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Aisha > Dunedin- Endocrine > Flashcards

Dunedin- Endocrine Flashcards

1
Q

What antibodies are associated with LADA or slowly evolving immune mediates diabetes of adults?

A

GAD (glutamic acid decarboxylase)

note- insulin not required at diagnosis
often >35 years

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2
Q

What is fulminant Type 1 diabetes

A

20% of acute onset T1DM in Japan
abrupt onset <7 days
frequent flulike and gastrointestinal symptoms
ketoacidosis at diagnosis
no c-peptide secretion

negative for island autoantibodies

increased levels of pancreatic enzymes

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3
Q

What is ketosis prone type 2 diabetes?

A

diabetes that typically presents with ketosis and evidence of severe insulin deficiency

goes into remission and doesnt need insulin treatment

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4
Q

What Is the mode of inheritance of monogenic diabetes?

A

autosomal dominant

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5
Q

What type of monogenic diabetes is most common?

A

Type 3

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6
Q

How can you treat MODY3?

A

sulfonylurea

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7
Q

How do you treat MODY 2 (GCK)?

A

dont need to

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8
Q

How do you treat MODY MODY5, MODY6, MODY7, MODY8?

A

Insulin

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9
Q

List some strongly diabetogenic drugs

A

glucocorticoids, immunosuppressives, antipsychotics

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10
Q

List some weakly diabetogenic drugs

A

Thiazides, B-blockers, statins

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11
Q

Post-transplant diabetes/NODAT (new onset diabetes after transplantation)

Is it more common with solid or non-solid Organs?

A

Solid organs

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12
Q

What drugs are linked to NODAT?

A

Glucocorticoids
calcineurin inhibitors (tacrolimus >cyclosporin)

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13
Q

What do immune checkpoint inhibitors cause diabetes?

A

Beta cells have PDL-1 receptors
often presents with DKA

does not reverse! life-long insulin

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14
Q

When to think about MODY?

A

if they act like T1DM but antibodies negative
often young and well

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15
Q

What is the lifetime risk of T1DM depending on family members affected?

A

Sibling 8%
Father 5%
Mother 3%
Mono Twin:
* 150-fold increased risk
* 50% concordance (greater the younger age that 1st twin affected)

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16
Q

What are common haplotype of T1DM?

A

1st chromosome - DR3
2nd chromosome DR4-DQ8

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17
Q

List some Genes related to T1DM?

A

Insulin VNTR (variable number tandem repeats)
PTPN22
CTLA4
IL2RA

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18
Q

List some viral precipitants for T1DM

A

enteroviruses esp coxackie viruses
congenital rubella infection

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19
Q

Briefly describe the pathogenesis of T1DM?

A

B cell destruction, further excaberated by the release of pro inflammatory cytokines

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20
Q

Describe what islet cells look like in T1DM?

A

Marked heterogeneity of islet lesions:
– Normal (no inflammation and normal beta cells)

Intense insulitis (marked infiltration of inflammatory cells)
* CD8 + T cells main inflammatory cell * Only 10-30% show insulitis at any time. * Can persist for many years (>10yr) after diagnosis

– Pseudoatrophic (lack of beta cells and no inflammatory cells)

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21
Q

Describe autoantibodies to T1DM

A

note, these are not actually relevant to the pathogenesis
and they also go away over time

– Insulin autoantibodies (IAA)
– Glutamic Acid Decarboxylase antibodies (GAD)
– Islet cell tyrosine phosphatase-2 (IA-2)
– Tetraspanin-7
– Zinc Transporter-8 (ZnT8)

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22
Q

What is teplizumab?

A

anti-CD3 monoclonal antibody

in stage 2 diabetes, and delays Type 1 diabetes by 2years.

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23
Q

Describe some stage 3 studies/drugs for T1DM

A

verapamil, teplizumab, baricitinib

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24
Q

What are some benefits of short acting insulin analogues?

A
  • better control of postprandial hyperglycaemia
  • reduced late hypoglycaemia and nocturnal hypoglycaemia
  • decreased severe hypoglycaemia by 30%
  • no evidence of reduced complication and only very small reduction in HBA1c
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25
Q

How long does Glargine (Lantus) last for?

A

24 hours, begins to wane at 15 hours

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26
Q

How to reduce risk of nocturnal hypoglycaemia with glargine (Lantus)?

