diabetes

Question 1

what is the basal insulin response in t1dm

Answer 1

intermediate or long acting insulin

Question 2

what is the bolus response in t1dm

Answer 2

short acting or rapid acting insulin

Question 3

what is the most common regimen in t1dm

Answer 3

short acting insulin 6-8 hours (regular) + intermediate acting 12-20hours (NPH)

Question 4

name the onset/peak/duration of rapid acting insulin and list their names

Answer 4

onset - 5 to 15 mins
peak 45-75 mins
duration 2-4 hours

lispro
aspart
glulisine

Question 5

name the onset/peak/duration of short acting insulin and list their names

Answer 5

onset - 15-30 mins
peak - 1-3 hours
duration 4-8 hours
regular/neutral/soluble

Question 6

name the onset/peak/duration of intermediate acting insulin and list their names

Answer 6

onset - 1-2 hours
peak - 2-8 hours
duration 18 to 20 hours
NPH/isophane

Question 7

name the onset/peak/duration of long acting insulin and list their names

Answer 7

zn suspension
onset - 2-4 hours
peak - 6-16 hours
duration 20-24 hours

protamine zn
onset - 3-8h
peak - 12-24 hours
duration = 24 hours

detemir
onset - 2 hours
no peak
duration 6-24 hours

glargine
onset 2-4 hours
no peak
duration approx 24 hours

Question 8

which part of the day does the t1dm regimen cover

Answer 8

NPH + regular insulin
pre breakfast
pre evening meals

NPH gives basal insulin for the day + covers the midday meal
&
basal + night

regular insulin - bolus (breakfast) + (evening meal) - hyperglycemia post food

Question 9

what is the starting individualized dose for t1dm patients

Answer 9

0.6-1 unit/kg/day

Question 10

other than exogenous insulin, what pharmacotherapy can be used in t1dm (@)

Answer 10

continuous sc insulin infusion - insulin pump - with rapid acting insulin only - release insulin slowly in small amounts - patients inject bolus insulin to cover food consumption

pramlintide - amylin analogue
regulates blood glucose levels
delays emptying of food to intestine - induces a feeling of satiety

Question 11

what are the risk factors for developing DM

Answer 11

1. lifestyle - sedentary lifestyle, high carb high fat foods, larger portion sizes, increased incidence of obesity
2. ethnicity - 18% higher risk in asian americans
3. age - as the population ages, incidence of developing t2dm increases
4. first degree family history of DM
5. cardiovascular diseases
6. history of GDM or delivery of a baby weighing greater than 4 kg
7. low HDL cholesterol
8. history of polycystic ovarian syndrome
9. hypertension
10. other conditions associated to insulin resistance

Question 12

what do b cells secrete and what do a cells secrete
what is their function on blood glucose levels

Answer 12

b cells secrete insulin and amylin - decreases blood glucose
a cells secrete glucagon - increases blood glucose

Question 13

what are the other hormones that increase blood glucose levels

Answer 13

growth factor, cortisol and epinephrine

Question 14

opposing actions of insulin and glucagon (& the counter-regulatory hormones) normally maintain fasting BG between __________.

Answer 14

79-99 mg/dL

Question 15

describe the 2 phases of insulin secretion response
how many minutes does it last
how does it affect physiology

Answer 15

1st phase insulin response: lasts approximately 5 to 10 minutes and causes suppression of hepatic glucose production and cause insulin-mediated glucose uptake by adipose tissue.
This bolus of insulin minimizes hyperglycemia during meals and during the postprandial period.

2nd phase of insulin response: characterized by a gradual increase in insulin secretion, which lasts 60 to 120 minutes and stimulates glucose uptake by peripheral insulin-dependent tissues, namely muscle.
Slower release of insulin allows the body to respond to the new glucose entering from digestion while maintaining blood glucose levels.

