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PR3152 Finals > DM > Flashcards

DM Flashcards

1
Q

symptoms of preDM
what does it predispose pt to

A

asymptomatic
- impaired fasting blood glucose and impaired glucose tolerance -> entities of pre-DM
predispose to T2DM and CVD

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2
Q

which asymptomatic people should screen for DM?
what test should be done?

A

asymptomatic individuals age >=40yo +/- RF for DM

screen:
1. fasting blood glucose (FPG)
2. HbA1c

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3
Q

asymptomatic individuals with results suggestive of DM, what next?

A

repeat test on a subsequent day
when 2 repeated tests are available and above threshold = DM confirmed

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4
Q

how to prevent T2DM for pre-DM (non pharm)

A

healthy diet
physical activity (150mins of moderate/ 75mins vigorous)

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5
Q

how to prevent T2DM for pre-DM (pharm)
- when should it be started?

A

metformin for pre-DM
- started when glycemic control not improved despite lifestyle intervention OR unable to adopt lifestyle interventions

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6
Q

what is DM? symptoms?
what are the different types of DM?

A

DM is a metabolic disorder characterised by resistance to insulin to insufficient insulin secretion or both
- main sx: hyperglycaemia
- types: type 1, 2, gestational DM

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7
Q

define type I DM

A

absolute deficiency of pancreatic beta cells function (no insulin)
- is an autoimmune disease
- with positive antibodies

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8
Q

stages in T1DM, glycemia level, symptoms

A
  • autoimmunity (positive antobodies)
    stage 1: normoglycemia, presymptomatic
    stage 2: dysglycemia, presymptomatic
    stage 3: new onset hyperglycemia, symptomatic
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9
Q

when is T1DM diagnosed

A

-> long pre-clinical period (from children - adults)
children (very early)
adults (LADA)

  • Latent autoimmune diabetes of adults
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10
Q

what is C-peptide? when is it absent?

A

is a short chain aa that is released into blood as a byproduct of formation of insulin by pancreas

  • absent when there is no insulin release (permanent DM)
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11
Q

define T2DM

A

progressive loss of adequate beta-cell insulin secretion + insulin resistance

early stage: high glucose, high insulin

  • insulin resistance: in presence of insulin, glucose utilisation is impaired and hepatic glucose output increased
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12
Q

differentiate T1 and T2 DM

A

T1:
- autoimmune, positive antibodies
- insulin/ c-peptide absent
- onset usually <30yo
- abrupt onset
- very thin
- prone to diabetic ketosis, diabetic ketoacidosis (emergency)

T2:
- insulin resistance, impaired secretion (later stage), negative antibodies
- insulin/ c-peptide normal/abnormal
- gradual onset
- often overweight
- uncommon for diabetic ketosis, diabetic ketoacidosis (emergency)

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13
Q

metabolic syndrome management

A

abdominal obesity (measure waist circumference)

  • need to recognise early and use aggressive CV reduction
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14
Q

S/S of hyperglycemia

A
  • 3Ps: polyuria, polydipsia, polyphagia
  • frequent urination
  • dry skin
  • blurred vision
  • drowsiness
  • decreased healing
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15
Q

S/S of hypoglycemia

A
  • shaking
  • fast HR
  • sweating
  • dizziness
  • anxoius
  • hunger
  • impaired vision
  • headache
  • irritable
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16
Q

parameters used to measure DM

A
  1. fasting plasma glucose (FPG)
    - no intake for past 8hrs
  2. random/casual plasma glucose
    - take at any time of the day
  3. postprandial plasma glucose (PPG)
    - glucose after meals/ OGTT 75mg glucose
  4. HbA1c: measure bld glucose over past 3 mths (FPG + PPG)
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17
Q

higher HbA1c range is due to …

A

FPG (basal hyperglycemia) -> use insulin that targets FPG

less high HbA1c is due to PPG

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18
Q

criteria for T2DM
- HbA1c, FPG, 2HOGTT ranges

A

see notes eL 2 pg 8

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19
Q

complications of DM

A

macovascular: CV
microvascular: retinoapthy, nephropathy, neuropathy

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20
Q

during diabetic foot screening what to advice pt

A
  • obtain glycemic control
  • encourage smokers to quit
  • good footcare and appropriate wound care
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21
Q

diabetic nephropathy test: what is tested?

A

SCr and/or eGFR
AND
uACR or uPCR

-uPCR used when albumin >= 300mg/g

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22
Q

how often to screen for macrovascular complications (HbA1c, lipid panel, BP)

A

HbA1c: every 3mth, 6mth if stable
lipid panel: every 3-6mths, 1yr if stable
BP: every visit

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23
Q

how often to screen for macrovascular complications (eye, kidney, foot)

A

eye, kidney: every 6mth, yearly if stable
foot: daily by pt, annually by podiatrist

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24
Q

treatment goals for HbA1c

A

<7%

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25
Q

tx goals for FPG

A

4.0 - 7.0 mg/dL

26
Q

tx goals for PPG

A

<10 mg/dL

27
Q

for t1dm <7% glycemic control, does it improve macro and micro complications?

A

improve micro
macro unknown

28
Q

for t2dm <7% glycemic control, does it improve macro and micro complications?

