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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the hormonal response to hypoglycaemia?

A

Decrease insulin, glucagon release, adrenaline release - giving symptoms of hypos

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2
Q

What is the pathophysiology behind the microvascular disease of diabetes?

A

Endothelial cells take up glucose (not dependent on insulin to do so) and form more surface glycoproteins. This thickens the basement membrane

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3
Q

What is the most common site affected by diabetic neuropathic arthopathy?

A

The foot - Charcot foot.
60% tarsometatarsal joints
30% Metatarsophalangeal joints 10% ankle

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4
Q

What are clinical features of LADA?

A
  • age of onset <25 kg/m2
  • personal or family history of autoimmune disease

The presence of two or more criteria had a 90 percent sensitivity and 71 percent specificity for identifying patients positive for anti-GAD antibodies.

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5
Q

What is the best test to distinguish T1DM from T2DM?

A

IA-2 and anti-GAD antibodies

- if one or more positive then diagnosis of T1DM is assumed

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6
Q

What is an example of a GLP-1 agonist?

A

Liraglutide
Exenatide

Activates GLP-1 receptors which stimulates insulin secretion
May increase medullary thyroid cancer - contraindicated in MEN2

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7
Q

What is gluconeogenesis?

A

Generation of glucose in the liver from non-carbohydrate substances (pyruvate, lactate, glycerol, amino acids)

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8
Q

What is glycolysis?

A

Conversion of glucose to pyruvate - provides energy in form of ATP

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9
Q

What is glycogenolysis?

A

Breakdown of glycogen to G-6-P

G6P is a substrate for glucose formation

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10
Q

What is glycogenesis?

A

Glycogen synthesis - where glucose molecules are added to chains of glycogen for storage

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11
Q

What is ketogenesis?

A

Formation of ketones from fatty acid breakdown, occurs withing mitochondria in liver
Fatty acids are broken down by b-oxidation to acetyl Coa which in starving states is made into ketone bodies from HMG-CoA

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12
Q

What is c-peptide?

A

Protein secreted with insulin by pancreatic beta-cells but is cleared more slowly therefore easier to measure - can help with discrimination of endogenous vs exogenous insulin administration

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13
Q

What is the process of insulin secretion?

A
  • triggered by BSL greater than 3.9
  • glucose transported into cell by GLUT 1 receptor
  • metabolised to g6p to generate ATP
  • ATP inhibits K channel inducing cell depolarisation which opens calcium dependant channels
  • insulin released from granules
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14
Q

What are incretins and there role?

A

Peptides released from neuroendocrine cells of GI tract after food ingestion
E.g. GLP-1 released from all cells mad stimulates insulin secretion in an insulin dependant manner and also suppresses glucagon secretion, slows gastric emptying, increases insulin sensitivity, decreases food intake)

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15
Q

Describe how insulin exerts action?

A

Released in the bloodstream, 50% degraded by liver, rest continues in blood stream
Binds to insulin receptor stimulating tyrosine kinase activity triggering widespread cell signalling
Activation of P13K pathway stimulates translocation of GLUT4 to cell surface allowing glucose uptake by skeletal muscle and fat

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16
Q

What are some anabolic effects of insulin?

A

Storage of triglycerides in adipose tissues
Increases glucose transport to fat and muscle
Increases glycolysis in fat and muscle
Stimulates glycogen synthesis
Inhibits glycogenolysis, gluconeofemesis, lipolysis, ketogenesis

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17
Q

Where is glucagon secreted from?

A

Pancreatic alpha cells

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18
Q

Major susceptibility genes for type 1 diabetes?

A

HLA DR3 and DR4

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19
Q

What are some examples of islet cell antibodies?

A

Glutamic acid decarboxylase (GAD)
IA-2
ZnT8

Antibodies are found in 85%

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20
Q

What are some types of MODY?

A 
MODY 1 - HNF4alpha
MODY 2 - glycokinase
MODY 3 - HNF1alpha
MODY 4 - IPF1
MODY 5 - HNF 1 beta
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21
Q

Diagnosis of diabetes?

A

Fasting glucose greater then 7.0
HbA1c greater then 6.5%
Symptoms of hyperglycemia and fasting glucose greater then 11.1
Oral glucose tolerance test - glucose greater then 11.1 after challenge

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22
Q

What is the definition of MODY?

A

Non insulin dependant diabetes at age less then 25

Usually autosomal dominant transmission with lack of autoantibodies

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23
Q

What is LADA?

