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Yr3 Medicine- Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the ideal plasma glucose concentration?

A

4.4-6.1mmol/L

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2
Q

Remind youself, for insulin and glucagon, of:

  • Where each hormone is produced
  • Effect on blood sugar
  • Anabolic or catabolic
A

Insulin

  • Beta cells in Islet of Langerhans
  • Decrease blood sugar
  • Anabolic

Glucagon

  • Alpha cells in Islet of Langerhans
  • Increase blood sugar
  • Catabolic
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3
Q

State some actions of insulin

A
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4
Q

Which of the common GLUT transporters is insulin dependent?

A

Glut 4

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5
Q

For GLUT 1-4 state whether they are:

  • Insulin dependent
  • Where they are found
A
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6
Q

State some actions of glucagon

A
  • Liver: stimulates glycogenolysis and gluconeogenesis
  • Adipose: break down fats into FA to be used as fuel
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7
Q

Discuss the pathophysiology of T1DM

A
  • Autoimmune destrution of beta-islet cells which causes pancreas to stop producing insulin
  • Cause is unclear; may be genetic component and it may be triggered by certain viruses e.g. Coxsackie B virus & entorovirus
  • When there is no insulin being produced, cells of body can’t absorb glucose from blood
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8
Q

State some risk factors for T1DM

A
  • Family history
  • Other autoimmune disease
    *
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9
Q

What gene mutations are thought to be associated with T1DM?

A

HLA D3 & HLA D4 (>90% children with T1DM)

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10
Q

Describe the typical presentation of someone with T1DM

A
  • Adolescent
  • Polydipsia
  • Polyuria
  • Weight loss
  • Blurred vision

If pt presents with DKA may also have:

  • Nausea & vomitting
  • Abdo pain
  • Tachypnoea
  • Lethargy
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11
Q

What investigations would you do if you suspect T1DM, include:

  • Bedside
  • Bloods
  • Imaging

*Where appropriate, justify why you would do each one

A

Bedside

  • Urine dipstick: check for glucosuria & ketones
  • Check plasma glucose:
    • Random plasma glucose
    • Fasting plasma glucose
    • 2-hour plasma glucose
  • Plasma ketones

Bloods

  • HbA1c
  • Then usual FBC, U&Es etc…: check for other causes/abnormalities
  • ? Fasting C peptide
  • ? Autoantibodies (NOT required but can distinguish other forms of diabetes from T1DM)
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12
Q

Discuss how many ‘abnormal’ diabetic results are required to diagnose diabetes according to WHO

A
  • If symptomatic, only need on abnormal result
    • e.g. fasting glucose ≥ 7mmol/L
    • e.g. random glucose ≥ 11.1mmol/L
    • e.g. glucose ≥11.1mmol/L after oral glucose tolerance test
  • If asymptomatic, must have abnormal result on two separate occasions
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13
Q

What is prediabetes?

What are Hba1c and fasting glucose values for pre-diabetes?

A
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14
Q

Explain what the fasting C-peptide result can tell you

A

C peptide is released at same time as insulin. It links A & B polypeptide chains but is removed by golgi before secretion of insulin. Hence, plasma C-peptide can tell you information about insulin secretion. C peptide has a longer half life than insulin (30 mins compared to 5 mins).

*NOTE: insulin is hepatic clearance & C-peptide is renal clearance

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15
Q

Discuss the long term management of T1DM

A

Lifestyle

  • Education
  • Dietary advice

Pharmacological

  • Subcutaneous insulin (basal-bolus)
  • NICE recommend considering adding metformin if BMI ≥25kgm2

Monitoring

  • Recommend monitor at least 4x per day (target of 5-7mmol/L on waking, target of 4-7mmol/L before meals)
  • HbA1c every 3-6 months with targe to ≤48mmol/L (6.5%)
  • Monitoring of other complications (e.g. retinopathy, diabetic foot disease etc..)
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16
Q

