinolones
radiographic contrast dye

Front 34

Scr limitations for Metfromin patients?

Back 34

Male Scr > 1.5
Female Scr > 1.4

Front 35

What does Metformin do to vitamin B12 absorption?

Back 35

decreases

Front 36

What should you warn the patient on rosiglitazone about?

Back 36

edema (look for s/s of heart failure)

Front 37

What 4 labs should be monitored if a patient is on Thiazolidinediones?

Back 37

LFTs, BG, A1C, and LDLs

Front 38

How long does it take the glitazones to work? Dpp-4 inhibitors?

Back 38

3-4 months

Hint 38

3-4 weeks for DPP-4 inhibs

Front 39

This diabeteic drug class increases satiety, slows gastric emptying, decreases postprandial glucagon release and preserves beta cells?

Back 39

GLP-1 Analogs
(byetta)

Front 40

For which diabetic med should the patient be educated about increases of UTI or sinusitis incidence?

Back 40

DPP-4 inhibitors

Front 41

Dose for Sitagliptin? Renal adjustment doses?

Back 41

50 - 100 mg qo

Hint 41

GFR 30-50 use 50mg/daily
GFR <30 use 25 mg/daily

Front 42

This DPP-4 Inhib is metabolized by CYP3A4 and must be dropped down to a dose of 2.5mg qd when on 3A4 inhibs.

Back 42

Saxagliptin (Onglyza)

Front 43

T/F. Sitagliptin has many drug-drug interactions.

Back 43

False
(none to date)

Front 44

This diabetic drug increases hepatic glucose production.

Back 44

glucagon
(emergency med, given IV, IM or SQ)
VOMITING

Front 45

A mild hypoglycemia patient can receive what 3 things to raise BG rapidly?

Back 45

4 oz of OJ
4 oz of regular soda
4-8 breath mints
(all followed by a high carb meal)

Front 46

After a diabetic patient exercises, how long should they monitor BG for low levels? Why?

Back 46

at least 2 days

Hint 46

bc 24-48 after exercise the body is replenishing the glycogen stores - making hypoglycemia still a risk

Front 47

Glucagon, epinephrine, norepinephrine and growth hormones all _____ during exercise.

Back 47

increase

Front 48

During exercise hepatic BG production ___ and FFA breakdown ___.

Back 48

increases

Hint 48

increases

Front 49

What is the benefit of exercise in a Type 1 patient?

Back 49

decrease CAD risk
(but A1C doesn't typically decrease)

Front 50

What 3 things can worsen in diabetic's exercise?

Back 50

Retinopathy
Nephropathy (inc proteinuria)
Peripheral neuropathy (feet)

Hint 50

weight lifting can be a huge cause

Front 51

Which patients are more so prone to get lactic acidosis while taking metformin?

Back 51

RENAL INSUFFICIENCY!!!
heart failure
hypoperfusion
older age
chronic pulmonary dis

Front 52

_____ (drug) has shown an association with the risk of ischemic myocardial events.

Back 52

Rosiglitazone (Avandia)

Front 53

Insulin causes an ______ shift of K+ in the body.

Back 53

Intracellular
(pulls K+ into the cells from the blood --> why insulin used for hyperkalemia)

Front 54

What % of insulin used in the ICU is given when patient is moved to the floor?

Back 54

75-80%

Front 55

While giving an inpatient insulin you should monitor BG ____ and Scr and K+ ____.

Back 55

check BG hourly, then every 2-3 hours

Hint 55

daily

Front 56

Which insulin brand is typically used for basal insulin? For nutritional insulin?

Back 56

Lantus

Hint 56

Novolog

Front 57

What 3 components must be covered to a non-ICU type 1 patient?

Back 57

basal
nutritional
supplemental or correctional

Front 58

Insulin aspart?

Back 58

Novolog

Front 59

Insulin lispro?

Back 59

Humalog

Front 60

Insulin glulisine?

Back 60

Apidra

Front 61

Which insulin is used in ICU patients?

Back 61

Regular (Humulin)
Why is no benefit in using analog insulin with these patients?