A

Latent autoimmune diabetes of adulthood
Patients aged 30-75 who have positive autoantibodies, usually have a period of insulin independence but progress to insulin within 6 years

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24
Q

5 distinguishing features of LADA fro type 2 diabetes?

A 
Younger
Symptomatic onset
BMI less than 25
Autoimmune history
Family history
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25
Q

Diagnosis of impaired glucose tolerance?

A

Fasting glucose 5.6-6.9
OGTT 7.8- 11
HBA1c 5.7-6.4

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26
Q

How many pregnancies get gestational diabetes?

A

7%, higher risk in ethnic group

27
Q

Complications of gestational diabetes

A

Macrosomia, neonatal jaundice, neonatal hypoglycemia
Still birth, premature delivery
Pre-eclampsia
Fetal malformations
Increased risk of childhood obesity
Increased risk of developing type 2 diabetes (35-60%)

28
Q

Screening for gestational diabetes?

A

Screen before 20 weeks with HbA1c

Screening at 24-28 weeks with OGTT

29
Q

Goals of treatment in gestational diabetes?

A

Fasting glucose less than 5.3

Post prandial less then 7.8

30
Q

What is the distinguishing factor between DKA and HHS?

A

Ketones (urine and blood)

Though some HHS can have ketones

31
Q

What is the pathogenesis of Hyperosmolar hyperglycaemic state HHS?

A

Insulin deficiency leads to Increased gluconeogenesis/glycogenolysis and decreased glucose uptake by muscle. Leads to hyperglycemia, glycosuria, osmotic dieuresis and volume depletion

32
Q

Diagnosis of HHS?

A

High glucose (usually very elevated)
Hyperosmolarity (greater then 320)
Hypernatremia
Absence of ketones

33
Q

Diagnosis of DKA?

A

Ketosis (urine or blood)
Metabolic acidosis with high anion gap
Hyperglycemia (can be only minimally elevated)
Total body deficit of K (but can be elevated in serum)

34
Q

What are the two types of diabetic retinopathy?

A

Non-proliferative - microanerysms, blot haemorrhage, cotton wool spots
Proliferative - neo vascularisation near optic nerve and macula which rupture easily causing vitreous haemorrhage, fibrosis and retinal attachment - needs laser photo-coagulation

35
Q

Natural history of diabetic renal disease?

A

Glomerular hyper perfusion and renal hypertrophy (increased GFR)
Thickening of GBM, glomerular hypertrophy, mesangial expansion (normal GFR)
Microalbuminuria after 5-15 years
Macroalbuminemia leads to steady decline in GFR - 50% lead to ESRF in 7-10 years

36
Q

Example of an amylin mimetic?

A

Pramlintide

Activated amylin receptor which slows gastric emptying, decreases glucagon secretion and promotes satiety

37
Q

Example of an SGLT-2 inhibitor?

A

Dapagliflozin

Inhibits glucose absorption at proximal tubule leading to glycosuria (increased risk of UTIs, genital infections and volume depletion)

38
Q

What is an example of alpha-glucosidase inhibitors?

A

Acarbose

Inhibits intestinal enzyme which cleaves oligosaccharides to simple sugars for absorption

39
Q

Example of DPP-4 inhibitors?

A

Sitagliptin

- inhibit degradation of native GLP-1 and enhance incretin effect

40
Q

Example thiazolidinediones?

A

Pioglitazone

  • activates nuclear transcription factor PPAR-gamma on adipocytes
  • contraindicated in heart failures, liver failure
  • increase osteoporosis And fractures
41
Q

Example of sulphonylurea?

A

Gliclazide, glipizide

  • act on ATP sensitive K channel to stimulate insulin secretion by assisting membrane depolarisation
  • CYP2C9 drug interactions (rifampicin, amiodaeone)
42
Q

Example of biguanides?

A

Metformin

  • inhibits MGPD enzymes that prevents glycerol from contributing to glucogenosis
  • also activates protein kinase which suppresses lipogeneisis
  • contraindicated GRF less than 30
43
Q

General targets for HbA1c and BSLs for diabetes?

A

HbA1c less than 7 (evidence that tighter control improves complications but do worse in terms of mortality and morbidity due to hypos)
Pre- prandial BSL 3.9-7.2

44
Q

Dosing of insulin?

A
  1. 5-1 units/kg per day

- 50% as basal, 50% divided between meals

45
Q

Time for screening for diabetic retinopathy?