Flash glucose monitoring (e.g. Freestyle Libre) is a relatively new technology used to monitor plasma glucose. It is quite expensive and NHS funding only available in certain areas (at present time). Describe how it works

A
  • Sensor on skin measure interstitial glucose concentration
  • Interstitial glucose concentration lags 5 mins behind plasma glucose concentration
  • Sensor records glucose readings at short intervals allowing pt to see what glucose levels are doing over time
  • User uses a reader to swipe over sensor and the reader shows the blood sugar readings
  • Sensors need replacing every 2 weeks

*NOTE: due to 5 min delay, if you suspect hypoglycaemia but sensor doesn’t show hypoglycaemia do capillary blood glucose

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17
Q

Discuss the pathophysiology of T2DM

A
  • Insulin resistance
  • Repeated exposure to glucose & insulin makes cells in body become resistant to effect of insulin; therefore more insulin is required. Over time pancreas- particularly beta cells- become fatigued and damaged (after having to produce extra insulin) resulting in the Beta cells dysfunctioning and producing less. Insulin resistance which can then be later combined with decreased insulin secretion leads to chronic hyperglycaemia
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18
Q

State some risk factors for T2DM (think about modifiable & non-modifiable risk factors)

A

Modifiable

  • Older age
  • Ethnicity (black, chinese, south asian)
  • Family history

Modifable

  • Obesity
  • Sedentary lifestyle
  • High carbohydrate diet (particularly refined carbohydrates)
  • Dyslipideamia
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19
Q

Describe the typcial presentation of someone with T2DM

A

Pt may not necessarily have symptoms and hence you should screen for T2DM in those with risk factors. However, symptoms & signs include:

  • Fatigue
  • Blurred vision
  • Polydipsia
  • Polyuria
  • Slow healing
  • Glucosuria
  • Acanthosis nigricans
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20
Q

What investigations would you do if you suspect T2DM, include:

  • Bedside
  • Bloods
  • Imaging

*For each, justify why where appropriate

A

Bedside

  • Urine dipstick: check for glucosuria & ketones
  • Check plasma glucose:
    • Random plasma glucose
    • Fasting plasma glucose
    • 2-hour plasma glucose
  • Plasma ketones

Bloods

  • HbA1c
  • Then usual FBC, U&Es, LFTs, lipids etc…: check for other causes/abnormalities
  • ? Fasting C peptide (NICE recommend doing this if T1DM suspected but clinical presentation has atypical features e.g. >50yrs old, BMI >25, slow evolution/long prodrome)
  • ? antibody titres (same as above)
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21
Q

Discuss the long term management of T2DM, consider:

  • Lifestyle
  • Monitoring (include HbA1c targets)
  • Pharmacological
A

Lifestyle

  • Patient education
  • Diet & lifestyle:
    • Regular exercise
    • Veg & oily fish
    • High fibre diet
    • Limited sugar and saturated fats
  • Weight loss
  • Stop smoking
  • Optimising treatment for other conditions e.g. hypertension, hyperlipidaemia, CVD
  • Frequent monitoring & treatment of complications

Monitoring

  • HbA1c every 3-6 months until stable then 6 monthly
  • Targets should be agreed with pt to encourage motivation, example targets:
    • Lifestyle only= 48mmol/L
    • Lifestyle + metformin= 48mmol/L
    • Taking a drug that can cause hypoglcyaemia (e.g. sulphonylurea)= 53mmol/L
    • Taking two or more antidiabetic medications= 53mmol/L

Pharmacological

  • First line= metformin
  • If pt has high risk CVD (QRISK >10%), established CVD or chronic heart failure SGLT-2 inhibitor should also be started (start and titrate metformin first before starting)
  • If HbA1c has risen to 58mmol/L, add second line: add any of the following:
    • DPP-4 inhibitor
    • Pioglitazone
    • Sulfonylurea
    • SGLT-2 inhibitor (if NICE criteria met and not already on one)
  • Add a third agent
  • Consider insulin and GLP-1 mimetics
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22
Q

