397 DM Mgt Flashcards
Chap 397. Diabetes Management and Treatment
OHA with proven cardiovascular safety
Empagliflozin
OHA not given to patients with CHF FC III- IV
Pioglitazone
OHA given for patients with renal disease
Linagliptin
Anti diabetic agent with proven cardiovascular safety for DM type 1
Liraglutide
Anti diabetic agents what may be given to DM type 1
Amylin agonist
Alpha glucosidase
Anti diabetic agent that can decrease appetite
GLP 1 agonist: exenitide and liraglutide
Why is NaHCO3 is not given immediately to patients with DKA?
It can cause Hypokalemia, decreased cardiac output and decreased oxygenation
Name 2 fruits with low sucrose
Grapes
Avocado
Main component of mediterranean diet
Olive oil
US equivalent of gliclazide
Glibenclamide
Which is a main advantage of Metformin
Weight loss
Lowers Lipid profile
Target HbA1c for most individuals
HbA1c less than 7
Target HbA1c for DM Type 1
HbA1c less than 6.5
Target HbA1c for elderly, chronic illness and bedridden
HbA1c less than 8 or 8.5
Reflects glycemic status over the prior 2 weeks
fructosamine assay (measuring glycated albumin)
Reflects glycemic history over the previous 2-3 months
glycated hemoglobin
insulin- carbohydrate ratio
1-1.5 units/ 10 grams CHO
What is amylin and name an example of amylin analogue
Amylin is secreted by pancreatic beta cells together with insulin. A decrease in insulin also means a decrease in amylin
Example of amylin analogue is pramlintide
What is the side effect of pramlintide
slowing gastric emptying
Major toxicity of metformin
lactic acidosis
Analogue of GLP-1 identified in the saliva of the Gila monster
Exenatide
Reduce insulin resistance by binding to PPAR-gamma
Thiazolidinediones
Highest levels of PPAR gamma is found where?
Adipocytes
Contraindicated in CHF Class III and IV
Thiazolidinediones
Necessary for DKA to develop
insulin deficiency and glucagon excess
At what pH is HCO3 given in DKA
ph less than 7.0
How is metabolic acidosis treated in DKA
HCO3 50 meq in 200 Sterile water with 10 meqs KCL per hour for 2 hours until pH more than 7.0
Two ketones produced by DKA
beta hydroxybutyrate and acetoacetate
How can a patient have DKA when urine ketone is negative
Only acetoacetate and acetone are detected by urine assay; the other ketone iin DKA, beta hydroxybutyrate is detected in the serum
Why is IVF changed to 0.45% once CBG reaches 250 mg/dl
To avoid hyperchloremia
Underlying cause of HHS
relative insulin deficiency and inadequate fluid intake
Preferred diet for T2DM
Mediterranean diet rich in polyunsaturated fat
Sodium intake in T2DM
same as general population
True or false. Sucrose food allowed with adjustment in insulin dose
True.
Treatment goals T2DM. HbA1c
less than 7.0%
Treatment goals. Preprandial glucose
4.4-7.2 mmol or 80-130 mg/dl
Treatment goal T2DM. Postprandial glucose
less than 10 mmol or less than 180 mg/dl
Treatment goal T2DM. Blood pressure
Less than 140/90
Treatment goal T2DM. LDL
less than 2.6 mmol or less than 100 mg/dl
Treatment goal T2DM. HDL
more than 1 mmol or more than 40 mg/dl
Treatment goal T2DM. Triglycerides
less than 1.7 mmol or 150 mg/dl
True or false. To avoid exercise related hyper or hypolgycemia, individuals with Type 1 should monitor blood glucose before, during and after exercise
True.
blood glucose levels to delay exercise
more than 14 mmol or more than 250 mg/dl with ketones; less than 5.6 mmol or less than 100 mg/dl
What to do with insulin dose if planning to exercise
decease insulin dose before or after exercise and not to inject nonexercising area
relative contraindication to exercise and why?
untreated proliferative retinopathy and this may lead to vitreous hemorrhage or retinal detachment
reflects average glycemia control over the previous 2-3 months
HbA1c
standard method for assessing long term glycemic control
HbA1c
HbA1c equivalent. 6%
7 mmol or 126 mg/dl
HbA1c equivalent. 7%
8.6 mmol or 154 mg/dl
hbA1c equivalent. 8%
10.2 mmol or 183 mg/dl
hbA1c equivalent. 9%
11.8 mmol or 212 mg/dl
hbA1c equivalent. 10%
13.4 mmol or 240 mg/dl
hba1c equivalent. 11%
14.9 mmol or 269 mg/dl
hbA1c equivalent. 12%
16.5 mmol or 298 mg/dl
ADA recommendation of HbA1c
2x a year or every 3 months if there has been change in therapy or there is inadequate glycemic control
reflects glycemic status over the prior 2 weeks
fluctosamine assay
alternative indicator when HbA1c is inaccurate
1,5- anhydroglucitol
Frequency. Eye examination
annual or biannual
Frequency. Foot examination.
