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IPFC 3 - DM > DM Pathophysiology > Flashcards

DM Pathophysiology Flashcards

(59 cards)

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1
Q

Signs + symptoms of hyperglycemia

A

polyuria
polydipsia
weight changes: up or down
blurred vision
increased infections
neuropathy

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2
Q

T or F: T2DM can be asymptomatic

A

T

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3
Q

What are the consequences/complications of hyperglycemia

A

Microvascular: retinopathy, neuropathy, or nephropathy

macrovascular: heart and brain disease

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4
Q

What is the most common cause of death in those with DM

A

CV death

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5
Q

What is the average decrease in life expectancy of those with DM

A
  • 6 year decrease
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6
Q

T or F: 1/100 Canadians have DM

A

F- 1/10 diagnosed with it

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7
Q

T or F: there is the highest prevalence of DM in those bw 40-60yrs of age

A

F - highest prevalence in those bw 75-79yrs

  • sharpest increase occur after age 40yrs
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8
Q

T or F: DM is more common in M than F

A

T

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9
Q

Other than age + sex, what other factors impact DM prevalence

A
  • lower income
  • lower education
  • Indigenous
  • cultural/race: more common in those with South Asian background
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10
Q

What are the 4 groups of DM classifications

A

1) T1DM: includes LADA; absolute insulin Def
2) T2DM: problems with insulin secretion or use
3) GDM
4) Others: drugs, or genetic

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11
Q

FPG: what is it and what value —- DM

A

Fasting plasma glucose (no eat for past 8 hours)
- >/= 7: DM

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12
Q

What is A1c + what value —— DM

A

Standard assay that measure A1c levels; glyclated Hg subunit in RBC; weighted average of LS of RBC
—— gives BG control over 2-3 mths

DM: >/= 6.5%

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13
Q

Who do you not use A1c in

A

Kids, pregnant women, CF pt
- those with factors that impact A1c
——- Increase A1c due to decrease RBC turnover: anemia, chronic RF, decrease RBC production

——- decrease A1c due to increase RBC turnover: EPO/FE use, chronic liver Dx, use of ASA, Vit C or E, hemoglobinopathies, RA, chronic or acute blood loss

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14
Q

T or F: If get + A1c, we need to complete a confirmatory test

A

T - confirmatory test next day because results impacted by a lot of shit

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15
Q

What is the 2hPG in 75g OGTT test

A

give 75g of oral glucose + measure BG 2hours later to determine oral glucose tolerance
—— >/= 11.1: DM

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16
Q

What is Random PG

A

Test BG at anytime during the day
- if >/=11.1: DM indicated

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17
Q

How are the test thresholds determined? Like the values that indicate DM

A

based on the risk of retinopathy development

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18
Q

DM diagnosis if present w/ symptoms

A
  • only need 1+ test result
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19
Q

DM diagnosis + no symptoms present

A
  • need 2 + test results; if 1+—- need to do confirmatory test on another day
  • can be the same test (unless RPG)

2+ results —— DM

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20
Q

T or F: there is a single diagnostic test that can tell us if someone has T1 vs T2 DM

A

F- clinical diagnosis based on looking at factors

T1 less likely if:
- FH of T2, BMI> 28, age> 45, not white ethnic group, dyslipidemia, HDL< 1

T2 less likely if:
- FH of T1, BMI <28, age < 45, any autoimmune disorder, HDL>1.5

**

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21
Q

IF a pt has a lot of factors that indicate they may have T1DM, what tests can you look at

A

1) GAD ab: immune response
2) paired C peptide: indirect measure of insulin production

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22
Q

What is prediabetes

A

Condition where pt at increased risk of getting DM
- includes IGT and IFG or high risk A1c

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23
Q

T or F: If you have pre diabetes, you are at an increased risk of micro + macro vascular events

A

F: only CV risk (no MV risk yet)

