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Pharmacotherapy 4271 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

this type of diabetes ranges from insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance

A

type 2

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2
Q

this type of diabetes is due to pancreatic beta destruction and prone to ketosis

A

type 1

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3
Q

this type of diabetes presents as glucose intolerance with onset or first recognition in pregnancy

A

gestational diabetes

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4
Q

explain the pathophysiology of a normal individual when they have high blood sugar

A

when you have high blood sugar, your body promotes insulin release from the pancreas. Insulin release stimulates glucose uptake from the blood into the muscle, kidney, fat, etc. along with glycogen formation in the liver, which then lowers blood sugar to a favourable amount

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5
Q

explain the pathophysiology of a normal individual when the have low blood isgar

A

when you have low blood sugar, you body promotes glucagon release from the pancreas. glucagon release stimulates the breakdown of stored glucose (glycogen) which is then released into the bloodstream and raises blood sugar

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6
Q

does insulin increase or decrease glycogenesis (synthesis of glycogen)

A

increase

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7
Q

does insulin increase or decrease ketogenesis (production of ketones)

A

decrease

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8
Q

does insulin increase or decrease glycogenolysis (breakdown of glycogen)

A

decrease

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9
Q

does insulin increase or decrease gluconeogenesis (synthesis of new glucose molecules)

A

decrease

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10
Q

does insulin increase or decrease lipogenesis (synthesis of fatty acids)

A

increase

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11
Q

does insulin increase or decrease lipolysis (breakdown of lipids)

A

decrease

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12
Q

does insulin increase or decrease protein synthesis from amino acids

A

increase

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13
Q

if insulin decreases:
- ketogenesis (production of ketones)
- glycogenolysis (breakdown of glycogen)
- lipolysis (breakdown of lipids)
- gluconeogenesis (synthesis of new glucose molecules)
which hormone increases these processes?

A

glucagon

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14
Q

explain the post prandial glucose metabolism in a patient with diabetes

A

blood glucose remains high after meals due to decreased uptake, utilization and storage of glucose
(glucose remains inaccessible to cells, therefore the cells behave as if they were in fasting metabolism)

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15
Q

explain the pre prandial glucose metabolism in a patient with diabetes

A

extension of post prandial high blood glucose levels because glucose is still sitting in the blood

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16
Q

what are the two incretin (Gut) hormones

A

GLP (glucagon-like peptide) and GIP (glucose-dependant insulinotropic peptide)

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17
Q

enhanced insulin release upon ORAL intake of nutrients triggering gut derived hormones that bind to beta-cells

A

incretin effect

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18
Q

decreased glucagon release, beta cell proliferations, neogenesis and survival (inhibit apoptosis beta cells)

A

pancreatic effect

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19
Q

decrease appetite, delay in gastric emptying, decrease gluconeogenesis

A

extra-pancreatic effect

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20
Q

true or false: insulin response Is better if take glucose by mouth compared to IV

A

true - because with IV incretin hormones not actiavted because they recognize food in the gut!

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21
Q

what is a normal A1C?

A

4-6% (or 5.5-7.5 mmol/L)
- less than 7% is the goal for most people

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22
Q

this is your AVERAGE blood glucose, before and after meals, continuously over the past 2-3 months

A

A1C

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23
Q

true or false: A1C is the value you get when your prick your finger

A

false - A1C is average blood glucose over 2-3 months and fingerpick is blood glucose at that very second

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24
Q

what are the two main test used to make a diagnosis of diabetes, and what are the values of these tests that show that someone is diabetic

A

fasting blood glucose (FBG) greater than or equal to 7 mmol/L
A1C greater than or equal to 6.5% in adults

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25
Q

fasting = no caloric intake for at least how many hours?

