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Medicine year 3 ANNA > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Define Diabetes Mellitus

A

Diabetes Mellitus = a reduction in insulin action sufficient to cause a level of hyperglycaemia that, over time, will result in diabetes specific microvascular pathology; retinopathy, nephropathy and neuropathy (eyes, kidneys and nerves) and macrovascular pathologies; stroke, MI, renovascular disease and limb ischaemia

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2
Q

What are the 3 mechanisms by which ↓ insulin action occurs in Diabetes Mellitus?

A
  1. ↓ insulin production
  2. ↓ insulin sensitivity of target organs
  3. Overwhelming ↑ in catabolic hormones (the anabolic effect of insulin is balanced against 4 main ‘catabolic hormones’ e.g. catecholamines, cortisol, glucagon and growth hormone)
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3
Q

Describe Non-diabetic hyperglycaemia (NDH) also called pre-diabetes (for patients) and impaired glucose regulation (healthcare staff).

A

NDH = insulin action ↓ is sufficient to cause hyperglycaemia but not sufficient enough to cause microvascular damage

There are 2 main types of impaired glucose regulation:

  1. Impaired fasting glucose (IFG) - due to hepatic insulin resistance
    • Fasting glucose 6.1 - 6.9 mmol/L
    • Pts with IFG should have an OGTT to rule out diabetes - if ≥ 7.8 but < 11.1 then pt has IGT
  2. Impaired glucose tolerance (IGT) - due to muslce insulin resistance
    • Fasting glucose < 7.0 mmol/L + OGTT 2-hour ≥ 7.8 but < 11.1
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4
Q

What is HbA1c?

A

HbA1c = glycated haemoglobin

  • It is an indication of the previous 3-month average plasma [glucose]
  • Test is limited to 3-month average as lifespan of RBCs is 120 days i.e. 4 months
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5
Q

What are the presenting symptoms of type 2 DM?

A

T2DM patients often present asymptomatically and only present when hyperglycaemia is overt

Symptoms:

  • Polyuria
  • Polydipsia
  • Tiredness
  • Polyphagia
  • Blurred vision
  • Candidal infections e.g. genitals or skin folds
  • Unexplained weight loss (this if for T1DM)
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6
Q

What are the diagnostic criteria for T2DM for each of the following investigations, with symptoms and then without symptoms:

  1. Random plasma glucose
  2. Fasting glucose
  3. Oral glucose tolerance test (OGTT)
  4. HbA1c
A

If patient is SYMPTOMATIC + ONE of:

  • Fasting glucose ≥ 7.0 mmol/L
  • Random plasma gucose ​≥ 11.1 mmol/L
  • Oral glucose tolerance test (OGTT) - ≥ 11.1 mmol/L (2h after 75g glucose given orally)

If patient is ASYMPTOMATIC the above criteria apply BUT must be demonstrated on two seperate occasions!

HbA1c:

  • Diabetes = HbA1c ≥ 48 mmol/mol (6.5%)
  • Pre-diabetes = HbA1c 42-47 mmol/mol
  • Not diabetic = HbA1c ≤ 41 mmol/mol (5.9%)
  • If asymptomatic the test must be repeated to confirm
  • Conditions that affects RBC turnover can produced misleading HbA1c - thus the it can’t be used in the following conditions:
    • Children
    • Pts with symptoms < 2 months
    • Haemoglobinopathies
    • Haemolytic anaemia
    • Untreated iron deficiency anaemia
    • Suspected gestational diabetes
    • HIV
    • CKD
    • Medication that may cause hyperglycaemia (e.g. corticosteroids)
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7
Q

What is the risk that gestational diabetes poses?

How can it be diagnosed via fasting glucose or OGTT?

A

↑ foetal morbidity/mortality

  • Fasting glucose ≥ 5.6 mmol/L
  • OGTT ≥ 7.8 mmol/L
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8
Q

Are men or women more likely to have Diabetes?

