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3rd year - Family Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Diabetes screening

A
  1. 5
  2. 6
  3. 8

1) screen by fasting plasma glucose (FPG) and / or HbA1C
FPG < 5.6 and HbA1C <5.5 = normal (repeat screen q3y)
FPG 5.6-6 or HbA1C is 5.5-5.9%
= if no risk factors patient is at risk and screening repeated yearly
= if > 1 risk factor go to OGTT
FPG 6.1-6.9 or HbA1C 6-6.4% = Go to OGTT
FPG >7 or HbA1C >6.5% = diagnosed with Type 2 diabetes

2) Secondary OGTT
FPG <6.1 and 2h blood glucose <7.8 = do HbA1C
= <6 patient is at risk and requires yearly screening
= 6-6.4 then patient diagnosed with pre-diabetes

2h blood glucose 7.8-11.0 = diagnosed with IGT (form of prediabetes)

FPG 6.1-6.9 = diagnosed with impaired fasting glucose

FPG >7 or 2h blood glucose is >11 = diagnosed with diabetes

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2
Q

What are variations of autonomic neuropathy?

A

Cardiovascular - exercise intolerance, sustained heart rate, syncope, dizziness, lightheadedness, balance

GI - dysphagia, bloating, N/V/D, constipation, loss of bowel control

GU - loss of bladder control, UTI, urinary frequency/dribbling, erectile dysfunction, loss of libido, dyspareunia

Sudomotor (sweat glands) - pruritus, dry skin, lib hair loss, calluses, reddened areas

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3
Q

What should be included in a diabetes physical exam?

A
  1. CVD assessment
    - metabolic risk factors (height, weight, WC, BMI)
    - complete CV and peripheral vascular exam
    - blood pressure
  2. Retinopathy assessment
    - fundoscopy
  3. Peripheral neuropathy assessment
    - 10g Semmes-Weinstein monofilament or tuning fork
    - Screening x 4 each big toe
    - If positive screening complete multi site testing
  4. Foot exam including insufficiency, pulses
  5. Thyroid, abdominal exam
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4
Q

What is considered microalbumineria and macroalbumineria

A

Urine ACR
Micro
Male 2-20
Female 3-28

Macro <20 in male and >30 in female

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5
Q

When should you screen for kidney function in diabetes

A

Type 1 diabetes - annually in postpubertal individuals with duration of diabetes 5+ years

Type 2 diabetes - at diagnosis and annually thereafter

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6
Q

What kidney function tests should be used to monitor kidney function in diabetes

A

Random urine ACR and serum creatinine for eGFR

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7
Q

What pharmacological agents can be used for vascular protection in diabetes and what are the indications for each?

A

Statins if any of:
a) 40+ years
b) Macrovascular damage
C) age <40 years with 1 of the following
i) age >30 years and diabetes duration >15 years
ii) microvascular complication: retinopathy, nephropathy iii) other risk factors acceding to Canadian cardiovascular guidelines
high risk (FRS >20%): start statin
intermediate risk (FRS 10-19%): start statin if LDL >3.5 or apoprotein B >1.2 or non-HDL cholesterol >4.3
low risk (FRS <10%): start statin if LDL >5 or familial hypercholesterolemia

ACEi/ARB even in the absence of HTN if any of

a) 55 years +
b) Macrovascular end organ damage (CAD, MI, stroke, PVD)
c) <55 years and microvascular end organ damage (nephropathy, neuropathy, retinopathy)

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8
Q

How frequently should a patient with diabetes have eye exam done?

A

Type 2 - at time of diagnosis and then every 1-2 years thereafter if no or minimal retinopathy

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9
Q

What patients with diabetes should have a baseline resting ECG completed?

A

> 40 years
Duration of diabetes >15 years and age >30 years
End organ damage (any micro or macro)
Cardiac risk factors

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10
Q

How often should an ECG be performed in patients with diabetes?