Question 16

what is the name of the hormone co secreted by be cells with insulin and what are its 3 functions

Answer 16

amylin

1.suppression of post meal glucagon production
2. regulates passage of food from stomach into intestine, increases satiety
3. regulates blood glucose concentration

Question 17

what happens to insulin secretion in t2dm

Answer 17

more insulin is secreted to maintain normal blood glucose levels until eventually the pancreas can no longer produce sufficient insulin.

Question 18

how is hyperglycemia in t2dm enhanced

Answer 18

extremely high insulin resistance, pancreatic burnout (β cells lose functional capacity) or both.

Question 19

what does impaired b cell function cause

Answer 19

fails to give 1st phase insulin response that sends signal to liver to stop post meal glucagon secretion

Question 20

what is the pathogenesis of t1dm

Answer 20

autoimmune disease manifested by macrophages, t lymphocyte and autoantibodies of b cell antigen like (islet cell antibody and insulin antibody) causes destruction of beta cells

also HLA - human leuckocyte antigen.. autoimmune destruction of beta cells

Question 21

what are the key problems in pathogenesis of t2dm

Answer 21

defect in insulin secretion, insulin resistance and hormonal abnormalities primarily involving glucagon

Question 22

how is insulin resistance manifested

Answer 22

increased lipolysis, free fatty acid production, increased hepatic glucagon production , decreased uptake of glucose by skeletal muscle

Question 23

where does resistance to insulin occur

Answer 23

resistance to insulin occurs in the adipose tissue, skeletal muscle and liver

Question 24

why is insulin resistance in the liver a double threat

Answer 24

liver becomes unresponsive to liver and continues to secrete glucose post meal leading to elevated fasting and post prandial blood glucose levels

Question 25

what are the hormones involved in the incretin effect where are they secreted from what is their effect how are they degraged

Answer 25

GLP - 1 glucagon like peptide 1 secreted by L cells of ileum and colon by endocrine and neural signals GIP - glucose dependent insulinotropic peptide secreted by K cells degraded by DPP4 - dipeptidyl peptidase 4 enzyme 1. when food enters git, GLP 1 levels rise and cause insulin secretion 2. suppresses hepatic glucagon secretion 3. git motility and increases satiety

Question 26

what is the age of onset of t1dm and t2dm

Answer 26

t1dm - Usually <30 years; peaks at 12–14 years; rare before 6 months; some adults develop it during the 5th decade t2dm - >40 years but also in childrena and young adults

Question 27

what are the presentation symptoms of t1dm and t2dm

Answer 27

t1dm mode to sev worseining relatively over days to weeks polyuria, polydypsia, fatigue, weight loss, ketoacidosis t2dm - mild polyuria, fatigue, diagnosed on routine physical or dental examination

Question 28

what is slow onset T1DM

Answer 28

latent autoimmune diabetes in adults type 1.5 occurs later at an unsual age of diagnosis patient thought to have t2dm because old and responds to oral antidiabetic drugs insulin resistance absent antibodies that destroy pancreatic beta cells present in the blood

Question 29

what is the clinical presentation and diagnosis in t1dm and t2dm

Answer 29

t1dm - polyuria, polydypsia, polyphagia, ketoacidosis, lethary and hyperglycemia t2dm - asymptomatic - polyuria, lethargy, nocturia, fatigue

Question 30

criteria for diagnosis of DM

Answer 30

1. signs and symptoms of DM + random FPG >= 200 mg/dl 2. FPG >= 126 mg/dl alone 3. 2 hour post load BG >= 200 mg/dl during an OGTT (75g anhydrous glucose in water) 4. Hba1c >= 6.5% (0.065 or 48 mmol/mol hgb)

Question 31

normal FPG ? IFP ? IGT ?

Answer 31

<100 mg/dl 100 - 125 mg/dl 140 - 199 mg/dl

Question 32

why and when should pregnant be assessed for GDM

Answer 32

first prenatal visit if 1. family history of DM 2. personal history of GDM member of high risk factor ethnic group 3. overweight/obese

Question 33

what condition needs to be asessed for during risk assessment of DM and how

Answer 33

metabolic syndrome by assessing BP and lipids

Question 34

what are the complications of DM

Answer 34

microvascular - retinopathy, neuropathy, nephropathy macrovascular - coronary heart disease, stroke, peripheral vascular disease 1. increased incidence of blindness among adults 2. end stage renal disease 3. non traumatic lower limb amputations 4. cardiovascular disease, stroke, peripheral vascular disease

Question 35

MNT for t1dm consists of? MNT for t2dm?