Further summary of T2DM management

A
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23
Q

State some short term complications of diabetes

A
  • Hypoglycaemia
  • Hyperglycaemia
  • DKA
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24
Q

State some symptoms & signs of hypoglycaemia

A

Sympathetic

  • Tremor
  • Sweating
  • Irritability
  • Dizziness
  • Pallor

Impaired CNS function

  • Reduced consciousness
  • Seizures
  • Focal neurology
  • Coma
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25
Q

Discuss how you would manage hypoglycaemia if pt is:

  • Alert & able to swallow
  • Confused/drowsy but able to swallow
  • Unconscious or swallowing concerns
A

Alert & able to swallow

  • Rapid acting glucose 15-20g (E.g. 200ml of orange juice)
  • Followed by slower acting carbohydrate (e.g. piece of toast) once glucose >4mmol/L

Confused/drowsy but able to swallow

  • Buccal glucogel
  • Consider IV access
  • Followed by slower acting carbohydrate (e.g. piece of toast) once glucose >4mmol/L

Unconscious or swallow impaired

  • IV glucose 20% (volume and time over depends on blood sugar- see UHL summary image)
  • Or glucagon 1mg IM
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26
Q

State some potential causes of hypoglycamia (don’t just think about diabetes)

A
  • Fasting
  • Exercise
  • Medications e.g. sulphonylureas
  • Insulinoma
  • Endocrine failures
  • Liver failure
  • Anorexia nervosa
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27
Q

Glucagon intramuscular injection may be considered in a hypoglycaemic pt who is unconscious or unable to swallow; discuss:

  • Indications for glucagon injection
  • How long it takes to work
  • Pts you shouldn’t use it in
  • Risks
A
  • Indications:
    • Refractory (other treatment not working)
    • Exogenous insulin induced
    • Dificult IV access
  • 15-20 mins
  • Requires glycogen stores hence don’t use in pts with liver disease and hence little glycogen stores. Don’t use in pts with insulinoma
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28
Q

State some symptoms & signs of hyperglycaemia

A

(similar to inital presentation). MUST CHECK not in DKA

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29
Q

Long term complications of diabetes can be classified into macrovascular, microvascular and infection related complications; state some of each

A

Macrovascular

  • Coronary artery disease
  • Peripheral vascular disease/ischaemia causing poor healing, ulcers
  • Stroke/cerebrovascular disease
  • Hypertension
  • Renal artery stenosis

Microvascular

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease (particularly glomerulosclerosis)

Infection Related

  • UTIs
  • Pneumonia
  • Skin & soft tissue infections
  • Fungal infections e.g. oral or vaginal candidiasis

*NOTE: diabetic foot is a combination of a microvascular (in terms of blood supply to nerves) and macrovascular complications

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30
Q

Discuss what should be monitored in a pt with T1DM (and include how we monitor it and how frequently we monitor it)

A
  • Plasma glucose: HbA1c (every 3-6 months)
  • Blood pressure (each visit_
  • CKD: urinary albumin excretion (yearly)
  • Diabetic retinopathy: opthamologist (yearly)
  • Diabetic neuropathy: diabetic foot clinic (yearly)
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31
Q

Explain how diabetes can lead to :

  • Coronary artery disease
  • Infection related complications
A
  • Coronary artery disease & hypertension: chronic exposure to hyperglycaemia causes damage to endothelial cells leading to endothelial dysfunction
  • Infection related complications: hyperglycaemia causes immunosupression & also provides optimal environment for organisms to thrive
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32
Q

What is meant by diabetic neuropathy?