by physician: 1-2 times/year; by patient: daily
Screening for diabetc nephropathy
annual
Frequency. Lipid profile and serum creatinine
annual
HbA1c goal for elderly, chronic illness and impaired activities of daily living
HbA1c 8.0- 8.5%
target HbA1c for most individuals
less than 7%
True or false. More stringent HbA1c target of less 6% is no beneficial
True.
Short acting insulin examples
aspart, glulisine, lispro, regular, inhaled human insulin
Onset. Peak. Duration. Regular insulin
O: 30- min 1 hr P: 2-3 hrs D: 3-6 hrs
Onset. Peak. Duration. Lispro
O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs
Onset. Peak. Duration. Aspart
O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs
Onset. Peak. Duration. Glulisine
O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs
Short acting insulin with same onset, peak and duration of action
lispro, aspart, glulisine
long acting insulin examples
degludec. Detemir, glargine, NPH
long acting insulin with no peak.
degludec. Detemir, glargine
Onset. Duration. Degludec
O: 1-9 hrs D: 42 hrs
Onset. Duration. Detemir
O: 1-4 hrs D: 12-24 hrs
Onset. Duration. Glargine
O:2-4 D: 20-24 hrs
Onset. Duration. NPH
O: 2-4 P: 4-10 D: 10-16 hrs
True or false. Aspart, lispro and glulisine is preferred over regular insulin in controlling prandial glucose
True.
how is insulin glargine differ from normal insulin
asparagine is replaced by glycine in amino acid 21 and two arginine residues added to C terminus of B chain
insulin the has a fatty acid side chain that reversibly binds to albumin
detemir
insulin that forms multihexamers in subcutaneous tissues prolong its duration of action
degludec
required prior to prescribing inhaled insulin
FEV1 should be measured;
side effect of inhaled thus avoided in this subset of patients
inhaled insulin can cause cough and bronchospasm; avoid in patients with lung disease or who smoke
insulin dose formula based on prepandial glucose
1 unit for every 2.7 mmol or 50 mg/dl over the preprandial glucose target
T2DM agents side effects. Flatulence
alpha glucosidase inhibitors. Acarbose. Voglibose
T2DM agents side effects. GI upset
biguianides. Metformin
T2DM agents side effects. Edema, CHF
thiazolidenediones. Pioglitazone
T2DM agents side effects. UTI, dehydration
SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin
T2DM agents side effects. Hypoglycemia
sulfonylureas. Glibenclamide, glimepiride, gliclazine
T2DM agents. Causes weight gain
insulin, sulfonylureas, thiazolidinediones
T2DM agents weight neutral
DPP4 inhibitors, alpha glucosidase inhibitors
T2DM agents causes weight loss
Metformin, SGLT2 inhibitors, pramlintide, GLP1 agonist
T2DM that doesn’t directly cause hypoglycemia
metformin, alpha glucosidase inhibitors, DPP4 inhibitors, GLP1 agonist, TZD, SGLT2 inhibitors
class of agents that reduces hepatic glucose production and improves peripheral glucose utilization
biguianides. Metformin
True or false. Metformin reduced fasting plasma glucose and insulin levels, improves lipid profile and promotes modest weight loss
True.
major toxicity of metformin
lactic acidosis
maximum dose of metformin
2000 mg daily
EGFR when metformin dose should be reduced
EGFR less than 45 ml/mim
class of agents that stimulate insulin secretion by interacting with ATP sensitive potassium channel on the beta cell
sulfonylureas. Glibenclamide, glimepiride, gliclazine
True or false. Weight gain is a common side effect of sulfonylurea therapy
True.
analog of GLP1 initially identified in the saliva of the Gila monster
exenitide
class of agents that amplify glucose stimulated insulin secretion
GLP1 agonist
class of agents that inhibit degradation of GLP1
DPP4 inhibitors
class of agents that reduce postprandial hyperglycemia by delaying glucose absorption
alpha glucosidase inhibitors. Acarbose. Voglibose
True or false. Alpha glucosidase inhibitors can increase levels of sulfonylureas
True.
