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Clinical Nutrition 1 Final McGill Uni > Diabetes > Flashcards

Diabetes Flashcards

1
Q

definition of Diabetes Mellitus

A
  • a metabolic disorder
  • characterised by elevated blood glucose concentrations and disturbance of CHO, lipids and protein
  • due to defective insulin secretion or action
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2
Q

classification (5)

A

DM1\DM2\Gestational diabetes(during pregnancy only)/pre-diabete/other: genetic defect, pancreatopathy

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3
Q

T/F insulin resistance can be indicated by a decreased insulin level

A

F IR can still maintain a normal insulin level or hyperinsulinemia. It cannot fully response to the level of blood glucose but the blood sugar level is just little impaired

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4
Q

mechanism of DM1

A

autoimmune or idiopthic destruction of pancreatic B cell. the cell degradation can because of aging

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5
Q

T/F all DM pts need insulin Tx

A

F

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6
Q

T/F all DM1 pts need insulin Tx

A

T

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7
Q

T/F all DM2 pts need insulin Tx

A

F

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8
Q

T/F all DM2 pts with ketosis prone need insulin Tx

A

T

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9
Q

T/F all DM pts who can resist ketosis do not need need insulin Tx

A

F

25% need insulin Tx

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10
Q

what is surveillance program for

and list two system/policies associated

A

it provides the equality to access the healthcare and education about DM
Canadian Diabetes Strategy/Aboriginal Diabetes Initiative/ Canadian Chronic Disease Surveillance System

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11
Q

List the factors affecting the DM prevalence

A

gender (M>F), region, age,
races, healthcare system, the trend of time
it is a global concern

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12
Q

List 4 common initial observation of DM2

A

polydipsia
polyuria
polyphagia
obesity

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13
Q

list three lab test reveal (more for DM2)

A

hyperglycemia
glycosuria
GTT: abnormal glucose tolerance

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14
Q

Why, in terms of metabolism, DM1 is suggested to fasting than eating under a severe condition?

A

A.A. do not used to do protein syn but go for gluconeogenesis and the CHO intake both NUTR components elevate the blood glucose level

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15
Q

definition of insulin resistance

A
  • a lesser sensitivity to insulin’s action

- in suppressing hepatic glucose production and stimulation of glucose uptake

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16
Q

why say the mechanism of glucose intake in brain is a good survival mechanism?

A
  • brain is insulin-independent, so it still can access fuel with IR exists
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17
Q

types of IR

which is common?

A
  1. receptor defects as decreased number and affinity

2. post receptor second message signalling failure (common)

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18
Q

the essential difference between MD1 and MD2

A

MD1: destruction of B cell, so no original insulin production

MD2: insulin resistance, so the signal cannot reach the cell’s regulation centre

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19
Q

what’s the cause of receptor-defect IR?

A

genetic mutations of INSR gene, but it is rare

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20
Q

T/F all DM2 is originated from over weight or obesity

A

F

genetic factor also

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21
Q

DM short-term complications

A
  1. Diabetic ketoacidosis: dehydration, skipped insulin, etc leads to coma [commonly in DM1]
  2. hyperglycemic hyperosmolar syndrome:dehydration or infection cause the burst of blood glucose ( >33M) [ commonly in DM2]
  3. Hypoglycemia: excess dose of insulin or impaired food intake to the dose, unplanned exercise
22
Q

DM long-term complications

A

microvascular system:
retinopathy–> blindness
nephropathy (20-40%)–> kidney transplantation
neuropathy (50%)–> amputation, decreased GI movement
- Macrovascular: CVD, CHD and stroke

23
Q

Hypoglycemia；
definition?
symptoms (early and late for 3 each)?
treatment?

A
  • BG < 3.9M
  • early: sweating, shaking, anxiety; late: confusion, blurred vision, coma
  • 15-15 rule: give 15 g of fast absorbed glucose and check the BG in 15min. If not be normal, repeat.[ the pt is conscious] /severe: injection of glucagon or glucose by care provider
24
Q

Explain how does DM affect CVD

A

the increased glucotoxicity makes more glycated proteins. As a result of endothelial damage, the acceleration of plaque expose the high risk of CVD

25
Q

What is A1C?
function?
measure value?

A
  • a glycated hemoglobin
  • an indicator of long-term glycemic control as its half-life is 3 m.o. ( which more effective than blood glucose measure)
  • normal 4.3-6.0%
26
Q

why serum TG may elevated in MD1? How about the level of HDL and LDL?

