Diabetes Flashcards

(50 cards)

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
What is A1C? function? measure value?
- 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
why serum TG may elevated in MD1? How about the level of HDL and LDL?
- 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
why serum TG may elevated in MD2? How about the level of HDL and LDL?
- 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
How to suggest DM pts to protect from CVD?
the ABCDEs
29
Who should be screened?
1.
30
4 diagnosis criteria
1. FPG 2. OGTT 3. A1C% 4. Random PG
31
what is FPG | & diagnosis range for PDM and DM
No cal intake for at least 8 hr PDM: 6.1-6.9 mM DM: no less than 7mM
32
what is OGTT | & diagnosis range for PDM and DM
2 test after a 75g OGTT PDM: 7.8-11.0 DM no less than 11.1
33
what is A1C | & diagnosis range for PDM and DM
- 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
what is random PG | & diagnosis range for PDM and DM
- no PDM criteria | - no less than 11.1 mM
35
if a pt does not have any DM symptom, what to do?
Must do a repeated confirmatory test of the first three diagnosing lab test
36
what does IGT stand for?
- Impaired glucose tolerance - when the result of 2hPG in a75g GOTT locates between 7.8-11.0 mM - indicate prediabetic
37
how to inter-print OGTT blood glucose curve?
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
what is the DPP study?
Diabetes Prevention Program | - Intervention can prevent diabetes onset
39
Who are the objects of DPP?
the pts with IFG or/and IGT, but w/o DM
40
what is the result of DPP
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
What is ABCDEs
the recommendation about vascular protection for all pts with DM
42
What is ABCDEs
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
What is ASA in ABCDEs?
the drug to protect from vascular disease: A= ACEi or ARB S= Statin A= ASA of indicated
44
T/F the target of a DM pt for A1C around 7.1%-8.5%
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
Who's target of A1C no more than 6.5%
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
the optimal DM target of A1C, fasting glucose, glucose 2hr PC
A1C no more than 7% FPG: 4.0-7.0 mM 2hr PC: 5.0-11.0 mM
47
the level of A1C, fasting glucose, glucose 2hr PC that has to take action
A1C: >8.5% FPG: > 10.0 mM 2h PC: > 14.0 mM
48
why to monitor the optimal gylcemic control
prevent the incidence and progression of complications
49
What is SMBG?
self-modification of blood glucose
50
why use SMBG
- 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