Diabetes Flashcards

1
Q

What is the pathophysiology behind T1DM

A

Autoimmune destruction of beta cells in the pancreas which causes an absolute deficiency of insulin

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2
Q

How does type 1 DM present

A

Shorter history

  • Weight loss - unable to use glucose for energy so use fat and muscle instead
  • Polydipsia - incresed thirst due to lots of urine produced
  • Polyuria - glucose lost in urine
  • tiredness
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3
Q

Which infections are more common in diabetics and why

A

Thrush and UTIs

Due to high sugar environment easier for bacteria to multiply

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4
Q

What is LADA

A

Latent autoimmune diabetes of adults

Form of T1DM with slower progression to insulin dependence

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5
Q

What are the glucose targets for T1DM patients

A

5-7mmol/L on waking

4-7mmol/L before meals and at other times of the day

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6
Q

How many times do T1DM patients need to monitor their insulin a day

A

4x a day including before each meal and before bed

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7
Q

How is DM diagnosed

A

Random blood glucose >11mmol/L
fasting glucose >7mmol/L
Oral glucose tolerance tests 2hrs later after 75g of glucose 2x venous gluose >11mmol/L
HbA1c >6.5% (>48mmol/L)

1 positive test result and symptomatic
or 2 positive test results and asymptomatic

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8
Q

Which HbA1c results suggest prediabetes

A

42-47mmol/L

5.7-6.4%

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9
Q

What is the pathophysiology behind T2DM

A

Normal or increased insulin secretion but relative insulin resistance
Resistance due to increased blood glucose levels so muscle and adipose tissue stop taking up glucose if oversaturated
Increased insulin production so increased absorption of glucose in cells (already overaturated)
therefore exhaustion of beta cells

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10
Q

How might T2dm present

A
Polydipsia
Polyuria 
Hx of blurred vision
Itchiness 
Peripheral neuropathy 
Recurrent thrush/UTIs 
Fatigue
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11
Q

How is T2DM managed

A

Diet and exercise to decrease insulin resistance
If HbA1c 6.5% (48mmol/L)
oral hypoglycaemics - metformin 1st line

1st intensification HbA1c (7.5%) 
Metformin + DPP4 i e.g. sitagliptin 
Metformin + pioglitazone 
Metformin + sulfonylurea e.g. gliclazide 
Metformin + SGLT 2 inhibitor 

Aim for a HbA1c of 7.0%

2nd intensification
Triple therapy on insulin based therapy
HbA1c therapy >7.5%

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12
Q

When are rapid acting insulins used

A

Taken before a meal used with long acting insulins e.g. Novorapid

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13
Q

When are short acting insulins used

A

30mins before meal e.g. Actrapid

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14
Q

When are intermediate acting insulins used

A

covers blood glucose when rapid stops working. Works for about 7hours
given at bedtme to cover night time
Patients should be aware of the risk of becomig hypoglycaemic

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15
Q

When are long acting insulins used

A
Given at bedtime to cover overnight 
Combined with rapid and short acting 
Taken OD or BD 
e,g. Levemir 
Glargine
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16
Q

What are the BM targets whilst on insulin therapy

A

Fasting 5-7mmol/L

before meals 4-7mmol/L

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17
Q

What is the MOA of metformin

A

Increases insulin sensitivity

Decrease hepatic gluconeogenesis

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18
Q

What are the side effects of metformin

A

GI upset - nausea, diarrhoea

Lactic acidosis

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19
Q

Which patients cannot take metformin

A

Patients with an eGFR of <30ml/min

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20
Q

What is the MOA of sulfonylureas

A

Stimulates beta cells to secrete insulin

  • Glicazide
  • Glimepinide
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21
Q

What are the side effects of Sulfonylureas

A

Hypoglycaemia
Weight gain
Hyponatraemia

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22
Q

What is the MOA of pioglitazone

A

Activates PPAR gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

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23
Q

What are the side effects of pioglitazone

A

Weight gain

Fluid retention

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24
Q

What is the MOA of DPP4 inhibitors (gliptins)