A

give with breakfast

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27
Q

Should you split Glargine?

A

similar results with splitting however splitting causes weight gain.

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28
Q

How long does insulin detemir work?

A

20 hours
given twice daily
reduces hypoglycaemia compared with isoprene

less weight gain

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29
Q

How long does Insulin degludec work?

A

40 hours

less nocturnal hypoglycaemia than evening glargine

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30
Q

How long does insulin isodec work?

A

half life of 8 days. given once a week

31
Q

What is 500/100 rule in diabetes?

A

carbohydrates ratio: 500/total daily unit of insulin

insulin sensitivity factor: 100/total daily unit of insulin

32
Q

What is the daily insulin requirement?

A

0.5unit/kg- 50% as basal and 50% as prandial

33
Q

Describe glycaemia targets for T1DM, and in the cause of continuous glucose monitoring.

A

pre-prandial: 4.4-7.2 mmol/L
post-prandial: <10mmol/ml

Time in range 4-10mmol/L: >70%

Time below range <5%

34
Q

What is the “dawn phenomenon”

A

Rise in blood glucose levels in the morning “dawn” as we have higher GH and cortisol.

when you are giving insulin in the morning it cant respond to that but pumps were good in overcoming dawn phenomenon.

35
Q

What is the somogy effect?

A

high BSL in the morning due to hypoglycaemic event in the night.

36
Q

How much does closed-loop pump improve time in range compared to non-closed loop pump?

A

10%

37
Q

What are methods of cell replacement therapy in T1DM?

A

Whole pancreas transplant
Islet cell transplantation
Stem cell therapy

38
Q

What are the different levels of hypoglycaemia?

A

Level 1: glucose 3-3.9
Level 2: glucose <3mmol/L
Level 3: hypoglycaemia with altered mental status and/or physical status

39
Q

What is the normal response to hypoglycaemia?

A

reduce insulin secretion
increased glucagon secretion
increased adrenaline secretion
increased GH and cortisol secretion
behavioural secondary to SNS activation

40
Q

What are symptoms of hypoglycaemia?

A

Autonomic
- adrenergic: palpitations, tremor, anxiety
- cholinergic: sweating, hunger, parasthesia

Neuroglycopenic
- brain glucose deprivation: confusion, fatigue, weakness, visual changes, seizure, loss of consciousness

41
Q

Describe the pathophysiology of T2DM

A

Characterised by both insulin resistance and initial hyperinsulinaemia followed by progressive beta cell dysfunction

42
Q

What is the action of insulin?

A

suppression of lipolysis
stimulation of glucose uptake

43
Q

When you gain weight, what occurs to adipose tissue?

A

hypertrophy more prominent than hyperplasia

creates hypoxic conditions and adipocyte death

macrophages are recruited to clear the dead adipocytes

dysfunctional adipocytes and macrophages release FFA’s and cytokines e.g. TNFalpha, IL-6

FFAs and these cytokines are toxic to Beta cells

44
Q

What are some methods of prevention of T2DM?

A

lifestyle intervention
Metformin
pioglitazone
liraglutide

45
Q

Describe the different diabetic drugs in terms of mechanism, cardiovascular effects, adverse effects

A
46
Q

What are the diabetic drugs proven to be cardioprotective?

A

SGLT2, GLP-1 agonist

+/- metformin

47
Q

What is the MOA of SGLT2 inhibitor?

A

Inhibiting glucose reuptake in
proximal tubule

48
Q

What is the MOA of sulphonylurea? main risk?

A

SU receptor on beta cells stimulating insulin secretion

hypoglycaemia risk

49
Q

What is the MOA of metformin? S/E?

A

insulin sensitiser
AMP kinase activation

S/E GI symptoms, vit B12 deficiency

50
Q

What is the MOA of GLP1 agonist

A

Stimulating insulin and inhibiting
glucagon secretion
Induces satiety
Delays gastric emptying

better stroke reduction
risk of pancreatitis and medullary thyroid cancer

51
Q

What are some of the new incretins?

A

orforglipron, cagrilinitide+semalgutide, retratrutide

52
Q

What are the risk of complications in diabetes?