A

8

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26
Q

what are some factors that may affect the efficacy of A1C

A
  • anemia
  • hemodialysis
  • pregnancy
  • type 1 diabetes
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27
Q

true or false: if a single test is in the diabetes range, a confirmatory glucose test must be done on another day

A

true

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28
Q

true or false: treatment can be delayed if confirmatory tests are not completed in those with symptomatic hyperglycaemia or suspected type 1 diabetics

A

false

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29
Q

what is the A1C level that represents pre-diabetes

A

6.0-6.4%

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30
Q

this is autoimmune destruction of beta cells in the pancreas leading to insulin deficiency. rate of beta cell destruction varies, but it is often abrupt (auto-antibodies). commonly seen in childhood or adolescence. often no family history

A

type 1 diabetes

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31
Q

describe the presentation of type 1 diabetes

A
  • polyuria (increased urination)
  • polydipsia (thirsty)
  • fatigue
  • weight loss
  • DKA (diabetic ketoacidosis)
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32
Q

what is used to treat type 1 diabetes

A

insulin -> immediately

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33
Q

this is insulin resistance and beta cell destruction. usually > 25 y/o. family history is strong and> 90% are overweight

A

type 2 diabetes

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34
Q

describe the presentation of type 2 diabetes

A
  • mild polyuria
  • polydipsia
  • fatigue

blurred vision, recurrent infections, often diagnosis on routine exam

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35
Q

what is used to treat type 2 diabetes

A

diet, exercise, weight loss, oral antihyperglycemics, and insulin (usually delayed)

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36
Q

what are some PERSONAL risk factors for type 2 diabetes

A
  • age > 40
  • first degree relative with type 2 DM
  • member of high risk population (African, Arab, asian, hispanic, indigenous or south asian descent, low socioeconomic status)
  • history of pre diabetes
  • history of gestational diabetes
  • history of delivery of macrosomic infant
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37
Q

what are some diseases and complications associated with diabetes

A
  • end organ damage (microvascular: retinopathy, neuropathy & nephropathy/ macrovascualr: coronary, cerebrovascular & peripheral arterial)
  • vascular risk factors (low HDL, high TGs, hypertension, overweight & abdominal obesity)
  • polycystic ovarian syndrome, obstructive sleep apnea, psychiatric disorders, HIV infection
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38
Q

what are some drugs that can affect insulin production or action

A
  • thiazide diuretics
  • beta blockers
  • protease inhibitors
  • atypical antipsychotics
    -corticosteroids should eb reversible upon discontinuation of drug
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39
Q

true or false: intensive lifestyle modification with weight loss can reduce the risk of progression from pre diabetes to T2DM

A

true

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40
Q

if you have 3 or more of the following, you have ________ (elevated waist circumference, elevated TGs, reduced HDL, elevated BP and elevated FPG) which puts you at high risk for CV disease and type 2 diabetes

A

metabolic syndrome

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41
Q

when should people be screened for type 2 diabetes

A

screen q 3 years if greater than or equal to 40 y/o or have risk factors for diabetes

screen q 6-12 months in people with additional risk actors or for those at very high risk

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42
Q

what should be done screening wise if the patients FBG is < 5/6 mmol/L and/or A1C < 5.5%

A

normal -> rescreen as recommended

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43
Q

what should be done screening wise if the patients FBG is between 5.6 and 6.0 mmol/L and/or A1C is 5.5 to 5.9%

A

at risk -> rescreen more often

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44
Q

what should be done screening wise if the patients FBG is between 6.1 and 6.9 mmol/L and/or A1C is between 6.0 and 6.4%

A

pre diabetes -> rescreen more often

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45
Q

what should be done if a patient has their FBG and A1C values, but one puts them in the pre diabetes category and the other puts them just at risk

A

use the worse number, therefore in this case the one that indicates pre-diabetes

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46
Q

this is defined as achieving A1C thresholds without any antihyperglycemic medications for a minimum of 3 months

A

remission

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47
Q

who are more likely to experience remission of T2DM

A

short diagnoses with T2DM (<6 yrs); overweight or obese, BG levels not extremely elevated, and those who do not use insulin

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48
Q

what are the goals of therapy for ALL types of diabetes

A
  1. tight blood glucose control (prevent both hypo- and hyperglycaemia)
  2. prevent acute & long term complications
  3. improve QoL
  4. prevent morbidity and mortality
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49
Q

what is the A1C treatment target for the majority of adults with type 1 or type 2 diabetes

A

less than or equal to 7

50
Q

what is the A1C treatment target for selected adults with type 2 diabetes with potential for remission to normoglycemia

A

< 6.0

51
Q

what is the A1C treatment target for adults with type 2 diabetes to reduce the risk of chronic kidney disease and retinopathy if at low risk for hypoglycaemia

A

less than or equal to 6.5

52
Q

what is the A1C treatment target for those who have
- recurrent severe hypoglycaemia and/or hypoglycaemia unawareness
- limited life expectancy
- frail elderly and/or with dementia