Answer 35

mod carbs and low fat + focus on balanced meals caloric restriction to promote weight loss

Question 36

weight mnamagement for t2dm? kcals? other 2 options?

Answer 36

1. therapeutic lifestye change 7% reduction in weight loss 0.45-0.91kg/week preferred PE for sedentary lifestyle to avoid worsening by activity cycling, swimming, walking for 150 mins / week over 3 days of week preferred 1000-1200 kcal/day women 1200-1600 kcal/day men gastric reduction surgery - gastric banding, bypass, transpose, resect small intestine for BMI>35kg/m2 drug therapy to aid weight loss in obese patients

Question 37

how does weight loss help DM

Answer 37

reduce cvd, stroke, HTN and eleated lipids reduce onset in high risk patient aerobic exercise improves glycemic control and increases insulin sensitivity better long term maintenance of weight loss and weight control

Question 38

vaccinations for DM2

Answer 38

yearly influenza vaccine for 6 mo of age and older one time pneumococcal vaccine for 2 years of age and older hep B vaccine series

Question 39

common dietary supplements believed to lower blood glucose? (4) do they work? what to advise patient?

Answer 39

chromium, magnesium, vit D, cinnamon they dont have efficacy and dont work differentiate between supplements and prescribed therapy and never stop prescribed therapy on your own

Question 40

goals of management for DM

Answer 40

1. reducing controlling and managing microvascular, macrovascular and neuropathic complications 2. preserving beta cell function 3. preventing acute complications from high blood glucose levels eg. diabetic ketoacidosis 4. minimizing hypoglycemic episodes 5. maintaining the patients overall qof managing CVD risk factors - smoking cessation, BP control, treatment of dyslipidemia, antiplatelet therapy to manage macrovascular disease

Question 41

lab goals for dm

Answer 41

1. hba1c < 7% 0.07 or 53mmol/mol every 3 months until in goal then every 6 months 2. average glucose <154 mg/dl 3. pre prandial 80-140 mg/dl 4. peak post prandial <180 mg/dl 5. BP <140/80 mm Hg at every visit 6. lipds at diagnosis of DM, age 40 then every 1-2 years 7. eye yearly dilated eye exam 8. feet feet examination at every visit 9. renal to see if kidney is leaking microalbumin

Question 42

biguanides moa and se hba1c FPG CI abilities why is it preferred when is it withheld what does it impair and main se susceptible in whom

Answer 42

metformin moa - increase insulin sensitivity and suppress hepatic glucose production se - Gi se, lactic acidosis, CI in renal insufficiency HBa1c reduction by 1.5-2% FPG reduction by 60-80mg/dl CI in abnormal creatinine clearance, alcoholics, liver disease, sepsis, dehydration, hypoxemia ability to lower BG even in glu toxicity > 300 mg/dl preferred because reduces MI, decrease risk of stroke compared to intensive therapy with SU and insulin , DM reated death, hypoglycemia is uncommon withheld before surgery or radiographic procedure which requires nephrotoxic contrast media (2 days before) assess renal function 48 hours later and resume therapy if func is normal impairs vit b12 absoprtion inhibits mitochondrial oxidation of lactic acid causing lactic acidosis which increased in elderly (advanced age) and those with renal impairment

Question 43

sulfonylureas moa and se name them state their inability state the se when do you need dose adjustment when do you need low starting dose HBa1c FPG

Answer 43

gliclazine glibenclamid glyburide stimulation of insulin release from the pancreas SE - hypogylcemia, weight gain inability to stimulate insulin release from pancreas in glucose toxicity prediposes pt to hypoglycemia dose adjustment in renal imapairment CI low starting dose in elderly and impaired hepatic or renal function reduction in hba1c by 1.5-2% reduction in FPG by 60-70 mg/dl