A

Retinopathy >nephropathy > neuropathy > microalbuminuria

53
Q

Other factors that can affect HBA1c

A

Increased A1c: iron deficiency, B12, deficiency, decreased eryhtopoiesis

Decreased A1c: use of erythropoietin, iron or B12, reticulocytosis, chronic liver disease

54
Q

What can occur to retinopathy if sudden improvement in BSL?

A

worsening retinopathy if advanced baseline retinopathy and higher HbA1c

55
Q

Describe screening for diabetic retinopathy

A

screening with retinal photography
- from diagnosis of T2
- within 5y diagnosis for T1DM

56
Q

What is the treatment for diabetic retinopathy treatment?

A

treat HTN
lower lipids (fenofibrate)
pan retinal photocoagulation (in severe PDR or vision threatening)
anti-VEGF in macular oedema eg ranibizumab

57
Q

Describe the pathology of diabetic kidney disease

A

thickened GBM
mesangial expansion
podocyte injury
glomerulosclerosis
tubulointerstital fibrosis

58
Q

Describe natural history of diabetic nephropathy

A

1) increase GFR (kidney hypertrophy)

2) microalbuminuria, hypertension (mesangial matrix expansion, glomerular basement membrane thickening, arteriolar hyallinosis)

3) proteinuria, nephrotic syndrome, decreased GFR (mesangial nodules- kimmesltiel-wilson, tubulo-interstital fibrosis)

59
Q

How to treat diabetic kidney disease

A

Glycemic control
BP control
RAS inhibition
SGLT2

60
Q

How do SGLT2s act in diabetic kidney disease?

A

when you use SGLT2 you get an increase of sodium which gets to the macula dense which causes vasoconstriction of afferent arterioles and dilation of efferent which reduces perfusion of glomerulus

61
Q

What are the common fibres affected in diabetic neuropathy?

A

large fiber neuropathy and small fibre neuropathy common

can also get proximal motor neuropathy, acute mono-neuropathy, compression palsies

62
Q

Does tight glycemic control in diabetes reduce CV outcomes?

A

NOPE

63
Q

What is the management of metabolic associated fatty liver disease?

A

lifestyle intervention
metformin may reduce risk of HCC
pioglitazone –> has side effects but good
Liraglutide
SGLT2

64
Q

What is the effect of gestational diabetes on childhood?

A

more likely to have impaired glucose tolerance in childhood

65
Q

What is the effect of inadequate glycemic control in the first trimester?

A

Increased risk of diabetic embryopathy:
– anencephaly, microcephaly, congenital heart disease,
renal anomalies, and caudal regression
– Risk directly proportional to HbA1c

66
Q

What are the glucose targets in pregnancy?

A

fasting plasma glucose < 5.3 mmol/L and
1-h postprandial glucose 7.8 mmol/L or 2-h postprandial 6.7 mmol/L)

67
Q

Can we use HBA1c in pregnancy?

A

No- HbA1c levels are reduced during pregnancy due to increased rbc turnover

68
Q

How to prevent risk of pre-eclampsia in patients with type 1 or type 2 diabetes?

A

low-dose aspirin 100–150 mg/day starting at 12 to 16 weeks of gestation

69
Q

What are the major categories of lipoproteins and their specific apoproteins?

A

chylomicrons - Apo B48
VLDL, IDL, LDL- Apo B100
HDL- Apo-A

70
Q

What is the main cause of familial chylomicronaemia syndrome?

A

LPL deficiency

71
Q

Why is the inheritance of familial hypercholesterolaemia?

A

autosomal dominant
usually see heterozygous, homozygous rare

lack of LDL receptor and APOB , can get gain of function of PCSK9

72
Q

What is the management of treatment of familial hypercholesterolaemia?

A

Statins
if LDL-C >2.6 still, add in ezetimibe

73
Q

Describe the diagnosis if familial hypercholesterolaeia

A

Simon Broome Criteria

Definite
* Total cholesterol >7.5mmol/L or LDL> 4.9mmol/L
PLUS one of the following:
* Tenon xanthomas in the patient or 1st or 2nd degree relative
* DNA based mutation of LDLR, apoB or PCSK9

Possible
* Total cholesterol >7.5mmol/L or LDL> 4.9mmol/L
PLUS one of the following:
* MI in 1st degree relative <60 years or 2nd degree relative <50 years
* Raised total cholesterol >7.5mmol/L in a 1st degree relative

74
Q
A

Aisha (12 decks)

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