A

7.1 - 8.5

53
Q

what is the A1C treatment target for those < 18 y/o

A

less than or equal to 7.5%

54
Q

what is the preprandial blood glucose target for most patients in order to achieve A1C of 7%

A

4.0-7.0 mmol/L

55
Q

what is the 2 hour post prandial blood glucose target for most patients in order to achieve A1C of 7%

A

5.0-10.0 mmol/L

56
Q

what are some non pharmacological recommendations for type 1 and type 2 diabetics

A
  • diet management (carbs that are adjusted to insulin or vice versa)
  • exercise
57
Q

examples of this type of insulin include:
- insulin aspart (Novorapid/Trurapi, Kirsty)
- insulin glulisine (apidra)
- insulin lispro (Humalog/admelog)

should be given 15 mins before a meal based on onset of action.

A

bolus (meal time) insulin -> rapid acting
best bolus

58
Q

examples of this type of insulin include:
- insulin regular (Humulin-R, Novolin ge Toronto)
- insulin regular U-500 (Entuzity)

should be given 30 mins before a meal based on onset of action

A

bolus (mealtime) insulin -> short acting

59
Q

examples of this type of insulin include:
- Insulin neutral protamine Hagedorn (Humulin N, Novolin ge NPH)

A

intermediate basal insulin
note: these have a peak therefore we don’t like these as much because more at risk for hypoglycaemia with a peak

60
Q

examples of this type of insulin include:
- insulin detemir (Levemir)
- insulin glargine U-100 (Lantus)
- insulin glargine U-500 (Toujeo)
- insulin glargine biosimiar (Basaglar/Semglee)
- insulin deluded U-100 (Tresiba)

A

long acting basal insulin

61
Q

this is a type of insulin therapy in T1DM. consists of 4-5 injections a day, where bolus insulin is used with meals and a basal insulin is used once or twice daily. insulin can be adjusted based on carb intake and BG values

A

basal-bolus injections

62
Q

this is a type of insulin therapy in T1DM. consists of rapid acting insulin only (e.g. lispro or aspart). continuous, small increment insulin given as 40-60% of total daily dose with boluses given with meals and snacks. more closely resembled physiological insulin release

A

continuous subcutaneous insulin infusion (CSII) - pump therapy

63
Q

true or false: 40% of total insulin requirement is given as short or rapid insulin divided between meals and the remainder is given as basal

A

false - 60%

64
Q

the goal is to attain A1C target by 3 months. the first step is lifestyle changes which is expected to reduce blood glucose levels (no pharmacotherapy. If the A1C is not at target at 3 months, what is the next step

A

start metformin

65
Q

true or false: when a patient is being started on metformin because their A1C was not at target after trying 3 months of lifestyle changes, and their A1C is > 1.5% above their target a second agent can be stated alongside metformin

A

true

66
Q

if a patients A1C is not at target after being on 3 months of Metformin, what is the next step

A

adjust or advance therapy and reassess A1C is 3-6 mth

67
Q

if advancing therapy from metformin, what may be added for a patient with Chronic kidney disease or heart failure

A

SGLT2 inhibitor

68
Q

if advancing therapy from metformin, what may be added for a patient with atherosclerotic cardiovascular disease

A

GLP1-RA or SGLT2 inhibitor

69
Q

if advancing therapy from metformin, what may be added for a patient > 60 yrs with CV risk factors

A

GLP1-RA

70
Q

these medications have benefits other than treating DM (e.g. CV safety, cardiorenal benefit)

A

GLP1-RA and SGLT2 inhibitors

71
Q

these medications have no additional advantage besides treating DM but have no risks either

A

DPP4i and Acarbose

72
Q

these medications may cause more harm than good when treating T2DM (e.g. high risk of hypoglycaemia, weight gain)

A
  • sulfonylureas
  • meglitinides
  • insulin
  • thiazolidinediones
73
Q

when is insulin initiated for T2DM

A
  • fasting BG and/or A1C NOT at target on metformin + other AHA
  • symptomatic hyperglycaemia
  • metabolic decompensation
74
Q

when starting insulin for T2DM, do you start with bolus or basal insulin? do you continue or take off other meds?

