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EXMD4743 > WK2 - T2DM > Flashcards

WK2 - T2DM Flashcards

1
Q

What are high levels of glucose in blood caused by?

A
  • inability to produce insulin
  • body unable to use insulin effectively
  • both ^^

Diabetes = siphon/pass through (greek)
Mellitus = honeyed/sweet

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2
Q

How does Medicare rebate work for T2DM in Australia?

A
  • receive rebates for group services! provided by diabetes educators, EP’s and dietitians on GP referral
  • Item 81110 - Ax for group service
  • involves comprehensive patient Hx, patient goals and preparing for appropriate group services program.
  • Initial Ax can be taken by diabetes instructor (81100), EP (81110) or dietitian (81120), it is generic in nature - covers factors relevant to all professions - patient then directed to any combo of group services
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3
Q

What is the prevalence of T2DM in Aus

A

1 in 17 adults (6%) - 1.2mil had T2DM in 2017

Indigenous Aus - 4x likely to have T2DM, hospitalisation, deaths

29,800 started using insulin in 2017 for T2DM

Since 2001, prevalence of Aus 18y+ has almost doubled from 3.3%

Since 2014-15 - trend relatively stable

men > females
lowest socioeconomic group>highest

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4
Q

What are the 4 classes of diabetes?

A
  1. T1DM
  2. T2DM
  3. gestational
  4. other - e.g. LADA (latent autoimmune diabetes) - rare 30y+, slow progression.
    Monogenic diabetes - rare, single gene mutation
    Brittle Diabetes - rare, chronic pancreatitis-associated

ADD. related conditions:
* intermediate hyperglycaemia/pre-diabetes/impaired glucose tolerance/impaired fasting glucose
* metabolic syndrome

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5
Q

What is the most common form of diabetes?

A

T2DM - insulin resistance (+/- secretory deficit
* gen. later onset
* produce insulin but not enough/cannot use effectively
* genetic component but largely preventable
* managed with lifestyle + med
* formally called - adult onset diabetes, non-insulin dependent diabetes
* often unDx until complications appear

Common >55y+

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6
Q

What is the burden of disease statistic?

A

12th largest contributor to Aus disease burden 2015

Just over 1 in 10 Aus deaths in 2017 - diabetes related

in 2015, 4.7% total disease burden could be prevented by reducing exposure to high blood plasma glucose levels

2015-16, est. 2.3% ($2.7bil) of total disease expenditure in Aus was attributed to diabetes

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7
Q

What is the West Moreton Diabetes Alliance?

A

2017-18 - diabetes leading cause of preventable hospitalisation
2000 preventable hospital stays

2013-2017 - diabetes caused avg. 45 local deaths/year (higher than state avg.

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8
Q

What are the risks of lower limb amputations?

A
  • T2DM damages nerves - peripheral neuropathy = poor circulation (peripheral vascular disease)
  • ischaemia, gangrene and impaired would healing = foot ulcers/infections and in severe cases –> amputations of affected toes/foot/lower leg
  • T2DM leading cause of non-traumatic lower-limb amputation
  • 2016-17, 4700 lower limb amputations provided to patients iwth Dx of diabetes/peripheral vascular disease
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9
Q

Provide the pathophysiology of T2DM.

A
  • marked insulin resistance with insulin secretory defect
  • decrease insulin action may be caused by genetics/ab-obesity
  • factors secreted by VAT (e.g. cytokines) act on liver to disrupt function
  • increased draining of FFA to portal vein = non-alcholic fatty liver disease = decrease glucose control
  • decrease insulin-mediated storage of glucose (liver, muscle)
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10
Q

What 4 factors are part of glycaemic control?

A
  1. liver
  2. adipose tissue
  3. pancreas
  4. muscle
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11
Q

What is the “Ominous Octet”?

A

They are the 8 factors that occur during hyperglycaemia.
1. impaired insulin secretion
2. neurotransmitter dysfunction
3. increased lipolysis
4. increased glucose reabsorption
5. decreased glucose uptake
6. decreased incretin effect
7. increased hepatic glucose production
8. increased glucagon secretion

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12
Q

What is the difference between insulin resistance and hepatic insulin resistance?

A

Insulin - reduced insulin-stimulated glucose uptake in skeletal muscle - impaired suppression of endogenous glucose production

Hepatic - impaired ability of insulin to inhibit glucose production

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13
Q

What is muscle (peripheral) insulin resistance?

