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Gastrointestinal Block > Diabetes Mellitis + DKA, HHS, Hypos > Flashcards

Diabetes Mellitis + DKA, HHS, Hypos Flashcards

1
Q

Compare the patho of Type I vs Type II Diabetes

A

Type I: Autoimmune destruction of the insulin-producing β cells of the islets of Langerhans in the pancreas

Type II: Relative deficiency of insulin due to an excess of adipose tissue ‘insulin resistance’

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2
Q

How does Type I diabetes present

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. May present with DKA: abdo pain, vomiting, ↓consciousness
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3
Q

How does Type II diabetes present

A
  1. Often picked up incidentally on routine blood tests
  2. Polydipsia
  3. Polyuria
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4
Q

What causes polyuria and polydipsia in a diabetes?

A

Water being ‘dragged’ out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).

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5
Q

List 5 ways to check blood glucose

A
  1. Capillary blood glucose - finger-prick glucose monitor
  2. One-off blood glucose, fasting or non-fasting
  3. HbA1c
  4. Glucose tolerance test
  5. Flash Glucose Monitoring (e.g. FreeStyle Libre)
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6
Q

What does HbA1c tell us?

A

Measures the amount of glycosylated haemoglobin and represents the average blood glucose over the past 2-3 months

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7
Q

Explain the glucose tolerance test

A

A fasting blood glucose is taken after which a 75g glucose load is taken

After 2 hours a second blood glucose reading is then taken

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8
Q

What is the WHO criteria for diagnosing type II diabetes?

A

If patient is symptomatic:

  • fasting glucose ≥ 7.0 mmol/l
  • random glucose ≥ 11.1 mmol/l (or after OGTT)

If patient is asymptomatic: above criteria must be demonstrated on two separate occasions

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9
Q

Answer the following:

HbA1c ≥ ______% (48 mmol/mol) is diagnostic of diabetes mellitus

But an HbA1c less than this does not exclude diabetes

A

6.5

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10
Q

3 Principals of Diabetes management

A
  1. drug therapy to normalise blood glucose levels
  2. monitoring for and treating any complications related to diabetes
  3. modifying any other risk factors for other conditions such as CVD
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11
Q

Management of Type I diabetes

A
  1. Subcutaneous insulin regimes
  2. Monitoring dietary carbohydrate intake
  3. Monitoring blood sugar levels on waking, at each meal and before bed
  4. Monitoring for and managing complications, both short and long term
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12
Q

List 2 S/Es of Insulin

A
  1. Hypoglycaemia
  2. Lipodystrophy
  3. Weight gain
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13
Q

What are the 2 main insulin therapies?

A
  1. Basal Bolus Regimes
  2. Insulin Pump
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14
Q

Explain the Basal Bolus Regime?

A

Basal → long acting insulin, typically in the evening, gives a constant background insulin throughout the day

Bolus → short acting insulin, usually 3 times a day before meals. Also injected according to the number of carbohydrates consumed during snacks

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15
Q

List 2 examples of Rapid-acting Insulin?

How long do these take to start working and how long do these last?

A

eg. Novorapid, Humalog, Apidra

Start working after around 10 minutes and last around 4 hours

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16
Q

List 2 examples of Short-acting Insulins?

How long do these take to start working and how long do these last?

A

eg. Actrapid, Humulin S, Insuman Rapid

Start working in around 30 minutes and last around 8 hours

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17
Q

List 2 examples of Intermediate-acting Insulin?

How long do these take to start working and how long do these last?

A

eg. Insulatard, Humulin I, Insuman Basal

Start working in around 1 hour and last around 16 hours

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18
Q

List 2 examples of Long-acting Insulins?

How long do these take to start working and how long do these last?

A

eg. Lantus, Levemir, Degludec (lasts over 40 hours)

Starts working in around 1 hour and lasts around 24 hours

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19
Q

What are Combination Insulins?

List 2 examples

A

Contain a rapid acting and an intermediate acting insulin.

In brackets is the proportion of rapid to intermediate acting insulin

eg.

  • Humalog 25 (25:75)
  • Humalog 50 (50:50)
  • Novomix 30 (30:70)
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20
Q

What is an Insulin Pump?

What are the 2 types?

