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year 2 core concepts > Endo: diabetes > Flashcards

Endo: diabetes Flashcards

1
Q

What is type 1 diabetes, what are the causes?

A
  • autoimmune destruction to beta cells causing decreased insulin
  • genetic + environmental trigger -> type 4 T-cell mediated hypersensitivity that destroys beta cells
  • genetic: HLA- DR3-DQ2 and HLA-DR4-DQ8
  • Environmental: viral or gestational infection
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2
Q

What are the symptoms of type 1 diabetes

A

Weight Loss, polyuria, polydipsia, polyphagia,
DKA: abdominal pain, vomiting, confusion

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3
Q

What are the different diagnoses of type 1 diabetes? When is each way suitable?

A
  1. Fasting glucose 7.0 mmol/l OR random glucose 11.1 mmol/l (twice if they have no diabetes symptoms ie, weight loss, polyuria & polydipsia)
  2. C- peptide (endogenous insulin production, low in T1DM) & autoantibodies (anti-GAD, ICA, IAA) used if patient is older & obese to distinguish from T2DM
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4
Q

What is the treatment of type 1 diabetes? Any side effects and how do you manage it?

A

Insulin injection in basal bolus regimen (basal is long acting once daily, bolus is short acting with each meal)
SE: hypoglycemia (give insulin analogue to help)

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5
Q

What is DKA? What are the causes?

A
  • Increased acidity in blood due to excessive lipolysis creating fatty acid & ketone bodies
  • Infection, miss insulin doses & myocardial infarction
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6
Q

What are the symptoms of DKA?

A
  • Abdominal pain, polyuria, polydipsia, dehydration
  • kussmaul respiration (hyperventilation to remove CO2 in blood to decrease acidity)
  • Hyperkalaemia (in acidity, H+ entering cells in exchange for K+ into blood stream/ extra cellular space)
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7
Q

How is DKA diagnosed?

A
  • Glucose of 11 mol/L +
  • ketones> 3 mmol/l or positive ketones on dipstick
  • pH> 7.3
  • Bicarbonate < 15 mmol/l
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8
Q

How is DKA treated?

A
  • Fluid replacement w/ isotonic saline (0.9% sodium chloride)
  • Fixed-rate IV insulin at 0.1 unit/kg/ hour
  • potassium if patient is hypokalemic
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9
Q

How is type 2 diabetes diagnosed?

A

Symptomatic + glucose levels (if no symps check twice)
Fasting blood glucose: 7.0mmol/ mol
Random blood glucose: 11.1mmol/L
Hb1Ac: 48 mmol/mol (6.5%)

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10
Q

What are the treatments for type 2 diabetes?

A

Life style: high fiber, low glycaemic index carb
Metformin
Metformin + (DPP-4i/ pioglitazone/ sulfonylurea)
Metformin + 2x (DPP-4i/ pioglitazone/ sulfonylurea)
Insulin based therapy or replacing one drug with GLP-1 ( weight loss)
SGLT-2 is given to any CVD patients, can be started at ANY point

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11
Q

What are side effects and contraindications for metformin?

A
  • GI upsets, reduce vitamin B12 absorption
  • Metformin associated lactic acidosis (MALA) from increased lactate production in gut and liver, lactate is cleared by liver and kidney
  • contraindicated in patients with kidney disease, sepsis (liver impaired), recent myocardial infarction
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12
Q

What are the symptoms of MALA

A

abdominal pain + severe diarrhea
increased lactate in report

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13
Q

how to minimize the side effects of metformin & what if it is contraindicated?

A
  • Titrate up slowly, modified-release (delayed administration) if severe side effects
  • SGLT-2 for CVD patients OR DPP-4i/ pioglitazone/ sulfonylurea
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14
Q

What are the target HbA1c for type 2 diabetes patients?

A
  • Aim for 48 mmol/mol (6.5%) if only on lifestyle and/or metformin
  • Aim for 53 mmol/mol (7.0%) for dual therapy or any treatment with sulfonylurea (may cause hypoglycemia)
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15
Q

what are the special factors of SGLT-2, GLP-1, and Sulfonyurea

A

SGLT-2: CVD patients only, pee sugar
GLP-1: weight loss
sulfonyurea: hypoglycaemia, no truck drivers

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16
Q

what is the mode of action of SGLT-2i (ie, empagliflozin)

A
  • inhibits sodium glucose transporter (filter in tubules of kidney that allows glucose reabsorption)
  • renal glucose loss resulting in glucose reduction and weight loss
17
Q

pros and cons of SGLT- 2i

A

pros: diuretic, improve myocardial energetic
cons: genital thrush from glycosuria, hypovolemia & hypotension

18
Q

what is the incretin effect? how is it diff in T2DM patients

A
  • insulin secretion difference between gut and intravenous intake due to GLP & GIP-1 hormones in the guts
  • In patients with diabetes oral glucose response to insulin is quickly lost
    (GLP-1 is broken down by DPP-4)
19
Q

mode of action & result of GLP-1 mimetic

A
  • act like GLP-1 hormones from L-cells that response to nutrient stimuli/ presence of high glucose
  • increase insulin and decrease glucose
  • Acts on hypothalamus to reduce appetite and intestines to reduce gastric emptying

year 2 core concepts (9 decks)

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