A
  • ability for muscles to utilise or store glucose
  • total glucose disposal by muscle cell - Glut 4 transport into cell
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14
Q

How to Dx and Ax diabetes?

A

HbA1c >6.5% (48mmol/mol)
fasting glucose >7mmol/L
random glucose >11.1mmol/L

On 75g oral glucose tolerance test
Fasting glucose >7mmol/L or 2hr glucose >11mmol/L

From The Royal College of Pathologists of Australiasia Criteria

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15
Q

How is fasting plasma glucose (FPG) performed?

A

Meausre of “acute” BG control

Easy to measure, but day-to-day variation limits reproducbility

FPG aim: 3-5.4mmol/L

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16
Q

What is the process of Glycated Haemoglobin (HbA1c)?

A
  • gold standard measure of glycaemic control
  • new diagnostic criteria
  • reflext 3M BG control
  • perform 2/year in well controlled DM, and every 3/12 in poorly controled DM or changes in Rx
  • HbA1c aim <7%
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17
Q

What is Postprandial Blood Glucose?

A
  • predicts CV outcome independently of fasting BG in some epidemiological studies
  • measured 2hrs after approx. BG peak
  • reflects different “component of glycaemic control

i.e. “good” fasting glycaemic control may accompany “poor” postprandial BG and vice versa: they are 2 independent processes contributing to HbA1c values

  • limited by poor standardisation (variation in meal nutrient content/caloric quantity etc)
  • postprandial (2hr) BG aim: <7.8mmol/L
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18
Q

What is the oral glucose tolerance test?

A
  • common clinical test for Dx of IGT and T2D
  • BG measured after fasting and then again 2hrs after drinking 75g anhydrose glucose dissolved in water

Interpretation:
- Normal <7.8mmol/L
- IGT 7.8-11mmol/L
- T2d> 11mmol/L

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19
Q

What are ketones?

A
  • produced in liver, from fat
  • used as fuel when glucose level low
  • production increases when insulin levels low (e.g. T1DM)
  • people with T1DM measure ketones (in urine or blood) if hyperglycaemia is suspected
  • in blood - measuring blood 3-beta-hydroxybutyrate - threshold >0.6mmol/L
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20
Q

What is the difference between ketosis and ketoacidosis?

A

Ketosis
- normal increase in ketones occurs when hungry/post Ex
- associated with hyperglycaemia in T1DM

Ketoacidosis
- life threatening
- Sx (rapid breathing, flushed cheeks, abdominal pain, sweet acetone (similar to pain thinner or nail polish remover) smell on breath, vomitting, dehydration

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21
Q

What are the risk factors for T2DM?

A
  • age, minority ethnicity, family Hx, low socioeconomic status
  • obesity (fat distribution - intraabdominal/visceral)
  • lifestyle factors: physical inactivity, diet
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22
Q

How is the role of exercise in prevention of T2DM?

A

Incidence:
* lifestyle: 58%
* metformin: 31%

Results from study:
* cumulative incidence of T2DM
- 4.8% lifestyle
- 7.8% metformin
- 11% placebo
* 58% reduction in risk
* 58% adherence

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23
Q

There is no “Tx”. How is T2DM managed?

A

All based on glycaemic control!

Glycaemic control is influenced by: diet, meds and exercise

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24
Q

What would be part of the multidisciplinary team for someone with T2DM?

A
  • GP
  • diabetes dietitian
  • ADEA - educator
  • clinical pharmacist
  • endocrinologist
  • EP
  • psychologist
  • clinical nurse specialist
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25
Q

The percentage of people achieving therapeutic goals is trending in the wrong direction. T or F?

A

True!
* despite control of glycated haemoglobin <7%, BP <140/90mmHg and non-HDL cholesterol <130mg/dL, the % of people achieving therapeutic goals is steady with slight decline

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26
Q

How did the Direct trial of a Very-Low Calorie Diet for T2DM go?

A

Diet: 825kcal/day for 3M

Results:
- avg. weight loss 10kg
weight loss and remission
- <5kg: 5%
- 5-10kg: 29%
- >15kg: 70%

Considerations
* rapid change in weight, glucose
* convenient, no tracking
* cost may not exceed food expense

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27
Q

What happened in the Direct trial for very-low calorie diet in responders and non-responders?

A

Responders = nondiabetic A1C
Non-responders = A1C remains high

Both:
* liver/pancreas fat decreases
* glucose-stimulated acute insulin secretion returns only in responders

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28
Q

What are the mechanisms of exercise?