Question 44

glinides moa and se

Answer 44

repaglinide rateglinide stimulation of insulin secretion from pancreas shorter half life, pre prandial administration, hypoglycemia, weight gain

Question 45

TZD moa and se

Answer 45

pioglitazone rosiglitazone increase insulin sensitivity by activation of peroxisome proliferator activated receptors-gamma increased risk for HF, fluid retention, weight gain, bone fractures rosi - CVD pio - bladder cancer concerns

Question 46

alpha glucosidase inhibitors moa and se

Answer 46

acarbose miglitol vocarbose reduce absorption of glucose in gut gi se, no systemic effects

Question 47

DPP4 inhibitors moa and se how does it affect DPP4 activtity and GLP1 and GIP concerns about unestablished se

Answer 47

siltagliptin viltagliptin saxagliptin lanagliptin increase glucose mediated insulin release and suprression of glucagon by prolonging half life of endogenous GLP 1 minor effect gi motility and satiety inhibits 80% of DPP4 activity GLP1 and GIP activity increased by 2-3 times medullary thyroid, pancreatic cancer and pancreatitis not established by FDA/EMA

Question 48

SGLT2 inhibitors moa and se name them why unique ttt ability wt gain or wt loss and how hyper or hypo glycemia other effects? se?

Answer 48

gliflozins dapagliflozin canagliflozin empagliflozin reducing glucose reabsorption of glucose and increasing glucose excretion genital infections possible diuretic effects weight reduction novel class, works independent of insulin action ability to lower blood glucose even in pancreatic beta cell failure or resistance negative energy balance and wt loss also reduction in BP owing to diuretic and volume depletion effects fungal infections mostly in females

Question 49

amylin analogue moa and se

Answer 49

pramlintide suppression of hepatic glucagon, Gi motility and satiety hypoglycemia when given with other agents like insulin

Question 50

bile acid seqquestrants moa and se

Answer 50

colesevelam possibly activation of farnesoid X receptor, bile acid receptor, no EMA approval primary lipid lowering drug with additional glucose lowering effects

Question 51

dopamine agonists moa and se

Answer 51

bromocriptine central modification of insulin resistance orthtostatic hypotension, nausea

Question 52

insulin moa and se commonly avaible in what unit storage? used for? maximum dose? inj technique? fast absorption where?

Answer 52

regular insulin, aspart, nph, lispro, determir, levemir, glargine lowers blood glucose afrezza inhaled insulin 2014 U-100 used for all types of dm no maximum dose, can be titrated to suit patient absorption varies accoring to inj site rotate sites to avoid hyperlipotrophy fastest abdomen slowest buttocks others arms and thighs 90degree with small needles, no pinch wait 10 seconds until flush within skin

Question 53

what are the first line drugs in monotherapy in order and used at what hbA1c?

Answer 53

hbA1c < 7.5% metformin glp 1 ra dpp4 i ag i sglt2 tzd su/gln

Question 54

what are the first line drugs in dual therapy in order and used at what hbA1c?

Answer 54

>= 7.5% or if >6.5% in 3 months metformin/other 1st line + glp1 ra ddp4 i tzd sglt2 basal insulin colesevelam bromocriptine ag i su/gln

Question 55

what are the first line drugs in triple therapy in order and used at what hbA1c?

