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Case 5 Diabetes > Diabetes > Flashcards

Diabetes Flashcards

(57 cards)

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1
Q

What is the dominant anabolic hormone?

A

Insulin

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2
Q

What are the 4 main catabolic hormones?

A

Glucagon, catecholamines, cortisol, growth hormone

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3
Q

What is the definition of diabetes mellitus?

A

A reduction in insulin action sufficient to cause a level of hyperglycaemia that, over time, will result in diabetes specific, microvascular (capillary) pathology in eyes, kidneys and nerves.

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4
Q

What does Non-Diabetic Hyperglycaemia (NDH)/IGT increase risk of?

A

Macrovascular disease (CHD, CVD, PVD)

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5
Q

How is DM diagnosed?

A
  • Fasting Glucose (x2 or + symptoms) >/=7.0mmol/L
  • 2hr post glucose load (or random glucose) >/= 11.1mmol/L
  • HbA1c greater or equal to 48mmol/mol – diagnosed DM.
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6
Q

How is IGT diagnosed? (3)

A
  • Fasting Gluc <7.0
  • 2h-post glucose load >7.8, <11.1
  • HbA1c 42-47 mmol/mol
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7
Q

What are the features of T1DM?

A

beta cell destruction, organ specific auto-immunity, mostly childhood onset, ketosis prone

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8
Q

What are the features of T2DM?

A

Insulin resistance + beta-cell dysfunction, Mostly adult onset, Ketosis resistant

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9
Q

What is a big modifiable risk factor for T2DM?

A

Obesity. Insulin resistance is closely linked to abdominal obesity.

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10
Q

What are the risk factors for T2DM?

A

Modifiable - Diet composition, lack of exercise, overweight and obese

non-modifiable - FH, ethnicity, age

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11
Q

What is diabetes insipidus?

A

Passage of large volumes (3L/day) of dilute urine due to impaired water resorption by kidney. This is because of reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of kidney to ADH (nephrogenic DI).

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12
Q

What are the signs and symptoms of hypercalcaemia?

A

Abdo pain, vomiting, constipation, polyuria, polydipsia, depression, anorexia, weight loss, tiredness, weakness, hypertension, confusion, pyrexia, renal stones, renal failure ectopic calcification, cardiac arrest (decresed QT interval).

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13
Q

What the symptoms of hyperglycaemia?

A

Thirst, polyuria, polyphagia, tiredness, weight loss

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14
Q

What investigations are used to diagnose diabetes? urine + blood tests

A

Urine Testing - Glucose, Ketones, Protein

Blood Testing - Glucose, Ketones, Glycated haemoglobin/fructosamine

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15
Q

What is proteinuria a sign of?

A

Diabetic Nephropathy (Nephrotic Syndrome)

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16
Q

What is involved in an annual care plan? (4)

A

Risk Factor Review, early detection of complications (eyes, kidneys, feet), patient and professional review of results, care planning

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17
Q

What is involved in a baseline management plan? (3)

A

Explanation and discussion of disease, referral to structured education programmed (e.g. XPERT, DESMOND), baseline annual checks

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18
Q

How many checks should a person with diabetes have?

A

9/year

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19
Q

What does a baseline annual check consist of? (5)

A

Lipid check, Urine ACR, eGFR, Foot exam, refer to diabetic eye screening programme

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20
Q

What are the treatment goals in diabetes? (4)

A

minimise side effects, blood glucose near-normal as possible, CVD risk management, effective self management

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21
Q

What is the treatment for T1DM

A

Insulin

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22
Q

What is foundation of T2DM management?

A

Lifestyle - particularly weight management diet and exercise

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23
Q

What drugs are used in T2DM?

Study These Flashcards
A
  • Biguanide e.g. Metformin
  • Thiazolidinediones e.g. Pioglitazone
  • Sulphonylureas e.g Gliclazide, Glipizide
  • Meglitinides e.g. Nateglinide, Repaglinide
  • Incretin based therapy - DPP4 inhibitors (e.g. sitagliptin) & Incretins, GLP1 agonists e.g. (exenatide, liraglutide)
  • SGLT2 antagonists (Dapagliflozin, Canagliflozin, Empagliflozin)
24
Q

How often do you measure HbA1C levels in adults with T2DM?