A

Glucose uptake from blood into skeletal muscle stimualted by 2 independent pathways:
1. insulin-mediated
2. exercise-mediated

Insulin-dependent glucose uptake
Insulin-independent glucose uptake

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29
Q

What are the acute exercise effects on blood glucose?

A

Immediate lowering of blood glucose
- dependent on intensity/duration of activity
- increase muscle glucose utilisation

Non-Insulin mediated glucose uptake
- persists for several hours

Increased insulin sensitivity
- up to 72hr following single bout

30
Q

Where are the exercise prescription/guidelines for T2DM published?

A

ADA/ACSM - 2010
AHA - 2009
ADA 2016
ACSM 2013

31
Q

What is the recommended aerobic training for T2DM and pre-diabetes?

A

Mode: large muscle group activities
Duration: >10mins
No more than 2 consecutive sedentary days (cosnider acute effects)
INTENSITY
- low at initial
- higher intensity if patient can tolerate
- vig/high intensity encouraged to promote increased aerobic fitness

Volume is likely insufficient to facilitate weight loss alone

32
Q

What is the Exercise prescription for Resistance Training in T2DM and pre-diabetes?

A
  • nonconsecutive days
  • each set to near-fatigue
  • acute gains in insulin action also apply to RT technique
  • risk of hypertensive responses: minimise sustained handgrip, static exercise and Valsalva manoeuvre
33
Q

What is the Ex prescription for all diabetics?

A
  • little/no different between “prescription” guidelines accorss various types of diabetes
  • compared to people w/o diabetes - frequency should be as high as possible
  • increases acute benefits of each Ex bout
  • important differences across types of diabetes come with special considerations needed during Ex delivery.
34
Q

What is included in the initial review of Ex prescription?

A
  • diabetic type
  • type/changes in med regimen
  • other relevant clinical data (e.g. resting BG, BP, HR, O2 saturation)
  • co-morbidities
  • other findings or observations which may impact on participation in Ex program
35
Q

What are the benefits of aerobic training in T2DM?

A
  • increase energy expenditure –> weight loss
  • improve glucose uptake (non insulin mediated) –> glycaemic control
  • improve insulin sensitivity (<72hr) –> glycaemic control
  • improve CRF (associated with decrease mortality risk)
  • improve myocardial/vascular function
  • improvement in risk factors for CV (lipids, BP etc)
  • QoL –> ADLs
36
Q

What are the benefits of RT in T2DM?

A
  • improve muscular strength/endurance
  • improve insulin sensitivity - glycaemic control
  • improve body comp. - glycaemic control/weightloss
  • improve QoL - ADLs
37
Q

What are key notes on the Ex guidelines?

A
  • not an Ex recipe
  • patients require tailored/individualised Ex programs
  • long-term Ex adherence is key - everything else is secondary
  • Ex dose-response

Anything > nothing
* guidelines > anything
* more than guidelines > guidelines

38
Q

What is included in the enhance primary care plan (now CDM) for Weight Problems?

A
  • increase PA // fitness
  • change diet/lifestyle
  • dietary discipline
  • reduce weight, CV risk

Required Tx:
* referral to dietitian and AEP

39
Q

What is included in the enhance primary care plan (now CDM) for Hypertension?

A
  • CV Ax
  • increase PA
  • reduce total cholesterol levels

Required Tx
* regular med, check ups, diet, Ex and investigation
* referral to cardiologist

40
Q

What is included in the enhance primary care plan (now CDM) for NIDDM?

A
  • routine ophthalmic Ax
  • Cv Ax
  • strict BSL control
  • increase PA
  • change diet/lifestyle
  • patient education
  • reduce total cholesterol levels
  • counselling
  • compliance with Tx
  • community services help, support/follow up
  • improve QoL
  • adequate physical and emotional support

Required Tx:
* dietitan/diabetic education
* EP
* endocrinologist
* regular med and GP

41
Q

What to consider for Anginine S/L tablet 600mcg; 1 s/l p.r.n?

A

Tx for acute angina pectoris

Ensure carry during Ex sessions

42
Q

What to consider for diamicro MT tablets 30mg; 1 daily?

A

Control blood glucose in T2DM

43
Q

What to consider for ditropan tablet 5mg; 1/day?

A

Tx loss of bladder control, a frequent need to pee and other Sx of an overactive bladder

Antispasmodic
Anticholinergic

44
Q

What to consider for Imdur tablet 60mg; 1 tab mane?