State and describe the 6 types of diabetic neuropathy

A

Damage to nerves caused by chronic hyperglycaemia, can cause:

  • Poly neuropathy
    • Parasthesia, loss of sensation (DCML or spinothalamic modalities), burning or shooting pains often worse at night. Bilateral & symmetrical
  • Mononeuropathy
    • ​One nerve affected. Often presents as sudden motor loss
  • Mononeuritis multiplex
    • ​​​​​More than one peripheral nerve
  • Autonomic neuropathy
    • ​Gastroparesis, incontinence, erectile dysfunction, irregular heart beats, problems with sweating
  • Diabetic amyotrophy
    • Acute, asymmetrical, focal lim pain then proximal lower limb muscle wasting. Reversbile.
  • Radiculopathy
    • ​Affects nerve roots- usually pain over spinal dermatomes
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33
Q

Discuss the management of diabetic neuropathy

A
  • Good glycaemic control
  • Regular attendance at diabetic foot clinics
  • Education
  • Pain relief e.g. gabapentin
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34
Q

What is meant by diabetic retinopathy?

A

Weakening and damage of small blood vessels in retina due to chornic hyerglycaemia. This may cause haemorrhages, exudates and even swelling of the retina.This then starves the retina of oxygen, and abnormal vessels may grow. May present with:

  • Sudden changes in vision
  • Floaters & spots
  • Double vision
  • Eye pain
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35
Q

State and describe the 4 types (stages) of diabetic retinopathy

A
  • Stage 1/Background retinopathy: developed microaneurysms on your retina. Microaneurysms are when there is a swelling of the capillaries. May leak small amount of blood.
  • Stage 2/pre-proliferative retinopathy: bleeding into retina
  • Stage 3/proliferative retinopathy: scarring has occured and new blood vessels have formed; new blood vessesl are weak and can bleed. Retinal detachment can occur
  • Diabetic maculpathy: diabetic macular oedema whereby blood vessels near to the macula leak fluid or protein onto the macula.
36
Q

Describe what you would see for each of the different types/stages of diabetic retinopathy

A
  • Background retinopathy/stage I:
    • Microaneuryseums
  • Pre-proliferative rentinopathy/stage II:
    • Cotton wool spots (soft exudates which represent retinal ischaemia)
    • Blot haemorrhages
    • Hard exudates (cholesterol exudates)
  • Proliferative retinopathy/stage III:
    • Visible new vessels
  • Diabetic maculopathy:
    • Swelling of macula
  • *NOTE: hard exudates have a more defined border/soft exudates have a more blurred border*
  • *NOTE: background & pre-proliferative can be grouped into mild, moderate and severe non-proliferative so may see differing info on what see in each.*
37
Q

Discuss the treatment for each of the types/stages of diabetic retinopathy

A
  • Background retinopathy/stage I: explain warning signs, improve glycaemic control
  • Pre-proliferative retinopathy/stage II: pan-retinal photocoagulation
  • Proliferative retinopathy/stage III: pan-retinal photocoagulation
  • Diabetic maculopathy: grid-laser therapy
38
Q

What is pan-retinal photocaogulation?

A

Use of laser to prevent new blood vessels growth, reduced size of existing blood vessels and prevent bleeding.

Exact mechanism by which PRP works is not entirely understood. One theory is that destroying the hypoxic retina decreases the production of vasoproliferative factors, such as VEGF, thus reducing the rate of neovascularization

39
Q

At what stages of diabetic retinopathy do you have visual deficits?