Study These Flashcards
A
  • 3–6-monthly intervals (tailored to individual needs), until the HbA1c is stable on unchanging therapy
  • 6-monthly intervals once the HbA1c level and blood glucose lowering therapy are stable
25
What is the HbA1C target level for T2 diabetics on a single drug?
48mmol/mol (6.5%), or 53 mol/mol (7.0%) if on drug associated w/ hypoglycaemia
26
How is a patient whose HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher managed?
- reinforce advice about diet, lifestyle and adherence to drug treatment and - support the person to aim for an HbA1c level of 53 mmol/mol (7.0%) and - intensify drug treatment.
27
What is first line treatment of T2DM?
standard release metformin
28
What is first intensification treatment?
- metformin and a DPP‑4 inhibitor or - metformin and pioglitazone or - metformin and a sulfonylurea.
29
What is second intensification treatment?
- Triple therapy with: metformin, a DPP‑4 inhibitor and a sulfonylurea or metformin, pioglitazone and a sulfonylurea OR - starting insulin-based treatment
30
What are the DVLA regulations for diabetes?
- Declare to DVLA if complication or on insulin therapy - Glucose Below <5mmol/L - not able to drive. - If feeling symptoms - turn off car, sit in passenger seat, treat hypoglycaemia. 'Rule of 15' - take 15g of glucose, re-check in 15 mins. - Refrain from driving until at least 45 mins after treatment of hypoglycaemia
31
What causes visual loss in diabetic eye disease?
Capillary leakage causes retinal haemorrhage and oedema. Capillary occlusion causes retinal ischaemia (cotton wool spots) which causes angiogenesis. The new vessels can causes a vitral bleed or fibrosis, which can lead to traction retinal detachment.
32
How is diabetic nephropathy prevented?
anti-hypertensive treatment, BG control
33
What causes a neuropathic foot ulcer?
Loss of protective sensation and abnormal foot function.  Foot ulceration occurs as a result of trauma (often trivial) in the presence of neuropathy and/or peripheral vascular disease with infection occurring as a secondary phenomenon following disruption of the protective epidermis.
34
What is charcot's foot?
It is a progressive condition affecting the bones and joints of the foot; it is characterised by early inflammation and then joint dislocation, subluxation, and pathological fractures of the foot of neuropathic patients, often resulting in debilitating deformity
35
What is the link between diabetes and CVD?
Multi -vessel disease and atheromatous involvement of smaller calibre arteries is more common with hyperglycaemia All hyperglycaemia is associated with increased risk of CAD, Stroke and total mortality
36
How is type 1 diabetes confirmed?
Anti-GAD antibody test or islet cell antibodies
37
Which diabetes medications cause an increased risk of hypoglycaemia?
Sulfonylurea, megatinides, insulin therapy
38
What are precipitating factors of DKA?
Alcohol binge (interrupts gluconeogenesis), stress and infection, missing meals, missing insulin doses
39
What causes DKA?
a severe insulin deficiency and increased catabolic hormones (glucagon, catecholamines, cortisol, GH). This leads to excess glucose, ketones (lipolysis) and impaired/saturated disposal
40
What electrolytes are lost in DKA?
Na+ and K+ due to osmotic diuretic effect of glucose
41
What causes K+ loss?
Osmotic diuresis, secondary hyperaldosteronism due to poor renal perfusion, increased H+ ions which displace K+
42
What are the symptoms of DKA?
polyuria, polydipsia, weight loss, weakness, nausea, vomiting (ketosis + hyperglycaemic gastric stasis), leg cramps, blurred vision, abdominal pain
43
What are the signs of DKA?
Dehydration (osmotic diuresis + vomiting), hypotension with warm peripheries (dehydration and vasodilation from acidosis), cold extremities, tachycardia, Kussmaul breathing, acetone on breath, hypothermia, confusion, drowsiness, coma (severe hypotension – CV shock), hyperventilation (met acidosis), hypokalaemia
44
What investigations are performed in suspected DKA?
Venous blood - gas, U&Es, bicarbonate Urine/Blood - ketones ECG Infection Screen
45
What ECG changes are seen hypokalaemia?
T wave inversion, U waves, increased P width, prolonged PR interval, depressed ST
46
How is DKA managed?
ABCDE, fluid replacement, insulin, correction of hypokalaemia (0.9% NaCl + KCl 40 mmol/L), VTE prophylaxis
47
How is Hyperglycaemic hyperosmolar state (HHS) characterised
Severe hyperglycaemia (>30mmol/L), hyperosmolality (serum osmolality > 320 mOsm/ kg), and dehydration in the absence of hyperketonaemia
48
What can precipitate HHS?
infection, myocardial infarction, cerebrovascular events or drug therapy
49
How is HHS managed?
Measure/calculate serum osmolality frequently, give fluid replacement with 0.9% NaCl (IV), Aim for positive fluid balance of 3-6L by 12 hours and replacement of remaining estimated loss over next 12 hours, correct osmolality, fluid, electrolyte and BG imbalances
50
How is T1DM managed?
Education in self management (i.e. DAFNE programme), lifelong insulin treatment
51
When is Continuous subcutaneous insulin (pump) infusion recommended?
Attempts to achieve target haemoglobin A1c (HbA1c) levels with multiple daily injections (MDIs) result in the person experiencing disabling hypoglycaemia or HbA1c levels have remained high (that is, at 8.5% [69 mmol/mol] or above) on MDI therapy
52
What is the mode of action of Liraglutide?
GLP-1 agonist
53
What are the side effects of liraglutide?
N and V due to delayed gastric emptying, early satiety, weight loss
54
Which anti-diabetic is contra-indicated in heart failure?
pioglitazone (Thiazolidinediones)
55
What is impaired fasting glucose?
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l
56
What is impaired glucose tolerance?
Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
57
What are the main complications of sitagliptins? (3)
Acute pancreatitis, vasculitic rash that can progress to steven-johnson syndrome

Case 5 Diabetes (1 decks)

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