A

Small devices that continuously infuse insulin at different rates to control blood sugar levels

Types:

  • Tethered pump
  • Patch pump
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21
Q

What is needed to qualify for an insulin pump funded by the NHS?

A

Child needs to be over 12 and have difficulty controlling their HbA1c

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22
Q

List 3 advantages and 3 disadvantages of an insulin pump over a basal-bolus regime?

A

Advantages:

  • Better blood sugar control
  • More flexibility with eating
  • Less injections

Disadvantages

  • Difficulties learning to use the pump
  • Having it attached at all times
  • Blockages in the infusion set
  • Small risk of infection
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23
Q

Medical management of Type II Diabetes?

In order of stepping up

A
  1. Initial drug treatment → Metformin
  2. Dual therapy → Metformin + pioglitazone or DPP‑4 inhibitor or sulphonylurea
  3. Triple therapy → using above medications OR insulin therapy
  4. metformin + sulfonylurea + GLP1 memetic
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24
Q

Medical management of Type II diabetes if Metformin is not tolerated?

In order of stepping up

A
  1. Gliptin or Sulfonylurea or Pioglitazone
  2. (Gliptin + Pioglitazone) or (Gliptin + Sulfonylurea) or (Pioglitazone + Sulfonylurea)
  3. Insulin
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25
Q

List 4 drug classes use to treat Type II Diabetes

A
  1. Biguanides
  2. Sulfonylureas
  3. SGLT-2 inhibitors
  4. DPP-4 inhibitors
  5. Thiazolidinediones
  6. GLP-1 analogues
  7. Intestinal Alpha-Glucosidase Inhibitors
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26
Q

Example of a Biguanide

Mechanism of action?

A

Eg. Metformin (first line)

MoA: Increases peripheral insulin sensitivity, decreases hepatic gluconeogenesis

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27
Q

Side effects of Metformin?

Contraindications?

A

S/E: diarrhoea, abdo pain, lactic acidosis

Contraindications: eGFR < 30 ml/min

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28
Q

Example of a Sulfonylureas

Mechanism of Action?

S/E

A

Eg. Gliclazide

MoA: Stimulate pancreatic beta cells to secrete insulin

S/E: Hypoglycaemia, weight gain, hyponatraemia

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29
Q

Example of a SGLT2 Inhibitor?

Mechanism of action?

S/E

A

Eg. Dapgliflozin

MoA: Increase urinary glucose loss

S/E: Glucoseuria, UTIs, Weight loss, DKA

30
Q

Example of a DPP4-Inhibitor?

Mechanism of action?

S/E?

A

Eg. Sitagliptin

MoA: inhibits DPP-4, this increases GLP-1 activity

S/E: GI upset, symptoms of URTI, pancreatitis

31
Q

What diabetic medication is contraindicated in heart failure?

A

Pioglitazone

32
Q

List the 3 main short term complications of diabetes

A
  1. Hypoglycaemia
  2. Hyperglycaemia (and DKA)
  3. Hyperosmolar Hyperglycaemic state (HHS) - rare
33
Q

List 4 causes of hypoglycaemia

A
  1. Insulin/sulphonylureas
  2. Liver failure
  3. Addison’s disease
  4. Alcohol
  5. Insulinoma
34
Q

How are symptoms of hypoglycaemia divided?

Why does each occur?

A

< 3.3 mmol/L → autonomic symptoms due to release of glucagon and adrenaline

< 2.8 mmol/L → neuroglycopenic symptoms due to inadequate glucose supply to the brain

35
Q

Features of hypoglycaemia < 3.3 mmol/L

A
  1. Hunger
  2. Irritability
  3. Sweating and Tremors
  4. Dizziness
  5. Pallor
36
Q

Features of hypoglycaemia < 2.8 mmol/L

A
  1. Weakness
  2. Vision changes
  3. Confusion
  4. Dizziness
37
Q

Pathophysiology of cardiac complications in diabetes?

A

Hyperglycaemia + free FA’s in blood can cause the lining of BVs to become thicker → impair blood flow

MI is commonly caused by a clot preventing supply to the heart

38
Q

Management of hypoglycaemia if patient is altert

A

15-20g fast acting carbohydrate ie. GlucoGel or Dextrogel, sweets or fruit juice

Eat some slower acting carbohydrate afterwards (e.g. toast)

39
Q

Management of hypoglycaemia if patient is unconscious or unable to swallow

A

1mg/kg IM glucagon or alternativly 200ml 10% dextrose IV

Treat seizure if prolonged or repeated

40
Q

What is DKA?