A

MEN

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9
Q

What Kidney condition is Diabetes the commonest cause of?

A

End Stage Renal Disease (ESRD)

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10
Q

What is the proportion of adults with Type 1 vs Type 2 diabets?

A

10% of adults diagnosed have type 1

90% of adults diagnosed have type 2

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11
Q

What % of patients with Non-diabetic Hyperglycaemia progress to T2DM per year?

A

5-10%

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12
Q

For Type 1 Diabetes describe the following:

  • Cause?
  • Onset?
  • Degree of Genetic influence?
  • Do obesity, sendentary lifestyle or social deprivation impact development of T1DM?
  • What acute condition are T1DM patients at risk of?
A
  • Cause: insulin deficiency due autoimmune destruction of pancreatic B-cells
  • Onset: Childhood (<30yrs)
  • Genetics: concordance in identical twins is ~30% (indicating environmental influence)
  • Obesity, sedentary lifestyle, social deprivation = no impact on developing T1DM
  • Risk of DKA - because lack of insulin results in abnormally high ‘burning’/metabolism of fat to produce ketone bodies for energy (as opposed to glucose)
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13
Q

For Type 2 Diabetes describe the following:

  • Cause?
  • Onset?
  • Degree of Genetic influence?
  • Do obesity, sendentary lifestyle or social deprivation impact development of T1DM?
A
  • Cause: combination of insulin resistance + B-cell dysfunction (no autoimmune associations)
  • Onset: Most adult onset (>30yrs)
  • Genetics: concordance in identical twins is ~80% (implying a STRONG genetic element)
  • Obesity, sedentary lifestyle, social deprivation = strong impact
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14
Q

What are the risk factors for T2DM?

A
  • Gender - type 1 and type 2 more prevalent in men
  • Age - prevalence of T2DM ↑ from 25yrs - 80yrs
  • Weight - as BMI ↑ so does risk of T2DM
    • Insulin resistance has been closely linked with abdominal obesity (i.e. visceral fat)
    • BMI is more impactful than age on development of T2DM
  • Black African / Caribbean (3 times risk) and South Asian (6 times risk)
    • T2DM affects these ethnicities 10yrs earlier than Europeans
    • Lower BMI thresholds are used for South Asians compared to Caucasians
  • Sedentary lifestyle
  • FHx of T2DM
  • HTN / CVD
  • Pre-diabetic state
  • Gestational diabetes - 60% of women with gestational diabetes will develop T2DM
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15
Q
  1. What are the blood pressure targets for T2DM for risk factor modification?
  2. What is the 1st line treatment for BP management in these patients?
  3. What drugs are used to ↓ CVD risk in T2DM?
  4. What drug is 1st line for ↓ CVD risk?
A
  1. BP target = < 140/80 mmHg (or < 130/80 mmHg if end-organ damage is present)
  2. ACE inhibitors are first line for BP
    • ACE-I are renoprotective in diabetes - hence they are 1st line
    • African or Caribbean pts whould be offered ACE-I + either thiazide diuretic or Ca2+ channel blocker
  3. Statins - only patients with 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin
  4. Atorvastatin 20mg once daily
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16
Q

What are the side-effects of Statins?

A
  1. Muscle aches/pain
    • Rhabdomyolysis - if muscle pain becomes severe or worsens contact GP immediately
  2. GI disturbances (constipation, diorrhoea, flatulence)
  3. Thrombocytopenia (prolonged bleeding / bruising)
  4. Headaches
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17
Q

What Lifestyle Interventions are suggested for managing T2DM and it’s risks?

A
  1. Weight loss - initial target of 5-10% weight loss
  2. Exercise - ↑ insulin sensitivity with or without weight loss
  3. Diet
    • ​​High fibre, low glycaemix index (charts online indicate what is high and low)
    • Include low-fat dairy, oily fish
    • Minimise saturated fats and fatty acids
    • Replace saturated fat intake with olive oil or rapeseed oil
  4. Smoking cessation
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18
Q

What medications can be used to manage T2DM?