Answer 55

not controlled on dual therapy for greater than 3 months glp 1 ra tzd sglt2 basal dpp4 i colesevelam bromocriptine ag i su/gln

Question 56

whcih drugs are used if hba1c is >9.0%

Answer 56

if no symptoms - dual or triple therapy symptoms = insulin +/- other agents eg. metformin

Question 56

whcih drugs are used if hba1c is >9.0%

Answer 56

if no symptoms - dual or triple therapy symptoms = insulin +/- other agents eg. metformin

Question 57

apart from lifestyle modification what is the foundational therapy for t2dm

Answer 57

In addition to lifestyle modification, metformin is considered foundational therapy for T2DM because it is the only oral antidiabetcic medication proven to reduce mortality and is available generically

Question 58

AACE recommends monotherapy with which agent if metformin is contrainidicated

Answer 58

sglt2 inhibitors gliflozins dapagliflozin empagliflozin canagliflozin

Question 59

Therapeutic goals of GDM:

Answer 59

Preventing ketosis Promoting adequate growth of the fetus Maintaining satisfactory blood glucose levels Preventing nausea and other undesired GI SE

Question 60

Complications of GDM:

Answer 60

Development of abnormally large fetus & complications associated with this. Infant hypoglycemia at delivery Hyperbilirubinemi

Question 61

what is the individualized meal plan in gdm

Answer 61

3 meals and 3 snacks per day

Question 62

glu intolerance in pregnancy may occur because of __________

Answer 62

increased maternal insulin resistance owing to circulating placental hormones

Question 63

excessive glucose left uncontrolled may lead to

Answer 63

increase in fetal insulin release and complications associated with this

Question 64

ttt of gdm

Answer 64

Insulin should be used when blood glucose levels are not maintained adequately by diet and physical activity. Insulin analogs (e.g. detemir, aspart, lispro), and regular insulin carry Category B safety ratings.

Question 65

study on glibenclamide in gdm found?

Answer 65

1. good glu control compared to insulin 2. low hypoglycemia 3. no diff in complications 4. nothing about teratogenensis

Question 66

describe dm care in hospital ICU not in ICU certain circumstances hyperglycemic value range glycemic control target

Answer 66

insulin therapy if hyperglycemia > 180mg/dl after initiating insulin glycemic control of 140-180 mg/dl is preferred oral antidiabetic drugs - home regimens continued in certain circumstances in ICU - IV infusion of insulin outside ICU - SC insulin infusion align with meals and bedtime or 4-6 h if n meals or if continuous then enteral parenteral therapy should be used

Question 67

DKA is characterized by

Answer 67

ketonaemia, hyperglycemia, acidemia

Question 68

DKA occurs. n t1dm and t2dm if ____...

Answer 68

sufficiently stressed eg. surgery, severe infection, MI

Question 69

most common cause of death in children and adolescents - in adults - in DKA

Answer 69

cerebrel edema severe hypokalemia, adult respiratory distress syndrome, comorbid states (pnuemonia, MI, sepsis)

Question 70

diagnosis of DKA

Answer 70

blood ketones >= 3mmol/L or significant ketonuria blood glucose >=11mmol/L or known DM serum venous bicarbonate <15mmol/L or venous pH <7.3

Question 70

diagnosis of DKA

Answer 70

blood ketones >= 3mmol/L or significant ketonuria blood glucose >=11mmol/L or known DM serum venous bicarbonate <15mmol/L or venous pH <7.3

Question 71

questions to ask the patient regarding DKA

Answer 71

1.Has insulin use been discontinued or a dose skipped for any reason? 2.If an insulin pump is being used, is the tubing clogged or twisted? Has the catheter become dislocated? 3.Has the insulin being used lost its normal activity? Is the bottle of rapid-acting/regular or basal insulin cloudy? Does the bottle of NPH look frosty? 4.Have insulin requirements increased owing to illness or other forms of stress (infection, pregnancy, pancreatitis, trauma, hyperthyroidism, or MI)? 5.Can the patient measure and/or administer insulin accurately?