A

Proliferative retinopathy

40
Q

Remind yourself of the pathophysiology/5 stages of diabetic nephropathy

A
  1. Hyperfiltration & hypertrophy- increase GFR
  2. Latent stage: GBM thickening and mesangial expansion
  3. Microalbuminuria: small amount of albumin detected in urine (not detected on conventional dipstick), further increase in GBM thickening and mesangial expansion, podoyte changes
  4. Overt proteinuria: lots of albumin in urine/can detect on conventional dipstick, diffuse glomerular histopathological changes, falling GFR
  5. ESRD
41
Q

Discuss the management of diabetic nephropathy

A
  • Good glycaemic control
  • Hypertension control
  • ACE inhibitors/ARBs
  • Smoking cessation
42
Q

For an insulinoma state:

  • What it is
  • What it produces
  • C-peptide levels
  • Triad of symptoms and what the triad is called
  • Diagnosis
  • Treatment
A
  • Rare tumour of beta islet cells of pancreas
  • Causes excess insulin to be produced
  • C-peptide will be raised
  • Whipples triad:
    • Hypoglycaemia
    • Symptoms of hypoglycaemia
    • Immediate reversal of symptoms with IV glucose
  • Diagnosis is by excluding medication causes e.g. too much exogenous insulin, excess sulphonylureas
  • Treatment= resection
43
Q

What does Whipple’s triad tell you?

A

?ASK. Sources say indicates insulinoma but how? Does it not just indicate hypoglycaemia

44
Q

DKA (dibetic ketoacidosis) is a potential complication of diabetes; dicuss the pathophysiology of DKA

A
  • Cells in body have no fuel, as no insulin to allow cells to take up glcuose, and think they are starving
  • Cells initiate ketogenesis: breakdown fatty acids and ketogenic aa to form ketones which can be used as energy. Ketones can be used by brain
  • Initially kidneys produce bicarb to neutralise ketones in blood and maintain normal pH
  • Over time ketones use up bicarb and blood starts to become acidic (due to acidic ketones in body)
45
Q

State some potential causes of DKA

A
  • Undiagnosed diabetes/first presentation
  • Inadequetely treated diabetes
  • Uncompensated stress e.g. infection
46
Q

Describe the pathophysiology of DKA

A

Uncontrolled lipolysis resulting in excess free fatty acids that are converted into ketones. Lipolysis occurs because there is insufficient insulin to allow cells to use/take up glucose.

47
Q

State the triad of DKA

A
  • Hyperglycaemia (>11.1mmol/L)
  • Acidosis with high anion gap (pH <7.3, HCO3- <15mmol/L)
  • Ketonaemia (>3mmol/L or >++ on urinalysis)
48
Q

DKA usually presents within how many hours of the cause (e.g. if cause is infection)

A

Develops in <24hrs (idea that develops over short period of time)

49
Q

Describe how a pt with DKA may present

A
  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Abdo pain
  • Acetone smell to their breath (pear drops)
  • Hyperventilation/Kussmaul respiration
  • Dehydration and subsequent hypotension
  • Altered Consciousness
  • They may have symptoms of an underlying trigger (i.e. sepsis)
50
Q

Alongside the hyperglycaemia, ketonemia and acidosis, what else are you concerned about in DKA?

What are the most dangerous aspects of DKA?

A
  • Dehydration (due to polyuria)
  • Potassium (acidosis causes H+ to move into cells and K+ to move out of cells)

The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. These are what will kill the patient. Therefore the priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.

51
Q

Discuss what investigations you would do if you suspect DKA/how you diagnose DKA.

NOTE: think about your usual bedside, bloods & imaging structure. But mainly focus on mian investgations

A

Bedside

  • Urine dip (ketones >++)
  • Plasma ketones (>3mmol/L)
  • VBG: pH<7.3, HCO3- <15mmol/L, glucose >11mmol/L

Bloods

  • FBCs
  • U&Es: check potassium
  • LFTs
  • CRP: infection as cause?
  • Others e.g. amylase for pancreatitis

Imaging

  • May consider CT head if altered consciousness to rule out other causes
52
Q

Dicuss the management of DKA

*Think FIG PICK BEV

A
  • Fluid replacement
  • Insulin (fixed rate Actrapid 0.1 unit/kg/hr)
    • REMEMBER keep long acting insulin, stop short acting
  • Glucose/dextrose once plasma glucose <15mmol/L
  • Potassium replacement & monitor closely
  • Infection
  • Chart fluid balance
  • Ketones
  • Bicarbonate (RARELY NEEDED- consultant decisioin)
  • Education/prevention
  • VTE prophylaxis (dehydrated, lots of glucose, hypercoagulable state)
53
Q