A
  1. Metformin
    • ↓ liver glucose production (gluconeogenesis), ↓ weight, ↑ insulin sensitivity
  2. Sulphonylureas
    • e.g. gliclazide, glipizide, glimepiride and glibenclamide
    • ​↑ insulin secretion via stimualting pancreatic ß-cells
  3. Thiazolidinediones (glitazones)
    • e.g. Pioglitazone or rosiglitazone
    • Stim nuclear receptor PPAR-gamma (perioxisome proliferator-activated receptor gamma) –> this causes gene modulation resulting in; ↑ storage of fatty acids in adipocytes (adipogenesis) - thus ↓ fatty acids in circulation, making the body depend on carbohydrates more (e.g. glucose)
    • ↓ insulin resistance, ↓ liver gluconeogenesis, ↑ adipogenesis
  4. Gliptins
    • e.g. sitagliptin, vildagliptin, linagliptin and alogliptin
    • Are DPP4-inhibitors
    • DPP4 breaks down GLP-1 (glucagon like peptide-1) - which is an incretin (↓ plasma glucose via ↑ insulin section and ↓ glucagon secretion)
  5. SGLT-2 inhibitors (-gliflozins)
    • e.g. dapagliflozin, canagliflozin, empagliflozin
    • Inhibit glucose reabsorption in kidney
  6. GLP-1 receptors agonists (-tides)
    • e.g. exanatide or liraglutide
    • Mimic GLP-1 –> ↓ plasma glucose via ↑ insulin section and ↓ glucagon secretion
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19
Q

What are the side-effects of the following drugs:

  1. Insulin
  2. Metformin
  3. Sulfonylureas
  4. Thiazolidinediones (pioglitazone)
  5. Gliptins
  6. SGLT-2 inhibitors
  7. GLP-1 agonists
A
  1. Insulin
    • Hypoglycaemia
    • Weight gain
    • Lipohypertrophy - small lump under skin due to fat accumulation at injection sites (insulin causes fat hypertrophy)
  2. Metformin
    • GI disturbances (diorrhorea, cramps, flatulence, nausea)
    • Lactic acidosis
  3. Sulfonylureas
    • Hypoglycaemia
    • Weight gain / ↑ appetite
    • Jaundice (is hepatically cleared so jaundice can occur in hepatic impairment)
    • Chlorpropamide - can ↑ ADH –> hyponatraemia
  4. Thiazolidinediones (pioglitazone)
    • Weight gain
    • Fluid retention
    • Fractures (2 x risk in women, but not men)
  5. Gliptins
    • ↑ risk of pancreatitis
  6. SGLT-2 inhibitors
    • UTIs
  7. GLP-1 agonists
    • Nausea / vomiting
    • Pancreatitis
20
Q

In what order are the pharmacological treatments for T2DM escalated?

  • Metformin
  • Sulphonylureas
  • Gliptins
  • Pioglitazone
  • SGLT-2 inhibitors
  • GLP-1 agonists
A
21
Q

By what two mechanisms does diabetic retinopathy occur?

A
  1. Capillary Leakage
    • Intra-retinal haemorrhages cause retinal oedema and leakage of lipid deposits which form ‘hard’ exudates
    • Hard exudates matter most if they occur in the macular region (maculopathy) –> causing loss of central vision
  2. Capillary Occlusion
    • If retinal ischaemia occurs in vessels supplying macula –> maculopathy
    • Retinal ischaemia can induce new retinal BV formation and potential vitreal haemorrhage (as newly formed vessels aren’t as structurally mature) –> this can eventually cause retinal detatchment or neovascular glaucoma (BV formation in anterior chamber over iris)
22
Q

What is DKA (Diabetic Ketoacidosis)?