A

micro improve
macro U shape (decrease until a certain point then increase macrovascular death)

29
Q

when to use stringent HbA1c target

A

Short disease duration
long life expectancy
no significant CVD

30
Q

when to use less stringent HbA1c target

A

hx of hypoglycemia
limited life span
advanced complications
extensive comorbidities
difficult to attain despite SMBG, counselling, effective tx

31
Q

MOA of metformin

A
  1. ↓ hepatic glucose production
  2. ↑ peripheral/muscle glucose uptake and utilization (i. e.↑ insulin sensitivity)
32
Q

onset of metformin

A

within days; max effects take up to 2 weeks

33
Q

how is metformin eliminated

A

renal, mostly unchaged

34
Q

max dose for metformin immediate release and extended release

A

immediate release: 2550mg/d (850mg TDS)
- can be used in children >= 10yo

extended release: 2000mg/d
- not to be used in children

35
Q

AE of metformin

A
  1. GI disturbances (D/N?V), loss of appetite,
    metallic taste
  2. decr vit B12 concentrations
  3. lactic acidosis
36
Q

CI of metformin

A
  1. eGFR <30mL/min (stage 4 CKD, severe renal impairment)
  2. hypoxic states or at risk of hypoxia (increase risk of lactic acidosis (eg HF, sepsis, repi failure, liver failure, alcholism)
37
Q

Sign and symptoms of lactic acidosis

A

nausea, vomiting, abdominal pain shallow/labored breathing, mental confusion
- see dr

38
Q

metformin DDI

A
  • alcohol
  • iodinated contrast material (eg CT scan)
    -> hold metformin for >= 48hrs
  • inhibitors of organic cationic transporters (cimetidine, dolutegravir, ranolazine) -> increase metformin by decreasing renal elimination
39
Q

metformin place in therapy

A
  • ↓ A1C by 1.5% (up to 2.0%)
  • Negligible weight gain and hypoglycemia
  • Possible reduction in CV events
  • Prevent and delay T2DM
  • Can be used for pregnant patients with T2DM
40
Q

TZD MOA:

A

PPARgamma agonist to promote glucose uptake into the target cells (increase insulin sensitivity, decrease insulin resistance)
- no effects on insulin secretion

41
Q

TZD how long to take effect?

A

Takes up to a month for maximal effect

42
Q

elimination of tzd

A

liver

43
Q

eg of tzd

A

pioglitazone

44
Q

ddi of pioglitazone

A

CYP3A4 and CYP2C8 inhibitors or inducers

45
Q

AE of TZD

A
  1. Hepatotoxicity (monitor LFT_
    - Do not initiate therapy/discontinue if ALT >3x UNL
  2. Fluid retention (caution in HF)
  3. Fracture
  4. Weight gain (dose related)
  5. Risk of bladder cancer (black box warning)
  6. Increased risk of hypoglycemia with insulin therapy
46
Q

CI of TZD

A
  1. Active liver disease
  2. Symptomatic or history heart failure
  3. Active or history of bladder cancer
47
Q

TZD (pioglitazone) place in therapy

A
  • ↓ HbA1c by 0.5 to 1.4%
  • beneficial in patients with Fatty Liver Disease
  • CV effects: reduce stroke, increase HF
48
Q

SU MOA

A
  1. block K+ channels of beta cells, stimulate insulin secretion
  2. ↓ hepatic glucose output and ↑ insulin sensitivity (like metformin)
  • Need functional Beta cells to work!
49
Q

Eg of SU and how they are cleared

A

tobulamide (H)
glipizide (H), glibeclamide (R), glicazide (R)
glimepiride (R)

50
Q

advantage of 3rd gen SU/ glicazide MR

A

once daily dosing improved adherece but higher cost

51
Q

AE of SU

A
  1. hypoglycemia
  2. weight gain
52
Q

CI of SU

A

hypersensitivity to any SU

53
Q

DDI of SU

A
  1. betablockers (mask sx of hypoglycemia)
  2. alcohol (disulfiram like reaction) (1 gen» 2/3 gen)
  3. CYP2C9 inhibitors (amiodarone, fluoxetine) may increase glimpiride, glipizide
54
Q

SU place in therapy

A
  • ↓ HbA1c by 1.5% (Require the presence of functioning β cells to work)
  • watch for hypoglycemia
  • exercise to reduce weight gain
  • cost effective therapy
55
Q

DPP4i MOA

A

Inhibit DPP4 enzyme and increase concentrations of endogenous incretins (decrease gastric emptying, increase insulin, decrease glucagon, makes you full)

56
Q

examples of DPP4i

A

sitagliptin
vildagliptin
linagliptin

57
Q

doing for DDP4i

A

sitagliptin
- 100mg OD
- eGFR 30-45 -> 50mg OD
- eGFR <30 -> 25mg OD

vildagliptin
- 50mg BD (with metformin or TZD)
- 50mg OD witth SU
- CrCl<50 -> 50mg OD

linagliptin
- 5mg OD

58
Q

AE of DPP4i

A
  1. sever joint pain that can be disabling
  2. headache
  3. acute pancreatitis
  4. hypersensitivity reaction
  5. bullous pemphigoid, skin rash (use prednisolone)
59
Q

DDI for DPP4i

A

sitagliptin: digoxin (increase DPP4i)
vildagliptin: none
linagliptin: cyp3A4 inducers (decrease DPP4i)

60
Q

DPP4i place in therapy

A
  • ↓ HbA1c by 0.5-0.8%
  • Usually used as dual or triple combination therapy
  • Not recommended to be used in patients with hx of acute pancreatitis

Advantages over GLP 1 agonists:
-PO, lower incidence of GI adverse events, cheaper
Disadvantages compared to GLP 1 agonists:
weight neutral, smaller HbA1c reduction, no “big 3” benefits (ASCVD, HF, CKD)

PR3152 Finals (4 decks)

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