Hint 61

because it's give IV not SQ thus get absorbed just as quickly as analogs (different in SQ admin)

Front 62

This insulin has an onset of 2-4 hrs, has no peak theoretically, and can last 20-24 hours.

Back 62

Insulin glargine (Lantus)

Front 63

Insulin glargine

Back 63

Lantus

Front 64

If blood glucose is 100-199, then what should the lag time be?

Back 64

10-20 minutes

Front 65

If blood glucose is 200-299, then what should the lag time be?

Back 65

20-30 minutes

Front 66

This insulin has an onset of 5-15 minutes, peaks in 60-90 minutes, and last for 4-6 hours.

Back 66

analogs
(used for nutritional purposes)

Front 67

Is NPH a good choice for inpatients?

Back 67

no

Front 68

How do you calculate the insulin sensitivity factor (or correction factor)?

Back 68

(1500 or 1800) / (total daily insulin)
more than likely always 1800
rapid analogs should be used for correction/nutrition

Front 69

Name 5 risk factors of Metabolic Syndrome?

Back 69

abdominal obesity (> 35, 40)
TG (>150)
HDL (<50, 40)
BP (>130/85)
Fasting Blood glucose (>100)

Hint 69

any of the 3 = metabolic syndrome

Front 70

The history of what 3 things increases the risk of Type 2 DM?

Back 70

baby > 9 lbs
HTN
dyslipidemia

Front 71

Above what age is a person at a higher risk of DM type 2? At what BMI?

Back 71

40

Hint 71

BMI > 26
(or greater than 120% of IBW)

Front 72

What is PCOS? What is it's significance?

Back 72

Polycystic ovarian syndrome

Hint 72

increases women's risk of type 2 DM

Front 73

What is Acanthosis nigricans due to? What is it's significance?

Back 73

due to insulin resistance

Hint 73

increases risk of type 2 DM

Front 74

What are the 3 P's of hyperglycemia's signs?

Back 74

Polyureia
Polydyspia (thirst)
Polyphagia (hunger

Hint 74

dry skin, yeast infections, blurred vision, Nausea, fatigue, wt loss, and ED are other signs of hyperglycemia

Front 75

DM diagnostic guideline...if FBG is over ___.

Back 75

126

Front 76

DM diagnostic guidelines...if admin a glucose load and BG is over ___ after 2 hours.

Back 76

200

Front 77

DM diagnostic guidelines...if casual BG is over ___.

Back 77

200

Front 78

Prediabetic BG range?

Back 78

100-125
(impaired glucose tolerance)

Front 79

How do you calculate the estimated average glucose (eAG)?

Back 79

(28.7 x A1C) - 46.7 = eAG

Front 80

Direct and indirect cost of DM in 2007 = ?

Back 80

$174 billion

Front 81

The DCCT trial implied that "Intensive treatment was possible and it ___ microvasc complications in Type ____ DM."

Back 81

lowered

Hint 81

type 1

Front 82

The UKPDS trial implied that" Intensive care for Type 2 DM was important. And that at least ___ meds were needed plus ____. (or an average insulin dose of ____ units/day)

Back 82

2

Hint 82

metformin
(100)

Front 83

In the ACCORD trail results showed that there was an ____ incidence of CVD death in the group with a target A1C of ___.%

Back 83

increased

Hint 83

<6

Front 84

In the ACCORD trial, which group was better off?

Back 84

the ones with A1C goal of 7-7.9%; SBP goal of <140; and cholesterol treatment of only a statin

Front 85

The ADVANCE trial, results showed that their was no significant changes in macrovascular events, cardio events, or death if the A1C was pushed down to ____ % vs an A1C of ___%.

Back 85

<6.5

Hint 85

7.5

Front 86

Could a virus lead to diabetes?

Back 86

Yes; an environmental insult like a virus could lead to Beta cell damage in the pancreas - leading to type 1 DM

Front 87

Due to IRS being blocked from insulin resistance, what happens?

Back 87

atherosclerosis and inflammtion

Front 88

(In DM) There is an increase in FFA because of a ___ in insulin secretion, increase in hepatic glucose production, and a(n) ___ in insulin sensitivity

Back 88

decrease

Hint 88

decrease

Front 89

What blocks tyroisin phosphorylation of IRS-1 (causing a dec in insulin sensitivity)

Back 89

FFA

Front 90

Which diabetic drug class increases IRS1 activity but also blocks the Shc activity?