A
  • Due to the lack of insulin, LPL activity decreases, which causes the defective removal of chylomicrons and VLDL
  • No change of LDL-C and HDL
27
Q

why serum TG may elevated in MD2? How about the level of HDL and LDL?

A
  • It is associated with obesity. The action of insulin to inhibit the hormone synthesis lipase fails. As a result, there is more lipids are broken
  • Low HDL and possible elevated LDL-C
28
Q

How to suggest DM pts to protect from CVD?

A

the ABCDEs

29
Q

Who should be screened?

A

1.

30
Q

4 diagnosis criteria

A
  1. FPG
  2. OGTT
  3. A1C%
  4. Random PG
31
Q

what is FPG

& diagnosis range for PDM and DM

A

No cal intake for at least 8 hr
PDM: 6.1-6.9 mM
DM: no less than 7mM

32
Q

what is OGTT

& diagnosis range for PDM and DM

A

2 test after a 75g OGTT
PDM: 7.8-11.0
DM no less than 11.1

33
Q

what is A1C

& diagnosis range for PDM and DM

A
  • the glycolated hemoglobin that lasts 3 months
  • not for suspected type 1 DM
    standardized and validated
    -PDM: 6.0-6.4%
    -DM= no less than 6.5%
34
Q

what is random PG

& diagnosis range for PDM and DM

A
  • no PDM criteria

- no less than 11.1 mM

35
Q

if a pt does not have any DM symptom, what to do?

A

Must do a repeated confirmatory test of the first three diagnosing lab test

36
Q

what does IGT stand for?

A
  • Impaired glucose tolerance
  • when the result of 2hPG in a75g GOTT locates between 7.8-11.0 mM
  • indicate prediabetic
37
Q

how to inter-print OGTT blood glucose curve?

A

IGT: fasting glucose level is the same origin as normal, but the peak is higher and takes longer time to go to the normal level

T2D: the area under the curve throughout the three hours are always higher than normal, which means the high FPG and high peak after intake (drastic change + a high starting point)

38
Q

what is the DPP study?

A

Diabetes Prevention Program

- Intervention can prevent diabetes onset

39
Q

Who are the objects of DPP?

A

the pts with IFG or/and IGT, but w/o DM

40
Q

what is the result of DPP

A

After 4 yrs, the change of lifestyle (58% less than Placebo incidence) is more effective than medication, Metformin (31% less than placebo incidence)
They are both important to prevent the DM.

41
Q

What is ABCDEs

A

the recommendation about vascular protection for all pts with DM

42
Q

What is ABCDEs

A

A— A1C: optimal glycemic control (no more than 7%)
B—BP: optimal blood pressure control (<130/80 mmHg)
C—cholestrol: LDL -C no more than 2.0mM if decision made to treat
D—drugs to protect: ASA
E: exercise/eating: regular PA, healthy diet to achieve or maintain a healthy body weight
S—smoking cessation

43
Q

What is ASA in ABCDEs?

A

the drug to protect from vascular disease:
A= ACEi or ARB
S= Statin
A= ASA of indicated

44
Q

T/F the target of a DM pt for A1C around 7.1%-8.5%

A

T

  • the average target of A1C is 7%
  • high range for pts with multiple co-morbidities, hypoglycemia unawareness or recurrence( severe) or difficult to achieve the 7%
45
Q

Who’s target of A1C no more than 6.5%

A

a target no more than 6.5% is for DM2 to further lower the risk of nephropathy and retinopathy, which must be balanced the risk of hypoglycemia

46
Q

the optimal DM target of A1C, fasting glucose, glucose 2hr PC

A

A1C no more than 7%
FPG: 4.0-7.0 mM
2hr PC: 5.0-11.0 mM

47
Q

the level of A1C, fasting glucose, glucose 2hr PC that has to take action

A

A1C: >8.5%
FPG: > 10.0 mM
2h PC: > 14.0 mM

48
Q

why to monitor the optimal gylcemic control

A

prevent the incidence and progression of complications

49
Q

What is SMBG?

A

self-modification of blood glucose

50
Q

why use SMBG

A
  • important to prevent the hypoglycemia to the pts with anti-hyperglycemic agents or insulin Tx
  • daily monitor more for DM1 with intensive conventional Tx \
  • this may not necessary for the one on the diet Tx

Clinical Nutrition 1 Final McGill Uni (8 decks)

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