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
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
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
4
Q
What are the 4 classes of diabetes?
A
- T1DM
- T2DM
- gestational
- 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
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+
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
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.
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
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)
10
Q
What 4 factors are part of glycaemic control?
A
- liver
- adipose tissue
- pancreas
- muscle
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
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
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
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
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
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%
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
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
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
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
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
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
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
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
25
The percentage of people achieving therapeutic goals is trending in the wrong direction. T or F?
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
26
How did the Direct trial of a Very-Low Calorie Diet for T2DM go?
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
27
What happened in the Direct trial for very-low calorie diet in responders and non-responders?
Responders = nondiabetic A1C
Non-responders = A1C remains high
Both:
* liver/pancreas fat decreases
* glucose-stimulated acute insulin secretion returns only in responders
28
What are the mechanisms of exercise?
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
29
What are the acute exercise effects on blood glucose?
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
Where are the exercise prescription/guidelines for T2DM published?
ADA/ACSM - 2010
AHA - 2009
ADA 2016
ACSM 2013
31
What is the recommended aerobic training for T2DM and pre-diabetes?
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
What is the Exercise prescription for Resistance Training in T2DM and pre-diabetes?
- 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
What is the Ex prescription for all diabetics?
- 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
What is included in the initial review of Ex prescription?
* 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
What are the benefits of aerobic training in T2DM?
* 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
What are the benefits of RT in T2DM?
* improve muscular strength/endurance
* improve insulin sensitivity - glycaemic control
* improve body comp. - glycaemic control/weightloss
* improve QoL - ADLs
37
What are key notes on the Ex guidelines?
* 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
What is included in the enhance primary care plan (now CDM) for Weight Problems?
* increase PA // fitness
* change diet/lifestyle
* dietary discipline
* reduce weight, CV risk
Required Tx:
* referral to dietitian and AEP
39
What is included in the enhance primary care plan (now CDM) for Hypertension?
* CV Ax
* increase PA
* reduce total cholesterol levels
Required Tx
* regular med, check ups, diet, Ex and investigation
* referral to cardiologist
40
What is included in the enhance primary care plan (now CDM) for NIDDM?
* 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
What to consider for Anginine S/L tablet 600mcg; 1 s/l p.r.n?
Tx for acute angina pectoris
Ensure carry during Ex sessions
42
What to consider for diamicro MT tablets 30mg; 1 daily?
Control blood glucose in T2DM
43
What to consider for ditropan tablet 5mg; 1/day?
Tx loss of bladder control, a frequent need to pee and other Sx of an overactive bladder
Antispasmodic
Anticholinergic
44
What to consider for Imdur tablet 60mg; 1 tab mane?
Angina medication - prevention
45
What to consider for Lipitor Tablets 60mg; 1/day?
Lower bad cholesterol and reduce stroke risk, heart attack, and other heart and blood vessel problems
46
What to consider for Nexium Tablet 40mg 1 tab nocte?
For GORD Sx
Tx conditions that cause too much stomach acid like stomach ulcers or reflux disease
47
What to cosnider for Plavix tablet 75mg; 1 daily?
To prevent blood clots
Platelet aggregation inhibitor
48
What to consinder for Tritace capsule 10mg; 1 tab mane?
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
What to consider for ibuprofin?
OA, only when flare up
Pain reliever
50
What are some general considerations prior to an Ex session?
* 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
What should we check before Exercising?
* 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
What is the Dawn Phenomenon?
More insulin resistance in morning
* due to increased release of cortisol and growth hormone in early morning, resulting in decreased insulin action
53
What to do for a phyoglycaemic patient?
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
What specific considerations are required for T2DM?
* 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
What to consider for peripheral neuropathy and foot care?
* peripheral neuropathy increases risk of foot ulcers/fracture
* limit weight-bearing activities for patients with advanced neuropathy
* may impact gait/balance during Ex
56
What are some extra considerations for retinopathy?
* 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
What are some extra factors to consider for nephropathy?
* 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
What are some random factors to consider?
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
What are the macro- and micro-vascular complications of T2DM?
CVD
* athersclerotic
* hypertensive
* peripheral arterial disease
Retinopathy
Neuropathies
* peripheral
* autonomic
* nephropathy
60
How can diabetic retinopathy (associated with vision loss) be prevented?
* intensive glycaemic control
* tight BP control (<130mmHg)
* comprehensive eye examinations
61
What is the prevalence of diabetic neuropathy?
~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
What are the Sx of diabetic neuropathy?
* pain
* paresthesia
* loss of vibratory sensation
Complications: pain, ulcers, stress fractures and amputation
63
What is symmetric polyneuropathy?
* most common form of diabetic neuropathy
* affects distal lower extremities and hands
64
What is autonomic polyneuropathy?
Affects autonomic nerves controlling internal orgrans
-peripheral
- genitourinary
- gastrointestinal
- CV
Classified as clinical or subclincal based on presence/absence of Sx
65
What drug stimulates the pancreas to make more insulin?
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
What drug sensitises the body to insulin and/or control hepatic glucose production?
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
What drug slows the absorption of starches?
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
What are the 4 medications that are used to treat T2DM?
* insulin
* sulfonylureas meglitinides
* biguanised (metformin) thiazolidinediones
* alpha-glucosidase inhibitors
69
What is Insulin?
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
What is Thiazolidinediones (Glitazones)?
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
What is the DPP4 inhibitor and what is the difference with SGLT2 inhibitor?
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
Why is GLP-1 Receptor Agonism special?
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