A

A state of severe, uncontrolled diabetes due to insulin deficiency

Complication of existing T1DM or may be the first presentation

(Rarely in T2DM)

41
Q

Pathophysiology of DKA

A

Uncontrolled lipolysis which results in an excess of FFAs that are ultimately converted to ketones

42
Q

List 3 of the most common precipitating factors of DKA

A
  1. Infection
  2. Missed insulin doses
  3. Myocardial infarction
43
Q

List 4 symptoms of DKA

A
  1. abdominal pain
  2. vomiting/ nausea
  3. lethargy, weakness, drowsiness
  4. polyuria, polydipsia
  5. leg cramps
  6. blurred vision
  7. Reduced consciousness ⇒ COMA
44
Q

List 4 clinical signs of DKA

A
  1. Kussmaul respiration (deep hyperventilation)
  2. Acetone-smelling breath (‘pear drops’ smell)
  3. Dehydration
  4. Electrolyte imbalance and Acidosis
  5. Hypotension ⇒ Shock
  6. Tachycardia
  7. Ketonaemia/ ketonuria
  8. Hyperglycaemia/ glycosuria
45
Q

Diagnostic criteria for DKA

“Joint British Diabetes Societies (2013)”

A
  1. Glucose > 11 mmol/l or known DM
  2. pH < 7.3
  3. Bicarbonate < 15 mmol/l
  4. Ketones > 3 mmol/l or urine ketones ++ on dipstick
46
Q

Management of DKA

A
  1. Fluid replacement: Isotonic saline used initially
  2. Fixed rate Insulin IVI, 5% dextrose infusion once BG is < 15 mmol/l
  3. Correct electrolyte disturbances: add K+ to replacement fluids
  4. Continue long-acting insulin, STOP short acting insulin
47
Q

What defines resolution of DKA?

A
  1. pH > 7.3 and
  2. blood ketones < 0.6 mmol/L and
  3. bicarbonate > 15.0mmol/L
48
Q

Complications of DKA or treatment itself?

A
  1. cerebral oedema
  2. hypoxaemia – pulmonary oedema
  3. fluid overload
  4. respiratory failure
  5. thromboembolism
  6. arrhythmias – cardiac arrest
  7. shock
  8. renal insufficiency – AKI
  9. hypoglycaemia
  10. coma
49
Q

Monitoring of DKA

A
  1. Glucose hourly for first 15 hours
  2. Finger prick ketones hourly until stable
  3. Blood gases/venous bicarbonate and electrolytes - 2, 4, 8 and 12 hourly
  4. Pulse, BP, temperature, neuro obs
  5. Urine output
50
Q

What is Hyperosmolar Hyperglycaemic state (HHS)

A

Hyperglycaemia in T2 diabetes

Results in osmotic diuresis, severe dehydration, and electrolyte deficiencies - Medical emergency

51
Q

In which popultion is HHS most common?

A

Typically presents in the elderly with T2DM

Note: increasing incidence in younger adults, can be the initial presentation of T2DM

52
Q

Pathophysiology of HHS

A

Hyperglycaemia results in osmotic diuresis with associated loss of Na+ and K+

Severe volume depletion results in a significant ↑ serum osmolarity, resulting in hyperviscosity of blood

Despite these, the typical patient may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume

53
Q

Diagnostic criteria for HHS

A
  1. Hypovolaemia and hypotension
  2. Severe Hyperglycaemia (≥ 30 mmol/L) without significant ketonaemia or acidosis
  3. Significant Hyperosmolality (> 320 mosmol/kg)
54
Q

How do we differentiate DKA from HHS

A

In HHS the hyperglycaemia is not accompanied by significant acidosis or ketosis (as it is in DKA)

In T2DM endogenous insulin production is sufficient to ‘switch off’ ketone production and prevent DKA

55
Q

Management of HHS

A
  1. Fluid resuscitation 0.9% saline → correction of osmolality and fluid and electrolyte losses (gradually)
  2. Insulin at 0.05 units/kg/hour → correction of hyperglycaemia (gradually)
  3. VTE prophylaxis - patients are high risk due to dehydration
56
Q

List the main long term complications of diabetes

Incl 2 macro and 2 microvascular complications

A

Macro: IHD, Stroke, CVD

Micro: retinopathy, nephropathy, and neuropathy

57
Q

What is the BP target in a person with type 2 diabetes?

