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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Which is better: venous BSL or capilliary BSL?

A

venous

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2
Q

When is HBa1c not accurate?

A

Haemoglobinopathy
recent red cell transfusion

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3
Q

Range of Hba1c for diagnosis of prediabetes, and diabetes?

A

<5.7% normal
5.7-5.6% prediab
>6.5% diabetes

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4
Q

Pathophys T1DM?

A

Immune mediated destruci5ton of beta cells of pancreas leading to absolute insulin def
- Prone to ketoacidosis, therefore always needs insulin

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5
Q

Does T1DM include destruction of beta cells from a specific cause ie CF or mitochondrial defects?

A

No, these are not classified as T1DM

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6
Q

Which HLA types are positively associated with T1DM? Which is protective?
Where is teh gene governing these specific HLA types located?

A

HLA DR3, HLA DR4 is risk
HLA DR2 is protective

Located on chrome 6

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7
Q

Risk of having T1DM in specific siutations:
- 1. Back ground population risk?
- 2. Sibling has T1DM?
- 3. RIsk for HLA identical twin
- 4. Risk for identical twins?
- 5. RIsk for baby of woman iwth T1DM?
- 6. RIsk for baby of man with T1DM?
- 7. RIsk of baby when both parents have T1DM?

A
  1. 0.6%
  2. 5-10%
  3. 15%
  4. 40%
  5. 2.1%
  6. 6.1%
  7. 30%

Risk of having it is dad has it is much more than the risk of having it if mum has it

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8
Q

Is risk of having T1DM biggest if father or mother has it? What about T2DM?

A

T1DM = Father
T2DM = Mother

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9
Q

When do autoantibodies develop relative to clinical T1DM?

A

Many years before
- mediate the gradual destruction of Beta cell prior to onset of clinical T1DM

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10
Q

T1DM autoantibodies? Why is more than one antibody measured?

A

Anti GAD (also implicated in stiffman syndrome)
Anti IA2
Ainc transport 8

Mooire than one are measured because it increases the sensitivity and specificity
- ie if you are positive in all 3 then much higher change of T1DM if only positive in 1 of them

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11
Q

Who is screened for T1DM? How are these pts screened?

A

Population is not screened as quite rare
But first degree relatives are screened

Screening:
- Anti GAD, IA1, Zn transporter 8
- HLA states for DR3,4
- Then screen insulin secreting potential (ie after IV glucose) every year for next 5 years

If found to have decreasing insulin secreting potential in addition to HLA DR3,4 and or antibodies then propbs will deve T1DM

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12
Q

Very basic pathophys of T2DM?

A

Insulin resistance, and variable defects in insulin secretion

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13
Q

Is the genetic basis for T1DM or T2DM strongest?

A

T2DM
- identical twins have >90% rate of T2DM

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14
Q

Is T1, T2 or both disease associated with HLA type?

A

ONLY T1DM
T2DM is not associated with HLA type

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15
Q

T2DM is polygenetics. What is a relevant genes for T2DM? what function in the body are most of the identified gene defects related to?

A

TCF7L2 is the most important
- Most are related to insulin secretion NOT insulin resistance

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16
Q

What is MODY (mature onset diabetes of the young)? What is the fundamental difference between T1DM and T2DM?

What are some features of MODY?

A

MODY is a form of inherited monogenetic diabetes that develops in pts <35yrs of age.
AD inheritance pattern

MODY is due to a single gene defect. T1DM and T2DM are not

Characterized by fasting hyperglycaemia without need for insulin and without ketotoic events

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17
Q

Does MODY behave more like T1DM or T2DM?

A

T2DM
- ie dont need insulin to survive
- nil ketotic events

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18
Q

Gene defects associated with MODY? What is the least serious of these diseases? What is the most common gene defect and how is this specific form treated and what is a common complication of treatment?

A

MODY1 - HNF-4 alpha
MODY2 - glucokinase
MODY3 - HNF-1 alpha
MODY4 - IPF-1
MODY5 - HNF-1 beta

MODY2 (glucokinase) is the least serious. Nil need to treat

MODY3 (INF-1 alpha) is the most common
- Treat with sulfonylureas
- Complication is that they are extremely sensitive and get hyypos at greatly reduced doses

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19
Q

Pt has MODY / diabetes + strange abdominal findings such as pancreatic or hepatic cysts etc. What disease?

A

MODY5 (INF-1 beta)

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20
Q

Woman with GDM is at risk of developing …?

A

T2DM in future

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21
Q

Complications of GDM?

A

Large baby
Increased perinatal mortality
Birth defects (although not as high as in preg T1DM pts)

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22
Q

Treatment for GDM? when can treatment be stopped usually?