A

start with basal insulin. Continue metformin unless contraindicated. review/adjust other meds

75
Q

if basal insulin is not getting the patient to their target and bolus insulin is to be added, what medications must be d/c

A

any that increase secretion of insulin, because bolus insulin + these meds can increase risk of hypo (e.g. sulfonylureas)

76
Q

in T2DM, insulin should be titrated to achieve target FBG levels of ____ to ___ mmol/L

A

4-7

77
Q

What is the suggested starting dose of basal insulin in T2DM

A

10 units at bedtime (titrate 1 unit per day until target is reached)

78
Q

true or false: there are no restrictions regarding dosing titrations for insulin in type 2 diabetes

A

false: the dose should not be increased if 2 or more episodes of hypoglycaemia (BG < 4mmol/L) are experienced in 1 weeks or any episode of nocturnal hypoglycaemia

79
Q

what is the starting dose for bolus insulin in type 2 diabetes

A

2-4 units

80
Q

when should bolus insulin be given in type 2 diabetes

A

largest carb meal of the day or breakfast

81
Q

true or false: when starting on bolus insulin with T2DM, all other oral AHA medications can be continued

A

fasle: continue metform, review/adjust other AHA

82
Q

how should bolus insulin dosing be titrated in T2DM

A

to safely increase dose, glucose levels should be measured at least prior to insulin dose then titrated by 1 unit daily to either of the following targets:
- 2 hour post-prandial glucose of less than or equal to 8 mmol/L
- pre-meal glucose of the next meal of 4-7 mmol/L

83
Q

KNOW the dosing of basal-bolus insulin in T2DM

A

40% of total insulin dose is basal insulin
20% of total insulin is as bolus (prandial) insulin 3 times per day using either rapid-acting insulin analogue or short-acting insulin

84
Q

this occurs when hormones (growth hormone, cortisol and catecholamines) produced by the body cause the lover to release large amounts of sugar (glucose) into the bloodstream. these hormones are released in the early morning hours. these hormones also may partially block the effect of insulin, whether its insulin the body produces or insulin from the last injection.

A

Dawn phenomenon

85
Q

if the blood sugar level drops too low in the early morning hours, hormones (such as growth hormone, cortisol and catecholamines) are released. these help reverse the low blood sugar but may lead to blood sugar levels that are higher than normal in the morning.

A

somogyi effect

86
Q

how can you differentiate between the dawn phenomenon and the somogyi effect

A

need to take blood sugar overnight.
both show high AM BG, therefore in dawn phenomenon, 3am BG will be in target and in somogyi effect, 3AM BG will be low

87
Q

what action may be took if a patient is experiencing dawn phenomenon

A

move suppertime basal insulin to HS or increase basal HS

88
Q

what action may be took if a patient is experiencing Somogyi effect

A

decrease suppertime basal or move suppertime basal to HS

89
Q

what are the two categories of diabetes in pregnancy

A

pre gestational diabetes -> pre-existing diabetes
gestational diabetes -> diagnosed in pregnancy

90
Q

what is the A1C target for pregestational diabetes

A

less than or equal to 7

91
Q

these two antihyperglycemic medications may be continued until pregnancy and then switch to insulin

A

metformin and glyburide

92
Q

when should ASA be started in pregnancy in order to prevent preeclampsia

A

12-16 weeks

93
Q

how is gestational diabetes diagnosed

A

all pregnancy women are screen between 24-28 weeks (if at high risk of GDM, screen at any time of pregnancy) => 50g glucose challenge test with PG 1 hour later => if PG is greater than equal to 11.1 = gestational diabetes

94
Q

what is the fasting and preprandial BG for gestational diabetes

A

< 5.3 mmol/L

95
Q

what is the 1h postprandial BG for gestational diabetes

A

< 7.8 mmol/L

96
Q

what tis the 2h postprandial BG for gestational diabetes

A

< 6.7 mmol/L

97
Q

what is the first line treatment in gestational diabetes

A

insulin

98
Q

this may be used as an alternative to insulin in pregnancy

A

metformin

99
Q

this may be used in women who refuse insulin and are not well controlled on metformin

A

glyburide

100
Q

this should be encouraged for a minimum of 4 months to prevent neonatal hypoglycaemia, childhood obesity and diabetes for both the mother and the child