creatinine threshold for alpha glucosidase inhibitors
cannot be given to patients with creatinine more than 2 mg/dl or 177 mmol
class of agent that reduce insulin resistance by bind to PPAR-gamma
TZD
PPAR-gamma receptors are found highest where?
adipocytes
class of agents that inhibit the sodium glucose co transporter
SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin
Where are SGLT2 co transporter expressed
proximal convoluted tubule in the kidney
associated BP reduced with use of SGLPT2 inhibitors
reduced in 3-6 mm Hg SBP
associated with Euglycemic DKA
SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin
what happens in euglycemia DKA
ongoing glucosuria masks stress induced requirements for insulin
PE finding in DKA not observed in HHS
nausea, vomiting, abdominal pain, Kussmaul respirations
underlying causes of HHS
relative insulin deficiency and inadequate fluid intake
when should ketone be measures in patients with diabetest
when CBG is more than 13.9 mmol or more than 250 mg/dl
what ketone is measured in blood? In urine?
blood: beta hydroxybutyrate; urine: acetoacetate and acetone
prominent features of DKA
nausea and vomiting
serious complication of DKA
cerebral edema
pathophysiology of DKA
relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catehcolamines, cortisol, and growth hormones)
biochemical characteristic necessary for DKA
insulin deficiency and glucagon excess
True or false. Insulin deficiency and glucagon excess shift the handling of pyruvate to glucose synthesis instead of glycolysis
True.
enzyme that alters hepatic metabolism to favor ketone body formation
carnitine palmitoyltransferase
characteristic of DKA
hyperglycemia more than 13.9 mmol or more than 250 mg/dl, ketosis and metabolic acidosis
metabolic acidosis in DKA
HCO3 less than 15 meq and increased Anion gap
True or false. In DKA, amylase is of salivary origin is not diagnostic of pancreatitis
True.
Laboratory tests to get is pancreatitis suspected in a patients on DKA
serum lipase
in DKA, ketone body synthesized 3x greater than the other
beta hydoxybutyrate
differential diagnosis of DKA
starvation ketosis, alcoholic ketosis (but HCO3 more than 15 meq/L)
fluid replacement in DKA
2-3 L of 0.9% saline over first 1-3 hrs (10-20 ml/kg/hr) then 0.45% at 250-500 ml/h; change to 5% glucose containing and 0.45% saline at 150-250 ml/hr when plasma glucose reaches 250 mg/dl or 13.9 mmol
how to administer insulin in DKA
0.1 units/kg bolus then 0.1 unit/kg per hour; increase 2x-3x if no response by 2-4 hrs
how replace K in DKA
if K is 5.0-5.2, give 10 meq/hr; if K is less than 3.5 meq/L, give 40-80 meq/h
what to watch out when planning to give insulin infusion
make sure serum potassiums is not less than 3.3 meq/L
how to adjust insulin once DKA resolve
infusion rate decreased to 0.02/0.1 units/kg/hr
when to transition from insulin infusion to long acting insulin in combination with SC short acting insulin
when patient starts to eat
why is insuliin infusion continued even when CBG is 250 mg/dl
to inhibit ketogenesis
True or false. As ketoacidosis improves, beta hydorxybutyrate is converted to acetoacetate and it can appear to be increased on urine assay using nitroprusside reaction
True.
how is metabolic acidosis treated in DKA
50 meq HCO3 in 200 cc sterile water to run for 2 hours until pH is more than 7.0
when to give HCO3 in DKA
when ABG ph is less than 7.0
when is do need supplement for serum phosphate
if less than 0.32 mmol or less than 1 mg/dl
prototypical patient with HHS
elderly, T2DM, diminished oral intake, polyuria that culminates in mental confusion, lethargy or coma
PE findings in HHS
tachycardia, hypotension, dehydration, altered mental status
laboratory findings of HHS
hyperglycemia usually more than 5.5 mmol or 1000 mg/dl, hyperosmolality more than 350 mOsm/L and pre renal azotemia
fluid replacement in HHS
1-3 L of saline over 2-3 hr; if serum sodium more than 150 meq/L to use 0.45%; free water deficit should be corrects in 1-2 days; once hemodaynamically stable, correct free water deficit with 0,.45% then D5W
what is steroid induced hyperglycemia
new onset hyperglycemia during chronic treatment with supraphysiologic dose of glucocorticoid (prednisone more than 5 mg or equivalent)
what to give with steroid induced hyerglycemia
if FBS is near normal, give oral agents; but if FBS is more than 11.1 mmol or more than 200 mg/dl give insulin
Three main goal of DM management
Improve/eliminate symptoms
Prevent complications
Back to normal or quality of life
