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pharmacotherapy 3 > diabetes > Flashcards

diabetes Flashcards

1
Q

what is the basal insulin response in t1dm

A

intermediate or long acting insulin

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2
Q

what is the bolus response in t1dm

A

short acting or rapid acting insulin

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3
Q

what is the most common regimen in t1dm

A

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

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4
Q

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

A

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

lispro
aspart
glulisine

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5
Q

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

A

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

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6
Q

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

A

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

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7
Q

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

A

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

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8
Q

which part of the day does the t1dm regimen cover

A

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

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9
Q

what is the starting individualized dose for t1dm patients

A

0.6-1 unit/kg/day

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10
Q

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

A

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

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11
Q

what are the risk factors for developing DM

A
  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
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12
Q

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

A

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

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13
Q

what are the other hormones that increase blood glucose levels

A

growth factor, cortisol and epinephrine

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14
Q

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

A

79-99 mg/dL

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15
Q

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

A

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.

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16
Q

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

A

amylin

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

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17
Q

what happens to insulin secretion in t2dm

A

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

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18
Q

how is hyperglycemia in t2dm enhanced

A

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

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19
Q

what does impaired b cell function cause

A

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

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20
Q

what is the pathogenesis of t1dm

A

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

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21
Q

what are the key problems in pathogenesis of t2dm

A

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

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22
Q

how is insulin resistance manifested

A

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

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23
Q

where does resistance to insulin occur

A

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

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24
Q

why is insulin resistance in the liver a double threat

A

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

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25
Q

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

A

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
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26
Q

what is the age of onset of t1dm and t2dm

A

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

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27
Q

what are the presentation symptoms of t1dm and t2dm

A

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

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28
Q

what is slow onset T1DM

A

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

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29
Q

what is the clinical presentation and diagnosis in t1dm and t2dm

A

t1dm - polyuria, polydypsia, polyphagia, ketoacidosis, lethary and hyperglycemia

t2dm - asymptomatic - polyuria, lethargy, nocturia, fatigue

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30
Q

criteria for diagnosis of DM

A
  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)
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31
Q

normal FPG ?
IFP ?
IGT ?

A

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

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32
Q

why and when should pregnant be assessed for GDM

A

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

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33
Q

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

A

metabolic syndrome by assessing BP and lipids

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34
Q

what are the complications of DM

A

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
35
Q

MNT for t1dm consists of?
MNT for t2dm?

A

mod carbs and low fat + focus on balanced meals

caloric restriction to promote weight loss

36
Q

weight mnamagement for t2dm?
kcals?
other 2 options?

A
  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

37
Q

how does weight loss help DM

A

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

38
Q

vaccinations for DM2

A

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

39
Q

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

A

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

40
Q

goals of management for DM

A
  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

41
Q

lab goals for dm

A
  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
42
Q

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

A

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

43
Q

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

A

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

44
Q

glinides moa and se

A

repaglinide
rateglinide
stimulation of insulin secretion from pancreas

shorter half life, pre prandial administration, hypoglycemia, weight gain

45
Q

TZD moa and se

A

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

46
Q

alpha glucosidase inhibitors moa and se

A

acarbose
miglitol
vocarbose

reduce absorption of glucose in gut

gi se, no systemic effects

47
Q

DPP4 inhibitors moa and se

how does it affect DPP4 activtity and GLP1 and GIP

concerns about unestablished se

A

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

48
Q

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?

A

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

49
Q

amylin analogue moa and se

A

pramlintide

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

50
Q

bile acid seqquestrants moa and se

A

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

51
Q

dopamine agonists moa and se

A

bromocriptine
central modification of insulin resistance
orthtostatic hypotension, nausea

52
Q

insulin moa and se

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

A

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

53
Q

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

A

hbA1c < 7.5%

metformin
glp 1 ra
dpp4 i
ag i
sglt2
tzd
su/gln

54
Q

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

A

> = 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

55
Q

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

A

not controlled on dual therapy for greater than 3 months

glp 1 ra
tzd
sglt2
basal
dpp4 i
colesevelam
bromocriptine
ag i
su/gln

56
Q

whcih drugs are used if hba1c is >9.0%

A

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

56
Q

whcih drugs are used if hba1c is >9.0%

A

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

57
Q

apart from lifestyle modification what is the foundational therapy for t2dm

A

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

58
Q

AACE recommends monotherapy with which agent if metformin is contrainidicated

A

sglt2 inhibitors
gliflozins
dapagliflozin
empagliflozin
canagliflozin

59
Q

Therapeutic goals of GDM:

A

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

60
Q

Complications of GDM:

A

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

61
Q

what is the individualized meal plan in gdm

A

3 meals and 3 snacks per day

62
Q

glu intolerance in pregnancy may occur because of __________

A

increased maternal insulin resistance owing to circulating placental hormones

63
Q

excessive glucose left uncontrolled may lead to

A

increase in fetal insulin release and complications associated with this

64
Q

ttt of gdm

A

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.

65
Q

study on glibenclamide in gdm found?

A
  1. good glu control compared to insulin
  2. low hypoglycemia
  3. no diff in complications
  4. nothing about teratogenensis
66
Q

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

A

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

67
Q

DKA is characterized by

A

ketonaemia, hyperglycemia, acidemia

68
Q

DKA occurs. n t1dm and t2dm if ____…

A

sufficiently stressed eg. surgery, severe infection, MI

69
Q

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

A

cerebrel edema

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

70
Q

diagnosis of DKA

A

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

70
Q

diagnosis of DKA

A

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

71
Q

questions to ask the patient regarding DKA

A

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?

72
Q

what to look for in a case of DKA

A
  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
73
Q

What the patient shall do if DKA occurred:

A

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

74
Q

management of DKA
(3 agents)

A
  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
75
Q

how is hypoglycemia defined and what is it caused by

A

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

76
Q

s&s of hypoglycemia

A
  1. sweating
  2. tremors
  3. palpitaions
  4. fatigue
  5. confusion
  6. headache
  7. dizziness
  8. flushing
  9. coma
  10. loss of consciousness
77
Q

causes of hypoglycemia

A
  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
78
Q

ttt of hypoglycemia

A
  1. test blood glucose, 15g of cho, wait 15 mins, then test again
    eg. of 15g og cho
  2. 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

79
Q

Sick Day Management

A

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.

80
Q

patient counselling

A

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.

  1. 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)
  2. Therapeutic goals:
    HbA1C
    Fasting, preprandial and postprandial BG levels
    Cholesterol
    Triglyceride
    BP
  3. Self Monitoring BG & Interpretation of results
  4. Foot care:
    Inspect feet daily
    Wear well-fitted shoes
    Avoid self-care of ingrown toenails, corns, or athlete’s foot; see a podiatrist
  5. Sick day management
  6. Cardiovascular risk factors:
    Tobacco use
    High BP
    Obesity
    Elevated cholesterol
  7. Importance of annual ophthalmologic examinations
  8. Tests for microalbuminuria
  9. Immunization
81
Q

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

A

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

pharmacotherapy 3 (2 decks)

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