A

q2 years

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11
Q

Exercise ECG stress testing is recommended for diabetc patients with:

A

Typical or atypical cardiac symptoms

Symptoms or signs of associated diseases (abnormal ABI, carotid bruit, TIA, stroke)

Resting ECG abnormalities such as Q waves

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12
Q

How often should lipid profile be completed in patient with diabetes

A

At time of diagnosis and then repeated yearly

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13
Q

What are the classes of diabetes drugs and the types of drugs in each?

A
  1. Insulin sensitizers
    - Biguanides, thiazolinedidiones
  2. Insulin secretagogues
    - Sulfonylureas, meglitindes
  3. Carbohydrate absorption inhibitors
    - Alpha glucosidase inhibitor
  4. Incretin agents
    - GLP-1 agonists and DDP4 inhibitors
  5. Weight loss agents
    - Lipase inhibitor
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14
Q

What is the only class of diabetes medication associated with significant risk of hypoglycemia

A

Secretagogues

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15
Q

Which antihyperglycemic agents are usually okay to use in end stage renal failure

A

Thiazolinedidiones and DPP-4 inhibitors

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16
Q

What antihyperglycemic agents are weight negative or weight neutral

A

Metformin
Alpha glucosidase inhibitor (acarbose)
Thiazolinedidiones
GLP 1 agents

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17
Q

What is an example biguanide medication

A

Metformin

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18
Q

What is the MOA of biguanides

A

Inhibit glucose production and output by liver by activation of AMP activated protein kinase

Enhance peripheral glucose uptake

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19
Q

What is the only oral anti hyperglycemic agent proven to decrease mortality by lowering CVD risk

A

Metformin

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20
Q

What are common and serious side effects of metformin

A

Common: diarrhea, B12/folate deficiency/anemia

Serious - lactic acidosis

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21
Q

What are contraindications to using metformin

A

Severe kidney, liver or heart failure

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22
Q

What are examples of drugs that are thiazolidinediones

A

End in glitazone (pioglytazone, rosiglitazone)

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23
Q

MOA of thiazolidinediones

A

PPAR gammaagonist resulting in

Decreased glucose production in liver
Increased glucose uptake

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24
Q

Indication for TZDs

A

ALMOST NEVER USED DUE TO SERIOUS SIDE EFFECTS

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25
Q

Adverse effects of TZDs

A

Common - weight gain

Serious - increased risk of CVD, CHF, osteoporosis, bladder cancer, anemia

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26
Q

Examples of drugs that are sulfonylureas

A

Names start with gli (glybride, gliclazide, glimepiride)

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27
Q

Sulfonylureas MOA

A

Activate sulfonylurea receptor on beta cell to stimulate endogenous insulin secretion

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28
Q

Indication for sulfonylureas

A

Usually 2nd line to add to metformin

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29
Q

Sulfonylureas adverse effects

A

Associated with hypoglycemia!!

Can lose its effectiveness over time

Common - weight gain, hypoglyemia

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30
Q

Meglitinides drugs

A

end with glinide (repaglinide)

31
Q

Meglitinide MOA

A

bind to a different domain of sulfonylurea receptor on beta cell to stimulate endogenous insulin secretion

32
Q

Meglitindes adverse effect

A

Hypoglycemia

33
Q

What is an incretin

A

peptides released by intestines in response to meal

34
Q

Drug examples of GLP1 agonists

A

end with “tide” exenatide, liraglutide

35
Q

MOA of GLP1 agonists

A

activation of GLP-1 receptor in beta cells to stimulate release of insulin, increasing beta cell response

inhibition of gastric emptying to decrease beta cell workload

36
Q

GLP1 agonists adverse effects

A

common: nausea and vomiting, significant weight loss
serious: pancreatitis (rare)

37
Q

DDP4 inhibitors names of drugs

A

end with “lipton”

sitagliptin (Januvia) saxagliptin (Onglyza) linagliptin (Tradjenta)

38
Q

DDP 4 inhibitors MOA

A

block DPP-4 degradation of GLP, thereby increasing GLP effect and incretin pathway (same mechanism of GLP-1 thereafter)

39
Q

DDP4 inhibitors adverse effects

A

common: GI upset, edema
serious: pancreatitis (rare)