Why is this important?

A

< 140/90 mmHg

BP control needs to be strict in diabetes because they are at higher risk of macro and microvascular complications

58
Q

How may physicians prevent CVD in diabetes?

Explain?

A

Lipid lowering through use of Statins

For T2DM use QRISK2 → >10% offer 20 mg Atorvastatin

59
Q

What is a recognised gastrointestinal complication of diabetes?

How/why does this occur

A

Gastroparesis - due to poor glycaemic control

Results in Autonomic Neuropathy - nerve damage to the ANS, specifcally to the vagus nerve (controls gastric muscles)

60
Q

How does Gastroparesis present?

A

Damage to vagus nerve leads to delayed gastric emptying and abnormal stomach wall movements. Presents as:

  1. offensive egg smelling burps due to bacterial overgrowth
  2. early satiety
  3. morning nausea
  4. fluctuations in blood glucose (mismatch between glucose absorbed in food and insulin injected)
61
Q

Treatment of Gastroparesis

A
  1. Motility agents ie. metoclopramide, domperidone
  2. Tight glycaemic control
  3. Antibiotics ie Erythromycin (bacterial overgrowth)
  4. Botox injections to relax the gastric outflow obstruction
  5. Gastric pacemakers if all else fails
62
Q

List a clinical feature of autonomic neuropathy in diabetics

How is this defined?

A

Postural/ orthostatic hypotension

Defined as a fall in systolic BP by 20mmHg or more after changing position or posture, typically lying to standing

63
Q

What is a consequence of orthostatic hypotension

A

Drop in BP on movement can lead to dizziness, falls and loss of consciousness

Can be exacerbated by dehydration (ie. if a patient has hyperglycaemia and consequent polyuria)

64
Q

Management of Autonomic Neuropathy in diabetes

A
  1. ↑ dietary salt
  2. salt retaining hormones ie. Fludrocortisone or Midodrine
  3. raising the head of the bed to retrain body’s baroreceptors
  4. wearing elasticated stockings to overcome venous pooling in peripheries
  5. sitting or standing slowly may help with light headedness
65
Q

How do we prevent Peripheral Arterial Disease in diabetics

A
  1. Patients and carers shold be educated about good foot self surveillance and care strategies
  2. Feet should be reviewed on a regular basis
66
Q

How may Peripheral Arterial Disease present?

A

If circulation is compromised, it can manifest in several ways:

  • foot discolouration
  • gangrene
  • intermittent claudication
  • rest pain
  • night pain
  • absent peripheral pulses (confirmed on doppler)
67
Q

What is the treatment for PAD based upon?

A

managing cardiovascular risk factors

68
Q

A patient with Type II diabetes presents with critical ischaemia on their left foot.

a) what is the biggest risk?
b) what is your first immediate step in management

A

a) at risk of losing their foot
b) need to be urgently seen by a multi-disciplinary specialist diabetic foot team which includes a vascular surgeon

69
Q

Most common causative organisms in diabetic ulcers?

A

Gram (+) → Staphylococcus aureus and Enterococcus

Gram (-) → Escherichia coli, Klebsiella species, Proteus species, Pseudomonas aeruginosa and anaerobes.

70
Q

Management of diabetic foot infections

A
  1. Good glycaemic and BP control
  2. Stopping smoking
  3. Improving the circulation (potentially with angioplasty or bypass surgery),
  4. Debridement of the wound and use of larvae therapy and antibiotics
71
Q

What is the risk if an ulcer is deep and probes down to bone tissue?

How do we diagnose this?

A

Osteomyelitis

Diagnosed by MRI (does not reliably show up on plain X-rays)

72
Q

What is the commonest cause of death for diabetics?

A

Heart and circulation problems (75% of all deaths), with heart attacks accounting for 30% of all deaths

Gastrointestinal Block (26 decks)

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