A

Increases incretin levels which inhibit glucagon secretion e.g. sitagliptin

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25
What are the side effects of gliptins
increased risk of pancreatitis | however generally well tolerated
26
What is the MOA of SGLT-2 inhibitors (-gliflozins)
Inhibits reabsorption of glucose in the kidney e.g Dapagliflozin
27
What are the side effects of SGLT-2 inhibitors
UTIs | Typically result in weight loss
28
What is the MOA of GLP-1 agonists
Incretin mimetic which inhibits glucagon secretion e.g. Exenatide Given via SC
29
What are the side effects of GLP-1 agonists
Nausea and vomiting Pancreatitis typically result in weight loss
30
What is the MOA of insulin
Direct replacement for endogenous insulin
31
What are the side effects of insulin
Hypoglycaemia Weight gain Lipodystrophy
32
What is given if Metformin is not tolerated or contraindicated e.g. eGFR <30ml
Gliptin Sulfonylurea Pioglitazone
33
When is insulin therapy considered in T2DM
Considered when the HbA1c reaches 7.5% and drug therapy is not controlling blood glucose (after first intensification)
34
Which drug should be continued when insulin therapy is started and why
Metformin because it reduces insulin resistance, reduces hyperinsulinaemia and counteracts weight gain
35
What is the target BP for diabetics
140/80 for diabetics with no end organ damage | 130/80 for end organ damage
36
What are the microvascular complications of Diabetes
Neuropathy Nephropathy Retinopathy Cardiomyopathy
37
What is the pathophysiology of diabetic neuropathy
Less blood flow to nerves due to narrowing of blood vessels due to damage of walls becuase high glucose content of blood
38
How may diabetic neuropathy present
Stock and glove distribution - same as b12 | Absent ankle relfexes
39
How does diabetic nephropathy present
Proteinuria - turbid, frothy urine Oedema - decreased serum protein Increased BP
40
How is diabetic nephropathy treated
first line is ACE inhibitors
41
How might diabetic retinopathy present
Floating spots in vision blurred vision sudden loss of vision
42
What would fundoscopy show in diabetic retinopathy
``` Cotton wool spots microaneurysms haemorrhages new vessel formation papilloedema ```
43
What are the macrovascular changes in Diabetes
Peripheral vascular disease - ulcers Atherosclerosis Coronary heart disease Stroke/TIA - statins given
44
What is acanthosis nigricans
Dark velvety patches - sign of insulin resistance in obesity, diabetes, in cushings, hypothyroidism, PCOS
45
What are secondary causes of hyperglycemia
Drugs - steroids, beta blockers, adrenaline, thiazides, some antipsychotics Acute stress events - stroke, MI, sepsis, encephalitis endocrine dysfunction - pancreatic disease and pancreatitis - CF Thyroid, adrenal or pituitary dysfunction Endocrine tumours - increased production of GH, glucocorticoids, catecholamines, glucagon, somatostatin
46
Why do diabetics get foot ulcers
Loss of sensation therefore cannot feel damage to feet so will continue to walk on them There will also be reduced circulation to the feet decreasing the healing More likely to become infected because of high glucose in blood - better environment for organisms to grow
47
Which staging system is used for diabetic ulcers
Wagners Grade 1: superficial Grade 2: involves ligament, tendon, joint capsule or fascia - no abscess or osetomyelitis Grade 3: deep ulcer with abscess or osteomyelitis Grade 4: gangrene to portion of mid foot Grade 5: extensive gangrene of foot
48
If an ulcer involves ligaments, tendons or the joint capsule which grade on the wagners classification is it?
Grade 2 - no abscess or osteomyelitis
49
How are diabetic foot ulcers treated
Prevention: remove dead skin regularly and keep foot clean to prevent infection Abx therapy Grade 1: mild - flucloxacillin QDS or Doxycycline OD 2 weeks Grade 2/3: moderate - flucloxacllin 1g QDS + Ciprofloxacin 500mg BD 2 weeks Systemic toxicity: Severe - In patient IV Tazocin + Vancomycin + Vascular surgery referral
50
How is osteomyelitis treated in diabetic foot ulcers
If confined to one bone, hole can be drilled into it and filled with abx cement
51
How can neuropathy be tested for in diabetic foot disease
Using a 10g monofilament on various parts of the foot
52
How would you investigate diabetic foot disease
``` Check foot pulses ABPI - may be higher than 1 due to calcification of arteries. may also be reduced due to peripheral arterial disease X ray foot - signs of osteomyelitis and charcots arthopathy measure depth of ulcer note which structures are affected Sensation of foot using monofilament Temperature of foot Check BP ```
53
What is charcots arthropathy
Microtrauma and peripheral neuropathy - fractures and progressive destruction and damage to bones and joints e.g. ankle Reduced autonomic nervous system Less vasoconstriction Increased blood flow to the bones Increase osteoclast activity and reabsorption of the bone Weakens bone
54
How may charcots arthropathy present
Warmer than other foot Red, swollen and oedematous Pain and soreness of foot - less than expected due to diabetic neuropathy Normally unilateral
55
How is charcots arthropathy diagnosed
Xray and MRI
56
What are the signs of charcots arthropathy on X ray
``` Distended joint Disorganisation Destruction Dislocation Increased density Production of debris ```
57
How is charcots arthropathy treated
Immobilise - prevent further destruction - full contact cast - walking brace
58
What is the definition of hypoglycaemia
Plasma glucose of <3mmol/L
59
What are the symptoms of hypoglycaemia
Autonomic - sweating - tremour - Anxiety - hunger - Palpitations - dizziness Neuroglycopenic - confusion - drowsiness - visual trouble - seizures - coma
60
When might post prandial hypoglycaemia occur
After gastric or bypass surgery (dumping syndrome - surge in insulin production) and in t2dm will have a prolonged OGTT
61
How would you investigate hypoglycaemia
``` Bedside Obs - BM, urine dip Bloods - FBC - blood glucose - U+Es - LFTs - CRP - TFTs ```
62
What are the causes of hypoglycaemia
In diabetics - insulin - sulfonylureas e. g. increased activity, missed meal, accidental/non-accidental OD ``` Non diabetic EXPLAIN Exogenous drugs e.g. insulin, oral hypoglycaemics, alcohol binge with no food, aspirin poisoning, ACE inhibitors Pituitary insufficiency Liver failure Addisons disease Islet cell tumour Non-pancreatic neoplasm ```
63
What are the risk factors for developing diabetes
``` Obesity Acromegaly Steroid use - long term Lack of exercise Calorie/alcohol excess Cushing's Pancreatic surgery/pancreatitis CF haemochromatosis ```