A

breastfeeding

101
Q

when should mothers be prescreened postpartum to see if they still have diabetes

A

between 6 weeks and 6 months post party with 75g OGTT

102
Q

this is an acute complication of diabetes/medications; is the development of autonomic (shakes, sweating) and neuroglycopenic (confusion, memory loss, blurred vision, slurred speech) symptoms; a low plasma glucose (< 4 mmol/L); symptoms respond to the administration of carbs

A

hypoglycaemia

103
Q

is this mild, moderate or severe hypoglycemia?
individual requires assistance of another person - unconsciousness may occur. typically PG < 2.8 mmol/L

A

severe

104
Q

is this mild, moderate or severe hypoglycemia?
autonomic symptoms are present. individual able to self-treat

A

mild

105
Q

is this mild, moderate or severe hypoglycemia?
autonomic and neuroglycooenic symptoms are present. individual able to self treat

A

moderate

106
Q

what can cause hypoglycaemia

A
  • not enough carbs
  • too much activity
  • missed meal or snack
  • too much SU
  • too much insulin
  • other medications
107
Q

what are the steps for treating mild-moderate hypoglycaemia

A
  1. recognize autonomic or neuroglycopenic symptoms
  2. confirm if possible (blood glucose < 4.0 mmol/L)
  3. treat with “fast sugar” (simple carbs - 15g) to relieve symptoms
  4. retest in 15 minutes to ensure BG > 4.0 mmol/L and retreat if needed
  5. Eat usual snack or meal due at that time of day or a snack with 15g carbohydrate plus protein
108
Q

what are some examples of 15g of carbohydrates

A

15g of glucose in the form of glucose tablets
15 ml (3 teaspoons) or 3 packets of sugar dissolved in water
175 ml (3/4 cup) of juice or regular soft drink
6 lifesavers (1=2.5g of carbohydrate)
15ml (table spoon) of honey

109
Q

this amount of glucose can increase BG by 2.1 mmol/L in 15-20 min

A

15g

110
Q

this amount of glucose can increase BG by 3.6 mmol/L in 45 min (used for severe, but conscious)

A

20g

111
Q

what is used for a hypoglycaemic emergency

A

1mg glucagon SC
(can increase BG from 3.0 mmol/L to 12.0mmol/L within 60 min)

3mg intranasal glucagon
(can increase BG from 3.0 mmol/L to 10.0 mmol/L within 60 min)

112
Q

this may occur when the threshold for autonomic warning symptoms are lower than the threshold for neuroglycopenic symptoms

A

hypoglycaemia unawareness

113
Q

this occurs when there are feelings of hypoglycaemia with BG > 4 mmol/L

A

relative (pseudo) hypoglycaemia
- recommended to treat symptoms with HALF the dose of glucose to make them feel better

114
Q

what are the two hyperglycaemic emergencies

A

diabetic ketoacidosis (DKA)
hyperosmolar hyperglycaemic state (HHS)

115
Q

absolute insulin deficiency causes lipolysis, TG’s are converted to FFA’s, which are converted to ketone bodies by the liver. ketones provide an alternative source of energy. the twi main ketones produced are beta hydroxybutyric acid andacetoacetate acid

A

DKA

116
Q

how does DKA usually present

A
  • pH less than or equal to 7.3
  • low bicarbonate
  • high anion gap (sodium + potassium) - (chloride + bicarbonate)
  • positive serum or urine ketones
  • high plasma glucose
117
Q

low insulin levels prevent lipolysis but not enough for body to use glucose. this takes longer to manifest, therefore BG levels are higher before diagnosis. patients are often older with decreased renal function

A

HHS

118
Q

how does HHS usually present

A
  • pH is greater than or equal to 7.3 (not acidodic)
  • low anion gap
  • BG is very high
  • negative to small ketones
  • increase bicarbonate
  • osmolality very high - dehydrated
119
Q

what is the treatment for DKA and HHS

A
  1. replacement of fluid loss
  2. replacement of electrolyte loses (Na and K+)
  3. correction of hyperglycaemia with low dose IV insulin and, in DKA, correction of metabolic acidosis (correct slowly to prevent cerebral edema)
  4. detection and tx of causes
  5. prevention and recurrence with specialized medical equipment
120
Q

when treating DKA and HHS, this electrolyte level must be > 3.3 before administering insulin

A

3.3

Pharmacotherapy 4271 (29 decks)

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