Explain how potassium balances occur in DKA

A
  • Insulin usually causes K+ to move into cells, however lack of insulin means less K+ moves into cells
  • Acidosis causes K+ to move out of cells (and H+ moves into cells)
  • Pts can therefore have a high serum K+ or they can have normal serum K+ (as kidneys are excreting K+) HOWEVER their whole body K+ will be low
  • When you start pt on insulin, this causes K+ to move back into cells and you get hypokalaemia
54
Q

Remember K+ cannot be infused at a rate of more than…?

A

10mmol per hour

55
Q

Discuss some general principles for administering K+ in DKA

A

DO NOT:

  • Give in boluses
  • Give in 1st 1L of IV fluids
  • If serum K+ >5.5mmol/L

General rule is to give K+ if between 3.5-5.5mmol/L. Consult specialist if K+ <3.5mmol/L

56
Q

State example fluid regime for DKA

A

-

57
Q

Discuss what monitoring you may do for a pt with DKA

A
  • Cap glucose (hourly)
  • Cap ketones (hourly until <0.6mmol/L then every 2-4hrs)
  • VBG to monitor K+ and pH every few hours
  • Fluid balance (check hourly)
  • Neurological obs (hourly if drowsy)

*NOTE: DKA sheets clearly show what monitoring should be done and how often

58
Q

What is the DKA resolution criteria?

A

PASSMED SAYS

  • Ketones <0.6mmol/L
  • pH >7.3
  • HCO3- >15mmol/L

UHL DKA DOCUMENT SAYS

  • Ketone <0.3mmol/L
  • pH >7.3
  • HCO3- >18mmol/L

Ensure oral intake established and subcut insulin established before stopping DKA treatment.

59
Q

Ketonemia and acidosis should have resolved within ______ hrs in DKA

A

24hrs; if not needs senior review

60
Q

State some potential DKA complications

A

Can be due to DKA itself or treatment:

  • Gastric stasis
  • Thromboembolism
  • Arrhythmias secondary to hyperkalaemia or iatrogenic hypokalaemia
  • Cerebral oedema (more common in children/young adults. Most commonly occurs 4-12hrs after starting treatment)
  • Acute respiratory distress syndrome
  • AKI
  • Hypoglycaemia
61
Q

What is hyperglycaemic hyperosmolar state (HHS)?

*NOTE: HHS also non as hyperglycaemic hyperosmolar non-ketotic syndrome

A

Medical emergency in which diabetic pt has:

  • Hyperosmolar plasma (osmolality >320mOsm/Kg
  • Hyperglycaemia (glucose >30mmol/L)
  • Marked hypovolaemia
  • DOES NOT have DKA (acidosis and ketosis criteria not fulfilled)
62
Q

Discuss the pathophysiology of HHS

A
  • Undiagnosed diabetes or inadequate insulin replacement leads to chronic hyperglycaemia
  • Chronic high plasma glucose levels lead to pt urinating a lot with associated loss of potassium and sodium. Volume depletion leads to hyperviscosity
  • Over time pt becomes very dehydrated leading to hyperosmolar plasma
  • In pts with HSS there is a higher insulin secretion (compared to pts with DKA); it is thought that this insulin concentration is high enough to suppress lipolysis and ketosis (hence preventing ketonemia and acidosis) but inadequate to prevent hepatic glucose production and glucose utilisation
63
Q

State some potential causes of HHS

A
  • Undiagnosed diabetes/first presentation
  • Inadequetely treated diabetes
  • Uncompensated stress e.g. infection, MI, pancreatitis
64
Q