Back 90

TZD's (glitazones)

Front 91

In a nutshell, what does insulin tell the liver?

Back 91

to stop making glucose (which doesn't happen in type 2 patients)

Front 92

T/F. DM patients lack gut factors that decrease hepatic glucose uptake.

Back 92

FALSE
(the gut factors INCREASE hepatic glucose uptake --> type 2 pts lack these factors, which is another reason why BG is high)

Hint 92

as a result of this there's an inc in PPG & a dec in hepatic insulin sensitivity

Front 93

What do GIPs do to insulin secretion? Is there enough GIPs in type 2 DM patients?

Back 93

increases insulin secretion

Hint 93

yes, but response to the GIPs in T2DM's = not normal

Front 94

Will GIPs help with T2DM patients? Why or why not?

Back 94

no

Hint 94

bc they won't increase insulin nor lower BG (remember levels = normal in type 2's)

Front 95

What will GLP-1's do to glucagon, beta-cells, GI, and insulin? Are they efficent in type 2 diabetics?

Back 95

dec glucagon
inc beta-cell fxn
dec GI emptying
inc glucose-depdt insulin release

Hint 95

yes (even tho levels are low in T2DM patients)

Front 96

What happens to posterior hypothalamus in obese subjects?

Back 96

it lowers sensitivity to glucose & causes over-eating

Front 97

About how much of 180gm of glucose is reabsorbed daily in a normal person? In a type 2 diabetic person?

Back 97

100%

Hint 97

up to 180%
(high BG!!)

Front 98

Do type 2 diabetic patients typically have insulitis? Beta-cell depletion?

Back 98

no

Hint 98

yes
(residual; chronically low)

Front 99

Which type diabetes has amyloid deposits? 50% concordance with monozygote twins?

Back 99

type2

Hint 99

type1

Front 100

Which diabetes has atrophy & fibrosis? Has a clinical age onset of 30+ and a typical BMI of >30?

Back 100

type1

Hint 100

type2

Front 101

During hyperglycemia, patients get _____ of polypeptides (of same protein) and a(n) ____ in lipid oxidation.

Back 101

crosslinking

Hint 101

increase

Front 102

During hyperglycemia, patients get ____ of PKC, thus leading to a(n) ____ in vascular permability and neovascularization.

Back 102

alterations

Hint 102

increase

Front 103

During hyperglycemia, cells that bind glucose get a(n) ___ in affectiveness. And ____ of NO.

Back 103

decrease

Hint 103

inactivation

Front 104

What do macrovascular effects include?

Back 104

Heart attack, stroke and HTN
(be aggressive in their treatment for a diabetic patient)

Front 105

What 2 drugs are good to use for the peripheral neuropathy (a microvasular effect of DM)?

Back 105

gabapentin or lyrica
(TCA's = too many SE's)
even capscian)

Front 106

Can you give a DM patient drugs for retinopathy?

Back 106

no prefer to tx with laser surgery

Front 107

DKA is primarily in type __ diabetics. HHS is primarily in type __ diabetics.

Back 107

1
(bc of ABSOLUTE insulin deficiency)

Hint 107

2
(bc of RELATIVE insulin deficiency)

Front 108

3 components of DKA? Of HHS?

Back 108

hyperglycemia
acidosis
ketosis

Hint 108

hyperglycemia
dehydration
hyperosmolality

Front 109

T/F. DKA and HHS share the following in common: increased counter regulatory hormone concentrations.

Back 109

true
(it's the absolute vs relative insulin def that leads to them specially)

Front 110

What is the major preceipitating factor of HHS/ DKA?

Back 110

infections!!! (most common)

Hint 110

others:
d/c of home insulin regimen
meds
MI's
pancreatitis
new onset of type 1 DM
dec water intake (esp in elderly)

Front 111

At what BG range do HHS present? What pH?

Back 111

>600

Hint 111

>7.3
(so not an acidosis disease unlike DKA)

Front 112

How do you find the anion gap?