A

Insulin

GDM usually resolves with placental delivery, therefore can cease Rx at this time

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23
Q

Prevention strategies for T2DM? in order of best to worst

A

Lifestyle (best approach)
Metformin (also good but not as good as metformin)
Rosiglitizone (not used anymore due to risk of oedema)
ramipril

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24
Q

Is weight loss required to reduce risk of DM when adopting a lifestyle approach to prevention?

A

No
other changes to lifestyle such as exercise without weight loss still reduced risk

25
Q

Does lifestyle measures in pts with T2DM change CVD risk?

A

It probably does, but has not been shown to
- despite better BSL control loss of weight etc

26
Q

What re sulphonylureas? how do they work and what are some examples and complications?

A

SU are class of OHG agent
- MoA: work by stimulating beta cell insulin secretion causing almost uncontrolled insulin secretion
- Example: Gliclazide
- Complication: As a result they can cause hypoglycaemia and obesity as complications

27
Q

What type of drug is gliclazide? why is it the preferred drug in its class?

A

SU
Preferred because it is not renally excreted therefore dont have to dose adjust in renal failure or in old age with decreased renal function

28
Q

What type of drug is metformin? How does it work and complications?

A

Metformin = Biguanide
- MoA: increases the action of insulin in the peripheries
- Complications: GI upset usually minor, lactic acidosis esp in renal failure and fasting pts

29
Q

Metformin is contraindicated in?

A

Advanced renal disease eGFR <30
Liver damage (ie CPC cirrhosis)
Pregnancy

30
Q

What is acarbose? MoA?

A

Acarbose is an alpha glucosidase inhibitor
- MoA: Inhibits the breakdown of Olio/disacharides in the gut thereby resulting in slower absorption of glucose in the gut
- Complication: dia and flatulence (complex carbs delivered to hind gut where bact break down and cause wind)

It is not used much because only has a very small effect. Maximum decrease in Hba1c is 1%, often does nothing overall

31
Q

What are some examples of thiozolidinediones? MoA, complications?

A

Powerful insulin sensatisers (similar to metforming but much more powerful)
- Examples: rosiglitazone, pioglitazone
- MoA: Increase peripheral insulin secretion by activating PPAR gamma
- Complications: weight gain (SC mopre than viceral), fluid retention, cardiac disease (CVA, IHD)

32
Q

What are the two types of incretin mimetic used? What is another related drug that is often used to amplify this pathway / effect?

A

GIP analogues
GLP-1 anolgoues

the incretins are normally broken down by DPP4
therefore by deactivating DPP4 we can increase the persistence of endogenous incretins

33
Q

What is the effect of a GLP1 anologue? What are 3 examples of GLP1s unsed currently?

A

Increased insulin secretion
Decreased glucagon secretion
Slows stomach emptying
Decreases appetite leading to loss of weight

Examples:
- exanetide
- Dulagletide (trulicity)
- Semaglutide (ozempic)

34
Q

What are some examples of DPP4 inhibitors? MoA? Complications?

A
  • Examples: SItagliptin, vidagliptin, linagliptin, saxagliptin
  • MoA: Inh DPP4 which would usually break down endogenous GLP1 and GIP

Unlike GLP1 they have no weight loss, nil CVD risk modification
Nil risk of hypoG

35
Q

How do DPP4 differ from GLP1? why is this deffernece present?

A

DPP4 are much weaker than GLP1. This is because pts with T2DM have less endogenous incretins overall

36
Q

What are SGLT2 inh? examples, MoA and side effects?

A

these inhibits SGLT2 transport in proximal tubule causing reduced re absorption of gluc in proximal tubule resulting in increase loss in urine
- Examples: dapa and empa
- Good cardiovascular outcomes
- Comp: UTIs, thrush, euglycaemic DKA (can also just have normal DKA)
-> SGLT2 cause propensity for ketone bodies to form, therefore never perscribe in T1DM

THis is the only drug which results in reduced glucose in the body

37
Q

SGLTt2 and fasting = DKA. What is teh mechanism?

A

fasting causes ketones
SGLT2 causes ketones

Together this is a signification risk of DKA
For this reason dont combine low calorie diet or ketogenic diet with SGLT2

38
Q

Normal BSL in evening, high BSL in morning. What is one cause that needs to be excluded?

A

hypoglycaemia overnight with rebound hyperglycemia due to counter regulatory hormones
- therefore always check 0200hrs or 0300hrs BSL to rule out this differential before increasing insulin

39
Q

Forms of long acting insulins routinly used?

A

Insulin glargine (optisulin, toujeo)
- single dose 24 hours in T1 and T2

Insulin detemir (levemir)
- best used BD
- Mostly used in T1DM to achieve better control than OD glargine

Insulin degludec (ultra long acting in ryzodeg)
- only used in ryzodeg

40
Q

What is the benefit of DPP4 with GLP1?