40
Q

Alpha glucosidase inhibitor drug names

A

acarbose (Prandase, Glucobay)

41
Q

Alpha glucosidase inhibitor MOA

A

slow absorption of starch and sucrose in gut on brush border of small intestine

42
Q

Alpha glucosidase indication

A

Usually used as adjunt therapy

43
Q

Alpha glucosidase adverse effects

A

common: flatulence, diarrhea

44
Q

Lipase inhibitor drug example

A

Orlistat

45
Q

Lipase inhibitor MOA

A

inhibit gastric and intestine lipase to prevent breakdown and absorption of dietary fat, thereby reducing calorie intake and weight

46
Q

Lipase inhibitor adverse effects

A

steatorrhea and flatulence

47
Q

Blood pressure pharmacological management in patients with diabetes

A

1st line = ACEI, ARB for diabetic and hypertensive patients with cardiovascular risk factors, cardiovascular disease or kidney disease

2nd line = dihydropyridine calcium channel blocker, then hydrochlorothiazide as adjunt to first line

48
Q

Anti platelet therapy in patients with diabetes

A

aspirin as primary prevention in diabetics without coronary artery disease is NOT currently recommended, because it does not reduces coronary artery disease events and increases GI bleed

aspirin 75mg to 162mg daily as secondary prevention in diabetics with history of coronary artery disease is currently recommended due to reduction in future coronary artery disease events

clopidogrel 75mg may be used in people unable to tolerate aspirin

49
Q

Treatment for serum triglyceride >10 mmol/L

A

Fibrate should be used to reduce risk of pancreatitis

50
Q

How big of an impact can nutrition therapy have on HbA1C?

A

Reduce by 1-2%

51
Q

Blood glucose targets

A
  1. HbA1C <7%
    if possible with low risk of hypoglycaemia, can decrease target to HbA1C <6.5 to lower risk of nephropathy
    target HbA1C should be above 6% (below is associated with increased mortality)
  2. fasting / pre-prandial blood glucose 4-7
  3. 2hr post prandial blood glucose 5-10

Note: if PPG 5-10 cannot achieve HbA1C <7%, than aim for PPG of 5-8

to assess response to meal, blood glucose should increase by <3 at 2hr post prandial reading

52
Q

Indications for Orlistat

A
  1. diabetic patients with BMI >30 with no comorbidities or risk factors
  2. diabetic patients with BMI >27 with obesity related comorbidities or risk factors
53
Q

Indications for bariatric surgery

A

when other interventions have failed:

  1. diabetic patients with class 3 obesity (BMI>40)
  2. diabetic patients with class 2 obesity (BMI 35 - 40) with comorbidities
54
Q

Indications for less stringent HbA1C control

A

less stringent HbA1C (7-8.5%) if patient have any of following:
limited life expectancy
high level of functional dependency
coronary artery disease with high risk of ischemic event
multiple comorbidities
history of recurrent severe hypoglycemia
hypoglycemia unawareness
longstanding diabetes that is difficult to control

55
Q

Approach to antihyperglycemic therapy

A

1st line = Metformin, especially if patient is overweight

2nd line = sulfonylurea: Glyburide (Diabeta), Gliclazide (Diamicron), Glimepiride (Amaryl)

3rd line =
DPP-4 inhibitor: Sitagliptin (Januvia), Saxagliptin (Onglyza), Linagliptin (Tradjenta)
alpha-glucosidase inhibitor: Acarbose

4th line = insulin usually
insulin is added as last line agent after multiple agents (usually after 2 or 3 oral agents) or if symptomatic hyperglycemia with HHS

if insulin, first start as basal (preferably long acting), then add bolus if diabetes is still uncontrolled

if bolus insulin is used, discontinue insulin secretagogues (e.g. Sulfonylurea) whereas metformin can be continued (insulin will control sugars, but metformin still has decreased mortality effect)

56
Q

What is HHS

A

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.

Symptoms include signs of dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness. Onset is typically over days to weeks.