A

DKA = acute metabolic complication of diabetes (most common acute hyperglycaemic complication of T1DM) – it is characterised by the triad of;

  1. Hyperglycaemia
  2. Ketonaemia
  3. Acidaemia
23
Q

What are the 3 most common events precipitating DKA?

(Besides new presentation of Diabetes as DKA)

A
  1. Inadequate insulin therapy (e.g. missed insulin dose)
  2. Infection (causes ↑ in bodies metabolic demands, for which there is insufficient insulin to accommodate for i.e. not enough to move enough glucose into cells)
    • Pneumonia and UTI are most common
  3. MI - cardiovascular events can stim release of counter-regulatory hormones that precipitate DKA (catecholamines, cortisol, glucagon, growth hormone)

The following are other known risk factors for precipitating DKA:

  • Pancreatitis
  • Acromegaly (↑ GH production due to benign pituitary adenoma)
  • Hyperthyroidism
  • Cushing’s Syndrome
  • Drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, anitipsychotics
24
Q

What is the mechanism underpinning the development of DKA?

A
  • Foundation is a combination of:
    • ↓ net effective insulin
    • ↑ counter-regulatory hormones (e.g. glucagon, catecholamines, cortisol and growth hormone)
  • ↓ net effective insulin –> hyperglycaemia (as body is unable to move glucose into cells)
  • The ↑ plasma [glucose] results in ↑ glucose in kidney nephrons –> this increases osmotic pressure (lowers H2O potential) causing solutes and H2O to move into the nephrons –> this is called osmotic diuresis
  • ​Osmotic diuresis causes:
    • Polyuria
    • Dehydration
    • Polydipsia
    • Electrolyte loss/disturbances
  • ↓ glucose moving into cells also causes ↑ lipolysis –> releasing fatty acids, which are converted by beta-oxidation (in the liver) into ketone bodies; acetoacetate and β-hydroxybutyrate
  • Ketone bodies are used as an energy source in starvation (i.e. absence of carbohydrate energy sources fat stores are used) –> however they turn blood acidic
  • The body initially buffers the ketoacidosis with bicarbonate (HCO3-), but is overwhelmed
  • The body hyperventilates (respiratory compensation) to lower blood CO2 (reduce acidity)
    • Kussmaul Breathing – is a form of hyperventilation involving deep + laboured breathing and associated with metabolic acidosis
25
Q

What are the signs / symptoms of DKA?

A
  • Polyuria
  • Polydipsia
  • Dehydration - dry mucous membranes, poor skin turgor, sunken eyes, ↑ HR, ↓ BP,
  • Abdominal pain - correlates with degree of acidosis
  • ↑ RR (Kussmaul breathing - deep hyperventilation)
  • Acetone breath (‘pear drops’ smell) - due to ketosis
  • Nausea/vomiting - correlates with degree of acidosis
  • Altered mental status
26
Q

How is DKA diagnosed from tests (excluding examination)?

A
  • Hyperglycaemia - blood glucose > 11.0 mmol/L or known diabetes mellitus
  • Ketonaemia - > 3.0 mmol/L or significant ketonuria (more than ++ on urine dipstick)
  • Acidaemia:
    • Bicarbonate (HCO3-) < 15.0 mmol/L and/or
    • Venous pH < 7.3
27
Q

What are some signs that might indicate SEVERE DKA and require consultant review?

A
  • Blood ketones > 6 mmol/L
  • Bicarbonate < 5 mmol/L
  • Venous/arterial pH < 7.0
  • Hypokalaemia < 3.5 mmol/L on admission
  • GCS < 12 or abnormal AVPU (alert, voice, pain, unresponseive)
  • O2 sats < 92% on air (assuming no respiratory disease)
  • Systolic BP < 90 mmHg
  • Pulse > 100 or < 60 bpm
  • Anion gap > 16 (elevated suggests acidosis) - normal = 6-16
28
Q

What tests/investigations might be useful in a patient suspected of DKA?