Question 72

what to look for in a case of DKA

Answer 72

1. S&S of hyperglycemia - thirst, excessive urination, fatigue, blurred vision, consistently elevated blood glucose >300mg/dl 2. S&S of acidemia- fruity breath odor, deep and difficult breathing 3. S&S of dehydration - dry mouth, warm, dry skin, fatigue 4. others- nausea, vomitting,stomach pain, loss of appetite

Question 73

What the patient shall do if DKA occurred:

Answer 73

Review “sick day management” Test blood glucose at least 4 times daily Test urine for ketones when BG is >300 mg/dL Drink plenty of fluids (water, clear soups) Continue taking insulin dose Contact physician or other healthcare provider immediately

Question 74

management of DKA (3 agents)

Answer 74

1. fluids 0.9% nacl NS fluid of choice if Na normal or elevated 0.45% Nacl 2. insulin Iv cont infusion or IM and return to SC insulin as soon as pt is biochemically stable and feels able to eat and drink 3. hyperkalemia- prompt cardiac function hyperkalemia due to insulin deficiency, when insulin administered potassium levels change rapidly .. should be monitored on admission and atleast every 2 hours to assess for requirements bicarbonate controversial because adequate fluid and insulin therapy resolves acidosis in DKA

Question 75

how is hypoglycemia defined and what is it caused by

Answer 75

<= 70mg/dl most serious se of insulin and SU

Question 76

s&s of hypoglycemia

Answer 76

1. sweating 2. tremors 3. palpitaions 4. fatigue 5. confusion 6. headache 7. dizziness 8. flushing 9. coma 10. loss of consciousness

Question 77

causes of hypoglycemia

Answer 77

1. inadequate or delayed food intake eg. carbohydrates 2. high dose of meds eg. SU or insulin 3. exercising when insulin levels are reaching peak effect 4. improper dose adjustment in pt with impaired renal or hepatic function

Question 78

ttt of hypoglycemia

Answer 78

1. test blood glucose, 15g of cho, wait 15 mins, then test again eg. of 15g og cho 1. orange, grapefruit or apple juice,, regular non diet soda 1/2 cup 2, fat free milk 1/2 cup 3. grape juice, cranberry cocktail 1/3 cup 4. 1 tsp of sugar or 3 cubes for loss of consciousness - glucagon emergency kit, roll pt to the side to prevent aspiration IV glucose as alternative to glucagon

Question 79

Sick Day Management

Answer 79

1.Continue taking your insulin even if you are not eating well or have nausea or vomiting. 2.Test your BG more frequently: every 3–4 hours. 3.Apply self-management protocol if indicated Begin testing your ketones (urine or blood) if you have T1DM. If you have T2DM, begin testing especially when glucose readings exceed 300 mg/dL. 4,Try to drink plenty of fluids (1/2 cup/hour for adults) 5. Call a physician if your BG level remains >300 mg/dL, or your urine ketones remain high after 2 or 3 supplemental doses of insulin, or your BG level remains >240 mg/dL for >24 hours.

Question 80

patient counselling

Answer 80

Diabetes: Pathogenesis and the complications Hyperglycemia: S & S and what to do Ketoacidosis: S & S and what to do Hypoglycemia: S & S and appropriate treatment Exercise: Effect on BG level and insulin dose Diet: Emphasis placed on carbohydrate counting because the carbohydrate is responsible for 90% of the rise in blood glucose after a meal. 7. Insulins: Injection technique Types of insulin Time action profiles (onset, peak, and duration) Storage and expiration once in use Stability (look for crystallization and precipitation with NPH insulin) 8. Therapeutic goals: HbA1C Fasting, preprandial and postprandial BG levels Cholesterol Triglyceride BP 9. Self Monitoring BG & Interpretation of results 10. Foot care: Inspect feet daily Wear well-fitted shoes Avoid self-care of ingrown toenails, corns, or athlete’s foot; see a podiatrist 11. Sick day management 12. Cardiovascular risk factors: Tobacco use High BP Obesity Elevated cholesterol 13. Importance of annual ophthalmologic examinations 14. Tests for microalbuminuria 15. Immunization

Question 81

GLP-1 RA name them moa hyper of hypo glycemia? relation w DDP4? Sc regimen

Answer 81

exenatide liralglutide albiglutide Stimulation of glucose dependent insulin release, suppression of elevated glucagon levels, reduction of GI motility, stimulating satiety, weight loss same hypoglycemia risk as placebo or slightly higher protected against DPP4 degradation sc once weekly adminstration