A

Type 1 - after 5 years of diagnosis

Type 2 - at time of diagnosis

46
Q

Physiological responses to low BSL?

A
  1. Insulin decreases
  2. Glucagon secretion increases
  3. AdrenalineIf
  4. Cortisol and GH (if hypoglycemia periositis for greater then 4 hours)
47
Q

If a woman has gestational diabetes which resolves after delivery, what should then happen?

A

Annual screening for diabetes

- risk of developing T2DM outside of pregnancy is 35-60%

48
Q

What target LDL should be achieved in diabetics?

A
49
Q

What should the target BP be for diabetics?

A

Aim 130/80

50
Q

What % of patients with diabetes can manage their BSLs with diet and lifestyle changes alone?

A

only 5-10%

51
Q

What is a usual insulin regimen?

A

0.5-1.5units/kg/day
50% long acting
50% short acting pre-meals

52
Q

When CHO counting, what correction factor is used?

A

1 unit for every 10-15g CHO

correction factor based on how much the pre-prandial BSL is above 5.6mmol/L
- usually 1 additional unit for every 1-2mmol above 5.6mmol/L

53
Q

What are the features of non-proliferative diabetic retinopathy?

A 
Chronic hyperglycaemia causes:
edema
hard exudates
tiny hemorrhages in the retinal layers.
cotton wool spots or soft exudates
- retinal infarcts caused by micro aneurysms
54
Q

What are the features of proliferative diabetic retinopathy?

A

proliferation of retinal vessels due to chronic retinal ischaemia

  • rupture of vessels - haemorrhages
  • fibrosis which can lead to retinal detachment
55
Q

When should diabetic eye screening occur?

A

T1DM - annually after 5 years after diagnosis
T2DM - annually after diagnosis (10% have diabetic retinopathy at diagnosis)

in pregnancy - every trimester and then closely monitored in the year post-partum

56
Q

What is the management of proliferative retinopathy?

A

laser photocoagulation
- improves central vision at the expense of loss of peripheral vision
injected VEGF (Bevasizumab)

57
Q

what is the basis of diabetic nephropathy?

A

chronic hyperglycaemia damages the GBM causing increase leakage of protein
- proteinuria is associated with worsening GFR, HTN and progression to ESRF

58
Q

What is the advised screening for proteinuria in diagnosed diabetics?

A

T1DM - test albumin:creat ratio annually 5 years after diagnosis
T2DM - test albumin:creat ratio annually from time of diagnosis

59
Q

What are the cut-off for albumin:creatinine and why is this important?

A 
30-300mg/g  = microalbuminuria
>300mg/g = macroalbuminuria

persistent microalbuminuria suggests increased risk of developing diabetic nephropathy in the future and 4 x increased risk of CVD

60
Q

Symptoms of hypoglycaemia and cause of them

A

Cholinergic - sweaty, hungry, parasthesias
Adrenergic - palpitations, tremor, anxiety, occur at less than 3.5
Neuroglycopenic - behavioural change, confusion, fatigue, occur at less than 2.5-2.8, loss of consciousness (less than 1.7), seizures (less than 1.3)

61
Q

Causes of hypoglycaemia

A

Drugs - alcohol, insulin
Critical illness - sepsis, hepatic, renal, cardiac
Hormone deficiency - cortisol, glucagon, adrenaline
Non islet cell tumour - produce IGF 2
Endogenous hyperinsulinaemia - insulinoma, post gastric bypass, functional beta cell disorder
Insulin autoimmune hypoglycaemia - antibodies to insulin

62
Q

Risk factors for hypoglycaemia in diabetic

A 
Excess insulin dose
Decreased exogenous glucose (skip meal)
Increased utilization of glucose (exercise)
Increased sensitivity to glucose
Decreased exogenous glucose (alcohol)
Impaired clearance (renal failure)
63
Q

What are features of hypoglycaemia associated autonomic failure

A

Two mechanisms:
Defective glucose counter-regulation - in response to low glucose insulin level doesnt fall and glucagon doesnt rise and adrenaline response occurs later

Hypoglycaemic unawareness - loss of warning adrengic/cholinergic symptoms due to decreased adrenaline response

Vicious cycle, worsened by recent hypoglycaemia

64
Q

Mechanism of hypoglycaemia due to alcohol

A

Blocks hepatic gluconeogenesis

Hypoglycaemia occurs if several day binge with little food as glycogen stores depleted

Endocrine (6 decks)

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