A
  • Blood ketones
  • Lactate - taken to exclude lactic acidosis (result should be normal in DKA)
  • Capillary and venous blood glucose
    • 5-10% of DKA patients present as being euglycaemic
  • VBG / ABG:
    • Generally VBG is easier, lower risk, and can be used to diagnose and determine response to treatment
    • VBGs can also provide glucose + potassium
    • ABG (gold standard for metabolic disturbances) is more accurate for determining hypercapnia and hypoxia
  • U+Es:
    • Serum K+ often ↑ but total body K+ ↓
    • Na+, Cl-, Mg2+ and Ca2+ are normally ↓
  • Urine Dipstick:
    • +ve for leucocytes in UTI (can precipitate DKA)
    • +ve nitrites (infection)
    • +ve for glucose
    • +ve for ketones
  • FBC:
    • Leucocytosis (↑ WBC) occurs during hyperglycaemic state and in infection
  • Blood culture - looking for infective pathogen
  • ECG - to identify MI as precipitant or examine cardiac effects of electrolytes disturbances (Hyperkalaemia = tall-tented T-waves and widened QRS, hypokalaemia = U-waves)
  • CXR - if pneumonia thought to be precipitant of DKA
29
Q

What 3 things are done to mange DKA?

A
  1. Fluid replacement:
    • Typical fluid deficit in DKA ~100ml/Kg e.g. 70kg = 7 litres
    • Always consider age, gender and concomitant medication and co-morbidites when replacing fluid
    • Cation when replacing fluid in following; Young aged 18-25yrs, Elderly, Pregnant, HF or kidney failure, Concomitant BP affecting medication
  2. Fixed rate Insulin infusion:
    • IV fixed rate infusion pump - made of up of 50 units insulin made up to 50ml with 0.9% saline –> infuse at rate of 0.1 unit/kg/hr
    • When blood glucose < 15 mmol/l an infusion of 5% dextrose should be started
    • Continue pts long-acting insulin at usual dose + times in diabetic patients
    • Only give bolus (stat) dose of IM insulin (0.1 unit/kg) if there is delay in setting up infusion
  3. K+ replacement - correction of hypokalaemia (caused by insulin)
    I
30
Q

What is the fluid replacement regime for DKA?

A

Fluid replacement

  1. Insert 2 large-bore cannula (one in each arm ideally)
  2. If systolic BP < 90 mmHg (and no concomitant HF or sepsis):
    • 500ml 0.9% sodium chloride (Saline) over 10-15 mins
    • If BP doesn’t improve then another 500ml over 10-15 mins + contact senior
    • If BP remains low –> contact ICU
  3. If/once systolic BP > 90 mmHg:
    • See image
31
Q

What are the potassium cut-offs which dictate potassium replacement during DKA?

A

Hypokalaemia and hyperkalaemia can occur in DKA:

  • K+ is normally ↑ on admission (even though the total body K+ is ↓)
  • But will ↓ post insulin treatment
32
Q

What are some causes of Polyuria?

Can you comment on how common each cause is?

A

Common (>1 in 10 cases):

  • Diuretics, caffeine & alcohol
  • Diabetes mellitus
  • Lithium
  • Heart failure

Infrequent (1 in 100)

  • Hypercalcaemia
  • Hyperthyroidism

Rare (1 in 1000)

  • Chronic renal failure
  • Primary polydipsia
  • Hypokalaemia

Very rare (<1 in 10 000)

  • Diabetes insipidus
33
Q

What types of Insulin classifications are there based on their profile of action/duration?

A
  1. Rapid-acting insulin analogues
    • Onset = 5 mins
    • Peak = 1 hour
    • Duration = 3-5 hours
  2. Short-acting insulin (also called soluable insulin)
    • Onset = 30 mins
    • Peak = 3 hours
    • Duration = 6-8 hours
  3. Intermediate-acting insulin
    1. Onset = 2 hours
    2. Peak = 5-8 hours
    3. Duration = 12-18 hours
  4. Long-acting insulin analogues
    1. Onset = 1-2 hours
    2. Peak = flat profile
    3. Duration = 24 hours
34
Q

What is a basal-bolus regime for Insulin?