A

Angina medication - prevention

45
Q

What to consider for Lipitor Tablets 60mg; 1/day?

A

Lower bad cholesterol and reduce stroke risk, heart attack, and other heart and blood vessel problems

46
Q

What to consider for Nexium Tablet 40mg 1 tab nocte?

A

For GORD Sx

Tx conditions that cause too much stomach acid like stomach ulcers or reflux disease

47
Q

What to cosnider for Plavix tablet 75mg; 1 daily?

A

To prevent blood clots

Platelet aggregation inhibitor

48
Q

What to consinder for Tritace capsule 10mg; 1 tab mane?

A

Tx for hypertension

ACE inhibitor

** Delay in onset of Ex program while HT addressed. resting DBP on initial visit 126 - Ex program commended 1M post with BP: 139/95

49
Q

What to consider for ibuprofin?

A

OA, only when flare up

Pain reliever

50
Q

What are some general considerations prior to an Ex session?

A
  • timing, amount/ type of previous food intake
  • meds used that day - including other medications secondary to treating diabetes (e..g beta-blockers - attenuate HR response to Ex - may mask hypoglycaemic Sx of palpitations/racing heart)
    *BGL and trend prior to Ex
  • Ax of any new Sx and current health status

Use these details + knowledge of mode, duration and intensity of Ex session for clinical decision making

51
Q

What should we check before Exercising?

A
  • feet should be checked before/after each session
  • Ex with partner/supervised
  • Med dosage may (likely) need to be adjusted)
  • ensure adequate fluid intake
  • avoid high environmental temp.
  • any Sx of patient feeling unwell sould be a contraindication to starting/continuing Ex
  • continuous glycose monitoring (CGM) - useful to better understand directions nad magnitudes of change in glucose/ allow more accurate adjustments in meds.
52
Q

What is the Dawn Phenomenon?

A

More insulin resistance in morning
* due to increased release of cortisol and growth hormone in early morning, resulting in decreased insulin action

53
Q

What to do for a phyoglycaemic patient?

A

BG <4mmol/L - relative decrease

Avoid Ex during peak insulin periods, do not inject into exercising limbs

Eat one serve of fast acting CHO and re-check in 15mins - refer to decisoin tree and action plan
–> wait until >7mmol/L before Ex

If pre/postEx BG <5.55mmol/L, ingest 1-2 serves (15-30g) of slow acting CHO, check after 15mins

Carry one serve of slow acting and one serve of fast CHO when Ex

54
Q

What specific considerations are required for T2DM?

A
  • Whether its insulin and/or sulfonylurea OR lifestyle and/or diabetes medications other than insulin/sulfonlurea - Separate Action Plans

INSULIN - be aware of patients insulin action profile important - patient taking short/rapid/intermediate acting insulin should avoid exercising when blood insulin level peaks

Hypoglycaemia - RED FLAG, action plan as per T1DM (initial Tx with fasting acting CHO) - depends on meds

Hyperglycaemia - RED FLAG >16.7mmol/L
* actions depend on recent food/med intake - See action plan

55
Q

What to consider for peripheral neuropathy and foot care?

A
  • peripheral neuropathy increases risk of foot ulcers/fracture
  • limit weight-bearing activities for patients with advanced neuropathy
  • may impact gait/balance during Ex
56
Q

What are some extra considerations for retinopathy?

A
  • risk of retinal detachment/vitreous hemorrhage with Ex - will not worsen with appropriate Ex

In practice:
* avoid higher intensities, activities that elevate BP significantly, movements involving jarring, head-down or elevated arms
* AVOID valsalva

57
Q

What are some extra factors to consider for nephropathy?

A
  • may limit Ex capacity
  • low-mod intensity Ex may be required

IN practice:
- avoid activties which elevate SBP 180-200mmHg, vig cardio or RT and Valsalva

58
Q

What are some random factors to consider?

A

Co-morbidities: hypertension, dyslipidemia, obesity, CVD and PVD

Medications

Hyperglycaemia may cause polyuria, polydipsia, weight loss and blurred vision

Dehydration may result from polyuria nad compromise thermoregulation

59
Q

What are the macro- and micro-vascular complications of T2DM?

A

CVD
* athersclerotic
* hypertensive
* peripheral arterial disease

Retinopathy

Neuropathies
* peripheral
* autonomic
* nephropathy

60
Q

How can diabetic retinopathy (associated with vision loss) be prevented?

A
  • intensive glycaemic control
  • tight BP control (<130mmHg)
  • comprehensive eye examinations
61
Q

What is the prevalence of diabetic neuropathy?