Back 112

Na - (Cl + HCO3) = anion gap

Hint 112

A DKA pt would have an increased anion gap (bc acidosis)

Front 113

What is the serum sodium concentration of a DKA patient? K+ concentration?

Back 113

decreases
(bc water comes out of cells thus diluting Na in blood)

Hint 113

increases
(bc acidosis causes K+ to leave cell and go into the blood -- opposite of insulin's effect on K+)

Front 114

When do you add dextrose to a DKA patient? To a HHS patient?

Back 114

at DKA pt with a BG >200

Hint 114

At a HHS pt with a BG of >300

Front 115

What is the primary goal of insulin therapy? Secondary?

Back 115

lipolysis
(no this is happening when bicarbonate goes back up)

Hint 115

get BG down

Front 116

When do you give K+ to a acidotic patient?

Back 116

if low (<3.3) or at normal levels
(rm: with acidosis the K+ serum levels will be artifical and lower than really are)

Front 117

At what pH would you start giving bicarbonate?

Back 117

pH < 6.9
(severe acidosis)

Front 118

What are the 2 drug interactions of glyburide and glipizide?

Back 118

alcohol (limits gluconeogensis --> why must be limited to <2 drinks/day)
fluoroquinolones

Front 119

These diabetic drugs have beta cell burn out, loss effect after 4-5 years, and can cause 5-15 lbs weight gain?

Back 119

sulfonylureas

Front 120

Why do liver and kidney functions be monitored while on sulfonylureas?

Back 120

bc if functions decline could cause an accumlation of insulin (their MOA) and thus more hypoglycemia

Front 121

Brand and use of Bosentan?

Back 121

Tracleer

Hint 121

treats pulmonary HTN

Front 122

What drug reaction occurs with glyburide and bosentan?

Back 122

increase liver damage
(CI!!!)

Front 123

Can a person skip meals while on a sulfonylurea? How much do they lower FBG/A1C?

Back 123

no!

Hint 123

50-80 points
(A1C lowered 2% if starts off at 9%)

Front 124

How much do glitazones lower FBG/A1C? Can they cause some weight gain?

Back 124

50-70 points of FBG
(1-1.5% dec in A1C)

Hint 124

yes can inc wt (due to edema and adipose)

Front 125

This diabetic drug class is a PPAR gamma agonist that inc insulin sensitivity especially in the periphery.

Back 125

glitazones

Front 126

Are glitazones beta cell sparing? Are GLP-1 agonists?

Back 126

yes

Hint 126

yes

Front 127

17% of patients on GLP-1 agonist get this?

Back 127

nausea

Front 128

T/F. Metformin and DPP-4 I's cause weight LOSS.

Back 128

true

Front 129

How much does Byetta decrease FBG/A1c? Can it be taken with insulin?

Back 129

50-60 points off FBG
(0.8-1.4% off A1c if starts at 8.5)

Hint 129

no
physically incapable with insulin

Front 130

Can Byetta and metoclopramide be taken together?

Back 130

no
spread apart (also for other fast acting meds)

Front 131

This diabetic drug class increases GLP-1 levels, is well tolerated, but has a smaller decrease in A1C than others?

Back 131

DPP-4 inhibs

Front 132

How much do DPP-4 I's decrease FBG/A1C? Are they inexpensive?

Back 132

15-20 points of FBG
(0.8% dec in A1C)

Hint 132

no they are expensive

Front 133

Does Metformin XL cause weight loss?

Back 133

no

Front 134

What rxn is there with metformin and fluoroquinolones? With cimetdine?

Back 134

causes hypoglycemia

Hint 134

dec metformin's clearance thus increases it's blood conc

Front 135

Can you get an increase in BP and TG on metformin?

Back 135

no
a decrease

Front 136

What 3 labs should be monitored while on metformin? is this drug beta cell sparing?

Back 136

CBC, SCr, LFTs

Hint 136

yes

Front 137

At what percent is it lactis acidosis?

Back 137

<0.03%
(rare ADR with metformin)

Front 138

How much does metformin decrease FBG/A1C?

Back 138

50 points off FBG
(dec A1C by 1.5% if start at 9%)

Front 139

For which diabetic drug class is osteoporosis an AE?

Back 139

glitazones