A

It is the combination of:

  1. Rapid/short-acting ‘bolus’ insulin before meals
  2. Intermediate/long-acting ‘basal’ insulin once or twice daily
35
Q

Name some examples of the following Insulin types:

  1. Rapid-acting insulin analogues
  2. Short-acting insulins
  3. Intermidate-acting insulins
  4. Long-acting insulin analogues
A
  1. Rapid-acting insulin analogues:
    • Insulin Aspart (Novorapid)
    • Insulin Lispro (Humalog)
  2. Short-acting insulins:
    • Actrapid
    • Humulin S
  3. Intermidate-acting insulins:
    • Isophane insulin
  4. Long-acting insulin analogues:
    • Insulin determir (Levemir) - once or twice daily
    • Insulin glargine (Lantus) - once daily
36
Q

What are ‘Premixed’ preparations of Insulin composed of?

A

Combinations of intermediate acting insulin + either a rapid-acting insulin analogue or short-acting insulin e.g.

  • Novomix 30:
    • 30% insulin aspart (rapid-acting)
    • 70% insulin aspart protamine (intermediate-acting)
  • Humalog Mix 25:
    • 25% insulin lispro (rapid-acting)
    • 75% insulin lispro protamine (intermediate-acting)
  • Humalog Mix 50:
    • 50% insulin lispro
    • 50% insulin lispro protamine
37
Q

Is Insulin typically administered; subcutaneously, intramuscularly, IV or oral?

A

Subcutaneously

38
Q

How often should HbA1c be check for type 1 and type 2 diabetes?

A

Every 3-6 months

(Then every 6 months when stable for Type 2)

39
Q

What are the DVLA regulations regarding 1) Cars 2) HGVs for diabetes mellitus patients?

A

Cars:

  • If on Insulin, pt can drive a car if:
    1. They have hypoglycaemic awareness
    2. No more than 1 episode of hypoglycaemia requires assistance of another person in the last 12 months
    3. No relevant visual impairement
    4. Drivers are normally contacted by DVLA
  • If on drugs than can cause hypos (e.g. sulphonylureas):
    • No more than 1 episode of hypoglycaemia requires assistance of another person in the last 12 months
  • If diet controlled:
    • No need to inform DVLA

HGV:

If on Insulin or other hypo causing medication (e.g. sulphonylureas);

  • Must not have had any severe hypoglycaemic event in the previous 12 months
  • The driver has full hypoglycaemic awareness
  • The driver must show adequate glucose control via regular blood glucose monitoring (at least twice daily and at times relevant to driving)
  • The driver must demonstrate an understanding of the risks of hypoglycaemia
  • There are no other debarring complications of diabetes
40
Q

What is MODY (Maturity-onset diabetes of the young)?

A
  • MODY = development of T2DM in patients < 25 years old
  • Genetic condition - typically autosomal dominant
    • ​Over 6 different mutations are known e.g. MODY 1, MODY 2 etc.
  • ~ 90% are misdiagnosed as having T1 or T2 diabetes
  • MODY 2 and MODY 3 are most common forms

Features:

  • Typically < 25yrs
  • FHx of early onset diabetes
  • Ketosis is not a feature on presentation
  • Responds very well to sulphonylureas (insulin not usually necessary)

MODY 2:

  • 20% of cases
  • Glucokinase mutation

MODY 3:

  • 60% of cases
  • HNF-1 alpha (hepatocyte nuclear factor 1 alpha) mutation
  • Associated with ↑ risk of hepatocellular carcinoma
41
Q

What is LADA?