57
Q

What is HONK

A

Hyperglycaemic Hyperosmolar Nonketotic Coma (HONK)

HONK is a dangerous condition brought on by very high blood glucose levels in type 2 diabetes (above 33 mmol/L).

58
Q

Suggested times to check blood glucose

A

before breakfast, which is best estimate of fasting blood glucose

before meal

2hr after meal, which is best estimate of post-prandial glucose

before bed

overnight occasionally

59
Q

Insulin MOA

A

endogenous insulin is synthesized and released by beta cells in islet of Langerhans of pancreas in response to increased blood glucose

insulin binds to tyrosine kinase insulin receptors on mainly myocytes in muscle, hepatocytes in liver and adipocytes in adipose tissue, activating PI3K -> PIP3 -> PDK&Akt signalling pathway

insulin elicits cell response to decrease blood glucose including
increased glycogenesis, lipogenesis, tracylglyceride synthesis overall

decreased lipolysis, glycogenolysis, ketogenesis in all tissue cells

increased glucose uptake from blood in liver and muscle cell

increased glycogenesis and protein synthesis in adipocytes

inhibition of lipolysis

60
Q

Rapid acting bolus insulin examples

A

Humalog
Novorapid
Apidra

61
Q

Rapid acting insulin onset of action, peak of dose response, duration

A

10-15 min

1-1.5 h

4-5 h

62
Q

Short acting bolus insulin examples

A

Humulin R
Novolin
Toronto

63
Q

Short acting insulin onset of action, peak of dose response and duration

A

0.5-1h

2-4h

5-8h

64
Q

Intermediate acting basal insulin examples

A

HumulinN

Novolin NPH

65
Q

Intermediate acting basal insulin onset of action, peak and duration

A

1-3 h

5-8 h

18 h

66
Q

Extended long acting basal insulin examples

A

Lantus

Levemir

67
Q

Extended long acting basal insulin onset of action, peak and duration

A

1.5 h

No peak

24 h

68
Q

Preferred bolus and basal insulin types

A

Rapid acting because fast peak and shorter acting

Extended long acting because longer acting and no peak, reducing the risk of hypoglycemia

69
Q

Premixed insulin examples

A

Humulin 30/70
Novolin 30/70
Humalog mix 25
NovoMix 30

70
Q

Premixed insulin onset of action, peak and duration

A

10-30 min

Mix of short and intermediate

18 h

71
Q

Methods of insulin therapy

A

Premixed insulin regimen vs intensive therapy (preferred)

Intensive therapy methods:

  1. MDI basal bolus analogue intensive therapy with basal insulin, bolus insulin (before meal according to carb counting) and high blood glucose correction (bolus)
    insulin
  2. Insulin pump intensive therapy same concept as MDI with basal insulin, bolus insulin and high blood glucose correction (bolus) insulin with pump, there is automatic continuous instantaneous injection of basal insulin, bolus insulin is manually added and adjusted by user based on carbohydrate counting of meal or blood glucose level
72
Q

Approach to starting basal and bolus insulin

A

1) Basal QHS to bring blood glucose reading before breakfast to 4-7
a) start with 5-10 units QHS SC and then titrate by increasing 10% every 3-4 days until blood glucose before breakfast is at target of 4-7
b) intermediate acting insulin usually need to be split into 2 doses one at breakfast and one at night

if hypoglycaemia event, then

a) switch to Lantus or Levemir; or
b) fix by splitting dose into BID dosing (one in morning, one at night)

2) post-prandial blood glucose (2 hours post breakfast, lunch and dinner)
a) start with 5 units with meals and titrate by increasing by 10% of current dose every 3-4 days until 2 hour post prandial blood glucose is at target of 5-10
b) aim for dose of 40% basal and 60% prandial

73
Q

Approach to starting premixed insulin

A

pre-mixed insulin usually only used to decrease number of injections, usually for poor glycemic control compared to basal + bolus insulin given separately

Usually start 5-10 U daily or BID before breakfast and / or dinner

if converting from basal + bolus insulin regimen: total amount of basal and bolus units daily divided in 2/3 - 1/3 over 2 equal doses in morning and night

3rd year - Family Medicine (9 decks)

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