How long does it take for HHS to develop? Compare this to DKA

A
  • HHS develops gradually, days-wks
  • DKA develops usually in <24hrs of cause
65
Q

Describe how a pt with HHS may present

A
  • Hypovolaemia symptoms/signs
    • Thirst/polydipsia
    • Dry mouth
    • Polyuria
    • Warm skin with anhidrosis
    • Poor skin turgor
    • Hypotension
    • Tachycardia
  • Hyperviscosity symptoms/signs
    • Visual impairment
    • MI
    • Stroke
    • Peripheral arteria thrombosis
  • General
    • Altered consciousness
    • Fatigue
    • Nausea & vomiting
66
Q

Which diabetic pts does HHS affect, T1DM or T2DM?

A

T2DM as their body produces some baseline insulin which prevents acidosis and ketosis. T1DM don’t produce any insulin hence they are more likely to develop DKA.

NOTE: DKA can occur in both T1DM and T2DM, CTF said in his experience about 50:50 split

67
Q

Discuss what investigations you would do if you suspect HHS, include:

  • Bedside
  • Bloods
  • Imaging

*Where appropriate, justify why you are doing each investigation

A

Bedside

  • Urine dipstick
  • VBG: check for acidosis, glucose
  • Plasma ketones

Bloods

  • FBCs
  • U&Es: check for electrolyte imbalances
  • LFTs
  • CRP: check for infection
  • ?Amylase: check for pancreatitis as cause

Imaging

  • ?CT head for confusion/focal neurology
68
Q

Describe the criteria for HHS

A

NOTE: a precise definition doesn’t exist but the below 3 criteria can be used as general rule to help distinguish between HHS and DKA

  • Hypovolaemia
  • Marked hyperglycaemia (>30mmol/L) without significant ketonaemia or acidosis
  • Raised serum osmolarity (>320mosmol/kg)
69
Q

If you don’t have serum osmolality, how can you estimate it?

*HINT: equation

A

(2x [Na+]) + glucose + urea

70
Q

If a pt, with HHS, presents with altered mental status this correlates with severity of hyperglycaemia & serum osmolality; true or false?

A

True; altered mental status is frequently present on admission, and correlates with the severity of hyperglycaemia and serum osmolality

71
Q

Discuss the management of HHS

A
  • Give all pts fluids (slowly over 24-72hrs. Typically 0.5-1L/hr)
  • Only give insulin if ketonemia or blood glucose not falling by 5mmol/L/hr with rehydration/glucose stops falling with fluids. Keep blood glucose 10-15mmmol/L for first 24hrs.
  • Potassium replacement (as per DKA guidelines, so nil if >5.5mmol/L, 40mmol/L if 3.5-5.5, <3.5 senior review/HDU or ICU opinion. Monitor K+)
  • VTE prophylaxis (pts at high risk of VTE due to hyperviscosity)
  • Investigate for & treat cause
  • Education/prevention
  • Consider HDU/ICU

*NOTE: fluid replacement alone (without insulin) will gradually lower plasma glucose and reduce osmolality hence insulin is NOT STARTED STRAIGHT AWAY

72
Q

When treating HHS, what should the rate of fall of plasma sodium not exceed?

A

Plasma sodium should not fall >10mmol/L in 24hrs

73
Q

State some potential complications of HHS

A
  • Thrombosis (as hypovolaemia increases viscosity)
    • PE
    • MI
    • CVA
  • Neurological complications due to treatment being too aggressive/correcting osmolality too quickly
    • Seizures
    • Cerebral oedema
74
Q

Compare the mortality of DKA with mortality of HHS

A
  • DKA= <1%
  • HHS= 5-15%

IDEA THAT HHS HAS HIGHER MORTALITY

75
Q

Discuss what monitoring you would want for somone with HHS

A
  • VBG (check glucose, osmolality)- hourly
  • Capillary ketones- hourly
  • Fluid balance/urine output- hourly
  • GCS with routine obs
  • Cardaic monitoring- at least in first 12 hours
76
Q

What fluid should you use in HHS?