A

Latent Autoimmune Diabetes of Adults

  • Autoimmune type diabetes which present later in life
  • Often misdiagnosed as type 2 - even though the pt is more likely to be:
    • Low BMI
    • Ketotic
    • Poor response to non insulin therapies
42
Q

What should be involved in the ‘Baseline’ care plan for a newly diagnosed diabetic patient?

A
  1. Book eduction programme
  2. Lifestyle changes:
    • Diet - minimise sugar, ↑ fibre, ↓ fat, ↓ calories
    • Exercise - 150 mins/week of moderate intensity or 75 mins/week of vigorous intensity
    • Smoking cessation
  3. Agree target weight loss e.g. 5% in 6 months and 10% in 1 year
  4. Refer to smoking cessation
  5. Review in 3 months
43
Q

What messages should be given to diabetic patients regdarding

Sick Days, so called ‘Sick Day Rules’?

A
  1. Increase frequency of blood glucose monitoring to 4-hourly or more
  2. Encourage fluid intake - aim for at > 3L in 24hrs
  3. If unable/struggling to eat –> keep sugary drinks to maintain blood glucose
  4. Advise pts to keep a box of ‘sick day supplies’ for if they become unwell
  5. Continue to take oral hypoglycaemic medication even if not eating - bodies response to stress is ↑ cortisol –> ↑ glucose
  6. If on insulin –> take doses as normal - if blood glucose + ketones are high –> give corrective insulin dose
    • Rule of thumb: total daily insulin / 6 (max 15 units)
  7. Advise pt to keep access to a mobile phone –> has been shown to reduce progression of ketosis to diabetic ketoacidosis
44
Q

Which of the following hormones oppose action of Insulin?

  • Glucagon
  • Thyroxine
  • GLP-1
  • Noradrenaline
  • Cortisol
  • Testosterone
A

Glucagon, Noradrenaline (catecholamine) and cortisol

45
Q

What test can be done to differentiate between Type 1 diabetes / LADA and T2DM?

A

GAD antibodies test (Glutamic Acid Decarboxylase autoantibodies)

  • Often done when pt > 30yrs + T2DM is in doubt (e.g. low BMI or weight loss)
  • In autoimmune style diabetes GAD antibodies often exist in circulation
46
Q

Which of the following are true about Diabetic Eye Disease?

  • Can be detected by checking visual acuity
  • Is related to HbA1c
  • Always lead to total blindness
  • May be present at diagnosis of Type 2 diabetes
  • Doesn’t occur in young people
A

Diabet eye disease:

  • Is related to HbA1c
  • May be present at diagnosis of Type 2 diabetes
47
Q

What is HHS (Hyperosmolar Hyperglycaemic State)?

A

General:

  • Medical emergency, difficult to manage, significant mortality
  • Typically seen in elderly T2DM
  • DKA present in hours whereas HHS comes on over several days - thus dehydration + metabolic disturbances are more extreme

Pathophysiology:

  • Hyperglycaemia –> osmotic diuresis:
    • Polyuria
    • Dehydration
    • Polydipsia
    • Electrolyte loss of Na+ and K+
  • Volume depletion causes –> ↑ serum osmolarity (typically > 320 mosmol/kg) –> causes hyperviscosity of blood
  • Despite electrolyte losses + total body volume depletion the typical patient with HHS, may not look dehydrated –> because hypertonicity leads to preservation of intravascular volume

Presentation:

  • General: fatigue, lethargy, nausea and vomiting
  • Neurological: altered level of consciousness, headaches, papilloedema, weakness
  • Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  • Cardiovascular: dehydration, ↓ BP, ↑ HR (tachy)

Diagnosis:

  1. ​Hypovolaemia
  2. Significant Hyperglycaemia ( > 30 mmol/L) without significant ketonaemia or acidosis
  3. Significant ↑ serum osmolarity (>320 mosmol/kg)

Mangement:

  • Normalise the Osmolarity (gradually)
    1. Replace fluid + electrolyte losses
    2. Normalise blood glucose (gradually)

Medicine year 3 ANNA (30 decks)

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