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24
Q

T or F: if you have prediabetes, you can revert back to normal

Study These Flashcards
A

T - 50% revert back

25
What are the diagnosis criteria for prediabetes
1) FPG: 6.1-5.9 (IFG) —- diabetes: if >/=7 OR 2) 2hPG in 75g OGTT: 7.8-11 (IGT —- DM >/=11.1 3) A1c: 6.0-6.4% —- DM: >/=6.5%
26
What are metabolic syndromes
group of different abnormalities that tend to group together than result in increased risk of CVD + T2DM includes: obesity, HTN, dyslipidemia, elevated glucose *** can have increased risk of DM without having elevated glucose **
27
What are the studied ways to prevent T2DM progression
- lifestyle changes (main ) : decrease weight + reduced progression risk from pre to DM by 60% - metformin: decrease progression risk by 30% (not approved for this ) DPP study
28
RF for T2DM
- age>/=40 - relative with T2DM - part of high risk pop: African, Asian, Arab, SA, Indigenous - history of pre - history of GDM - had baby 9+lbs - end organ damage associated with DM: retinopathy, neuropathy, nephropathy, CV - vascular RF: HT, overweight, smoking - gout, psychiatric HIV, CF - certain drugs: glucocorticoids, statins, some atypical antipsychotics
29
How often should people be screened for T2DM and when to start
If normal risk: start at 40+ and screen every 3 yrs High risk: screen every 3 years but start earlier - can screen more often/earlier (6-12mths) if have other RF for DM or super high risk
30
What are the 3 sources of PG
1) diet 2) glycogenolysis in liver : glycogen — glucose 3) New glucose production (gluconeogenesis) in liver + kidney from other carbon compounds (AA) —— liver does most of it
31
What are the main hormones that regulate glucose levels in the body
insulin + glucagon
32
T or F: if the BG conc < 3.0mmol/L in brain, impacts brain fxn
T - brain uses glucose as main energy source - can’t store or make it, so relies on supply ** if fasting for long time —- will use ketone bodies
33
Main tissues that use glucose
- brain - skeletal muscle - kidney - blood cells - splanchinic organs (shit in abdominal cavity) -adipose
34
What are the 3 metabolic states
1) fed/post prandial: lasts till about 4 hours after you eat —- glucose comes from meal; suppress liver production by 80% (neo) but gluconeogenesis in kidney keeps going — inhibition done by insulin 2) Fasting/ post absorptive : done digesting food + stored (overnight or if skip meals) - decrease in BG + insulin; must cut into storage( lasts 60 hours - glucagon released + increases glycogenolysis + gluconeogenesis - liver: 80-85% of glucose comes from ( at start —- mainly glycogenolysis 50%, decreases as time increases — increase in gluconeogenesis) - kidney: 15-20% 3) starving : deprived from glucose for 2-3 days - no glycogen (no glycogenolysis) - rely on lipolysis + gluconeogenesis from FA+AA - brain can’t use fats: so uses ketones made during FFA breakdown
35
What are the 2 fxns of the pancreas
1) make hormones to regulate glucose 2) make digestive enzymes
36
What are all the key regulatory factors of glucose
insulin glucagon catecholamines GH cortisol FFA incretins
37
Direct methods in which insulin regulates glucose
Decreases PG - increases uptake at tissues + suppress glucose release
38
Indirect regulation methods of insulin
- suppress FFA release —— FFA normally stimulate glucose production + stop glucose transport into cells - promote glucose storage
39
MoA of Caetcholamines on glucose
Ne+E - fast acting way to increase PG (increase glucose reduction + lipolysis)
40
GH mech of action
slow acting way to increase PG - increases production of the enzymes that help with glucose production + slow down glucose transport into cells
41
Cortisol MoA
stops insulin secretion
42
FFA: impact on PG and MoA
increases PG - general energy source for body (not brain) - stimulates glucose production + stops transport into muscle regulated by SNS, GH, insulin and hyperglycemia
43
Fxn of incretins
hormones secreted by gut that stimulate insulin secretion (GLP-1 and GIP) GLP-1: also increases satiety, decrease gastric emptying and inhibits glucagon secretion —— normally low in T2DM
44
General patho of T1DM
Autoimmune destruction of B cells (immune or genetic trigger)
45
T or F: T1DM symptoms can be detected before 50% of B cells destruction
F: 70% of cells must be destroyed before symptoms even start appearing —- not linear destruction (on and off overtime) - can have autoimmune markers (85-90% of cases have before B cell destruction)
46
Onset of T1DM: fast or slow
Rapid: once hit the 70% of B cells destruction —- absolute insulin D (need insulin to survive)
47
What is the Islet autoAb test
Can be used to help distinguish T1 nand T2 - GABA autoaB is the most common one screened for
48
C peptide test
Used to measure insulin production - useful 3-5 years after diagnosis - DM symptoms + high C peptide: likely T2DM - DM diagnosis + low C peptide: confirms T1
49
What is LADA
Latent autoimmune DM - slower progressive loss of B cells - normally misdiagnosed at T2DM - seen in those < 30 - normally have islet Ab at diagnosis (immune) —— slowly become dependent on insulin
50
T or F: We can prevent T1DM
F- can’t be prevented — RH: FH and environmental factors/trigger - no routine screening recommended
51
Patho of T2DM
Result from predominant relative insulin deficiency OR predominant insulin R OR BOTH - patho starts year before diagnosis; progressive loss of B cells fxn - abnormal insulin + glucagon activity
52
T or F: In T2DM , we lose the initial phase of insulin secretion in response to glucose
T - loss that initial spike that occurs with glucose uptake (within mins) —- instead get only one phase
53
When do Microvascular complications appear with T2DM
don’t appear till after diagnosis - CV risk complications start before
54
What are the Egregious eleven
11 core pathophysiologic defects of T2DM that can result in hyperglycemia/decrease in insulin —- changes in R or S that result in impaired glucose regulation 1) Change in B cells: less fxn or mass 2) Decrease incretin effect: less GLP-1 3) Alpha cell defect: glucagon weird (increased level — more glucose in blood) 4) Adipose: increase lipolysis (glucose P), increase insulin R 5) Muscle: less up take of glucose 6) Liver: increased G production 7) Brain: increased appetite 8) Colon: less GLP-1 secretion 9) Immune inflammation 10) Stomach/SI: increased rate of Absorption 11) Kidney: increase glucose reuptake
55
T or F: in T2DM , the loss of B cells is slower than T1
T - 4-5% year
56
Changes in Glucose + Insulin T2DM (meals)
Glucose: higher spike in level Insulin: lose phase 1 (delayer spike+ smaller); don’t get same spike to help with glucose control when eat Glucagon: not suppressed during meal (normally no release when eat bc glucose source is food); increase in release with food
57
What are the Goals of DM Care
1) Avoid symptoms of hyperglycemia 2) Avoid or minimize risk of acute complications (hypo if use insulin or hyper/DKA) 3) Reduce risk of chronic complications (LT goal): micro + macro
58
ABCDES of DM Care
1) A1c
59

IPFC 3 - DM (9 decks)

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