A

~60-70% of diabetics have mild to severe forms
of nervous system damage

Includes: Impaired sensation/pain in feet/hands * 1/3 of diabetics have pain
* Slow digestion of food
* Other nerve problems (e.g. carpal tunnel syndrome)
* Numerous types –> Most common - DPSN – diabetic peripheral sensory neuropathy (glove and stocking distribution)

62
Q

What are the Sx of diabetic neuropathy?

A
  • pain
  • paresthesia
  • loss of vibratory sensation

Complications: pain, ulcers, stress fractures and amputation

63
Q

What is symmetric polyneuropathy?

A
  • most common form of diabetic neuropathy
  • affects distal lower extremities and hands
64
Q

What is autonomic polyneuropathy?

A

Affects autonomic nerves controlling internal orgrans
-peripheral
- genitourinary
- gastrointestinal
- CV

Classified as clinical or subclincal based on presence/absence of Sx

65
Q

What drug stimulates the pancreas to make more insulin?

A

Sulfonylureas Meglitinides
* decreases FPG 3-4mmol/L
* reduces A1C by 1-2%

Effects:
- hypoglycaemia, weight gain

Brands:
1st gen. chlorpropamide (diabinese), tolazamide, acetohexamide (dymelor) and tolbutamide
2nd gen. Glyburide (micronase, glynase and DiaBeta), glimepiride (Amaryl), Glipizide (glucotrol, glucotrol XL

66
Q

What drug sensitises the body to insulin and/or control hepatic glucose production?

A

Thiazolidinides
&
Biguanides (Metformin)
* decreases FPG by 3-4mmol/L
* reduces A1c 1-2%

Effects:
* diarrhea and abdominal discomfort
* small decrease in LDL cholesterol and triglycerides
* possible modest weight loss
* contraindicated in patients with impaired renal function

Brands: metformin (glucophage), metformin hydrochloride extended release (glucophage XR)

67
Q

What drug slows the absorption of starches?

A

Alpha-glucosidase inhibitors
* decrease peak postprandial glucose 2-3mmol/L
* decrease FPG 20-30mg/dl (1.4-1.7mmol/L)
* decrease A1C 0.5-1%
Effects:
* flatulence/abodminal discomfort
Contraindicated in patients with IBS or cirrhosis

Brands: acarbose (Precose), Miglitol (glyset)

68
Q

What are the 4 medications that are used to treat T2DM?

A
  • insulin
  • sulfonylureas meglitinides
  • biguanised (metformin) thiazolidinediones
  • alpha-glucosidase inhibitors
69
Q

What is Insulin?

A

Used T1D and T2D
* only injected

Basal-bolus routine:
- longer acting form of insulin to keep BGL stable through periods of fasting (no peak, lasts 24hrs)
- separate injections of shorter acting insulin to prevent rises in BGL from meals (1-20min action; 1hr peak 3-5hr duration)

70
Q

What is Thiazolidinediones (Glitazones)?

A

Decrease insulin resistance (muscle/adipose cells more sensitive to insulin; suppress hepatic glucose production
* decrease FPG ~2mmol/L
* reduce A1C ~0.5-1%
* 6wks for max. effect
Effects:
* weight gain, oedema
* hypoglycaemic (if taken with insulin/agents that stimualte insulin release)
* contraindicated in patients with abnormal liver function or CHF
* improves HDL cholesterol and plasma triglycerides; usually LDL neutral

Brands: pioglitazone (actos); rosiglitazone (Avandia)

71
Q

What is the DPP4 inhibitor and what is the difference with SGLT2 inhibitor?

A

Dipeptidyl Peptidase-4 = enzyme that destroys hormone incretin
* incretins increase production of insulin when needed, reduce amount of glucose produced by liver when not needed

Sodium-Glucose Co-transport 2 helps reabsorb glucose into blood
* blocking allows kidney to lower BGL and excess glucose removed via urine

72
Q

Why is GLP-1 Receptor Agonism special?

A

Regulates body weight and glucose metabolism.

Tells…
* Liver - decrease gluconeogenesis and steatosis
* Intestine - decrease gastric emptying and GI motility
* Brain - decrease food intake, reward behaviour, palatability
* Muscle - increase insulin sensitivity and glucose uptake
* Pancreas - increase insulin secretion/synthesis and beta-cell survival - decrease glucagon secretion nad apoptosis

EXMD4743 (9 decks)

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