A
  1. 9% saline
    * *NOTE: 0.45% saline can be used but that decision can only be made by a senior*
77
Q

What is meant by pre-diabetes?

A

Blood sugars are higher than usual but not high enough to be classed as diabetes. Signifies pt at risk of diabetes and hence conservative management/lifestyle changes should be implemented

  • Oral glucose tolerance test: 7.8-11.1mmol/L
  • Fasting glucose test: 6.1- 6.9mol/L
  • HbA1c: >41 to <48mmol/L
78
Q

What is MODY, include:

  • What MODY stands for
  • What it is
A
  • Maturity onset diabetes of the young
  • Group of inherited disorders in which younger patients develop symptoms similar to those with T2DM
79
Q

What is LADA, include:

  • What LADA stands for
  • Age it generally presents
  • Is it T1DM or T2DM or neither
  • Treatment
A
  • Latent autoimmune diabetes in adults
  • 30-50yrs
  • Often seen as combintation/straddle between T1DM and T2DM. Comes on slower than T1DM but autoantibodies which are present in T1DM are present in LADA
  • There isn’t a definitive agreed method of managing LADA yet but usually start on e.g. metform then progress to insulin as necessary
80
Q

State some symptoms of diabetic foot ulcer

A
  • Pain
  • Visible ulcer
  • Foot erythema
  • Oedema of foot/ankle/calf
  • Absent pedal pulses
  • Malaise
  • Anorexia
    *
81
Q

Discuss what investigations you would consider in a pt with suspected diabetic foot ulcer, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Capillary plasma glucose
  • Wound swab & culture

Bloods

  • FBCs: WCC show infect
  • CRP: infection
  • U&Es

Imaging

  • X-ray foot: screen for osteomyelitis, foot fractures, deformities etc..
  • MRI foot: best imgaging for osteomyelitis. Will also show soft tissue better
82
Q

Discuss the management of a diabetic foot ulcer

A
  • Wound care
  • Dietary advice (pts with diabetes can be malnourished)
  • Antibiotics if infected
  • Drainge and/or debridement
  • Amputation if infection in bone
  • Education
    • Checking feet daily
    • Checking shoes daily
    • Appropriate footwear
    • Attending diabetic foot clinic
    • Good glycaemic control
83
Q

Remind yourself what metabolic syndrome is

A

“syndrome X” or “insulin resistance syndrome”, is a cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein (HDL)-cholesterol levels, elevated triglycerides, and hypertension

84
Q

What is the DVLA guidance regarding diabetes and group 2 licence/HGV?

A

Can drive with HGC/ group 2 license so long as:

  • No severe hypoglycaemic event in past 12 months
  • Driver has full hypoglycaemia awareness
  • Driver shows adequate control of diabetes by regular glucose monitoring (need to use blood glucose monitors with memory function to be able to supply 3/12 readings)
  • No other complications of diabetes that impact ability to drive

From a practical point of view patients on insulin who want to apply for a Group 2 (HGV) licence need to complete a VDIAB1I form.

85
Q

Further summary of T2DM mangaement

A
86
Q

What is the DVLA guidance regarding diabetes and group 1 drivers?

A

Other specific points for group 1 drivers:

  • If on insulin, can drive if they have:
    • Hypoglycaemic awareness
    • Not more than 1 episode of hypoglycaemia requiring the assistance of another person in preceding12 months
    • No relevant visual impairment
  • If tablets may induce hypoglycaemia (e.g. sulfonylureas) then there must not have been more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months. Don’t need to tell DVLA as long as meet requirements.
  • If on tablets or exenatide no need to notify DVLA.
  • if diet controlled alone then no requirement to inform DVLA

Yr3 Medicine- Endocrinology (9 decks)

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