A

Nil
- dont use in combination, there is no point using a DPP4 if already using GLP1

41
Q

Treatment of steroid induced hyperglycaemia due to dex and steroids?

A

Always use insulin because this is the strongest hypoglycaemic agent that can be easily tailored

Dex is long acting there fore use a long acting insulin such as toujeo or optisulin

Pred is short acting therefore use AM dose of protaphane (insulin protamine / NPH) to control becasuethis will peak in the middle of teh day with the peak in pred dose

42
Q

Why is intensive BSL control preferred in pts? Which complication of DM does it most significantly decrease the risk of occuring?

A

Significantly decreased risk of microvascular complications
- Most predominantly retinopathy

Complications was hypo (and therefore falls), therefore not used so much in elderly

43
Q

Does intensive BSL control decrease risk of micro and macrovascular complications in DM?

A

Yes it does
- There is a famous trial that showed an increase in CVD outcomes in pts with intensive BSL control however there were several flaws in this:
-> too intensive (aimed Hb1 of 6%)
-> Too quickly (used 3 or more agents to achieve this)

Therefore beware very intense rapid control of BSL in pts with long standing DM and CVD because can increase risk of CVD

44
Q

Describe the legacy effect of glucose control?

A

Early intense control of BSL is important in reducing CVD outcomes in the long term (ie better then poor initial control with subsequent good control)

45
Q

HbA1c targets in pts with T2DM?

A

generally 7% is target except:
- nil CVD + metformin - 6%
- Nil CVD + anything less than insulin - 6.5%
- Nil CVD + insulin - 7%
- CVD or long duration DM - 7%
- Recurrant hypos - 8%

46
Q

Do DPP4 have effect on CVD?

A

No effect (does not improve or improve)

47
Q

Why do we use sitagliptin not saxogliptin or aloglitin?

A

Sitagliptin showed no change in rates of CCF presentation
- Saxagliptin statistically significant increase in heart failure presentation
- Alogliptin trending towards this

48
Q

Does a pt need to have DM to have cardivascular benefits from SGLT2?

A

No, pts without DM show benefit as well

49
Q

What is the only agent to have a mortality benefit in HFpEF?

A

Empagliflozin

50
Q

Pt with renal disease, heart failure and T1DM. SHould you give them SGLT2?

A

No
Flozins never been shown to have benefit in T1DM pts with CCF or renal disease (ie T1DM pts were excluded from all these trials). But they are known to increase DKA in these pts

51
Q

What agent has been shown to improve CV oputcomes and renal outcomes in pts WITH T2DM? (aside from SGLT2, GLP1, ACE/ARB)

A

Finerenone
- non steroidal mineralocorticoid antagonist like spironalactone

Therefore there is a new indication for this medicartion for treatment of albuminuria CKD in T2DM

52
Q

Pt with albuminuric CKD, already on ACEI, flozin and GLP1. What other agent should you add?

A

Finerenone
- has been shown to improve CV and renal outcomes in pts with T2DM

53
Q

What cardiovascular disease does GLP 1 help with the most?

A

IHD, and CVA
- nil benefit in CCF or renal disease

Unlike SGLT2 which shows benefit in IHD, CCF, and renal disease

54
Q

Pt has hypo 1hr post OGTT. COuld this be an insulinoma?

A

No
Pts with insulinoma basically never get hypo post a glucose load (ie meal or OGTT). Furthermore, the glucose load from an OGTT often will overcome the relatively short duration spike in insulin that is typical of an insulinoma
- this is more likely impaired insulin tolerance

55
Q

Characteristic of pt with insulinoma?
How does this compare to impaired insulin tolerance as a cause for hypoG?
How does this compare to factitious hypo?

A

Insulinoma
- Very high C peptide
- late hypos (ie >8hrs post meal)

Impaired tolerance
- high-ish C peptide
- Hypo occurs rapidly after a meal (ie 1 hrs after)

Factitious:
- medical personnel
- not related to meals
- Low or zero C peptide

56
Q

Why can pts with imparied glucose tolerance het reactive hypoglycaemia following a meals with a high glucose load?

A

Pts with imparied tolerance have delayed recognition of glucose, this introduces a lag and consequently an overshoot into the system
- Manifests as delayed and large insulin spike and delayed hypoglycemia as a result

57
Q

WHat is the main cause of mortality post DKA treatment?

A

Not enough potassium infusion causing hypokalaemia and CV death

58
Q

Control of BP in pts with DM?

A

ACEI/ARB
CaC blocker second line

59
Q

Fenofibrate is good in the prevention of which DM compliucation?

A

retinopathy

Endocrinology (4 decks)

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