Lecture ILO’s Flashcards
1
Q
Normal blood sugar
A
What is ‘normal’?
NICE says:
Adult fasting: 4 - <6mmol/L, post-prandial <7.8 mmol/L plasma glucose
HbA1c
<59 mmol/mol (7.5%) under 18 <53 mmol/mol (<7) for adults
2
Q
Diagnosis measures of type 2 diabetes
A
• Random venous plasma glucose concentration ≥ 11.1 mmol/L
• Fasting plasma blood glucose level ≥ 7.0 mmol/L
• HbA1c of 48 mmol/mol (6.5%) or more (shows previous 3 months)
Must have diabetes symptoms
3
Q
HbA1C targets
A
• Educate the person about their individual recommended HbA1c target, and encourage measures to achieve and maintain it, where possible.
• Lifestyle including diet management—48mmol/mol(6.5%).
• Lifestyle including diet combined with a single drug not associated with
hypoglycaemia (such as metformin) — 48 mmol/mol (6.5%).
• Drug treatment associated with hypoglycaemia (such as a sulfonylurea): 53
mmol/mol (7.0%).
If HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher: Support the person to aim for an HbA1c level of 53 mmol/mol (7.0%).
4
Q
Glycaemic targets
A
HbA1c
Agree a personalised target usually between 48 and 58 mmol/mol (6.5% and 7.5%)
Avoid pursuing highly intensive management to below 48mmol/mol (6.5%)
Blood glucose
Before meals 4 – 7 mmol/l
Two hours after meals lless than 8.5 mmol/l
5
Q
Monitoring of type 2 diabetes
A
• The HbA1c should be checked every 3-6 months until it is stable, then every 6 months.
• Currently it is not recommended to offer self monitoring blood glucose levels in Type 2 unless
• The person is on insulin
• Evidence of hypoglycaemia episodes
• On oral medication that may increase their risk or hypo whilst driving or operating machinery
• The person is pregnant or planning pregnancy
• Short term on corticosteroids
• Continuous Glucose monitoring
• Type 2 on multiple daily insulin injections
• Recurrent hypos
6
Q
Lifestyle advice for type 2 diabetic
A
Diet:
Carbohydrates with a low glycaemic index (fruit and vegetables).
• High fibre, low saturated fat.
Stick to appropriate meal patterns to reduce risk of hypoglycaemia.
Control alcohol intake.
Exercise and weight loss- Can help reduce cardiovascular risk.
Smoking cessation.
• Type 2 diabetes may be completely manged through lifestyle changes alone!
7
Q
What is the Desmond programme
A
• “Diabetes Education and Self Management for Ongoing and Newly Diagnosed”
• Patient education and support programme.
• Can also provide training and guidance for health care professionals.
• Type 1 equivalent = DAFNE
8
Q
What is included in the yearly screening for type 2 diabetes?
A
• Retinopathy (Starting at diagnosis)
• Diabetic foot problems (Starting at diagnosis)
• Cardiovascular risk factors (Starting at diagnosis)
• Nephropathy
Also quite common:
Peripheral vascular
Infections due to increase sugar (breeding ground for bacteria) ie uti and thrush
9
Q
Retinopathy with diabetics
A
Common symptoms - blurred vision
• Caused by microvascular occlusion, which progresses to retina ischemia.
• Most common cause of serious sight impairment in people 18-55.
• Ideally should be screened for once a year in Type 2 diabetics.
Have a proper eye test
10
Q
Kidney disease and diabetes
A
• The glomerulus is very sensitive to vascular damage, and results in albumin excretion, which is not usually excreted in the urine.
• The Urine AcR (Albumin to Creatinine ratio) is routinely done in Type 2 diabetes to monitor for kidney disease.
(Protein leaking from kidney so protein tested to see if in urine)
11
Q
What is the target blood pressure for type 2 diabetics?
A
Type 2 DM
• Blood pressure should be checked annually, and kept below 140/90.
• Or below 130/80 if evidence of nephropathy, retinopathy, or cerebrovascular damage.
12
Q
Name the types of anti-diabetic medication for type 2 diabetes
A
1st step- diet and lifestyle
Metformin
Sulfonylureas
DPP- 4 inhibitors (gliptins)
GLP- I agonist
Thiazolidinediones (glitazones)
SGLT-2 inhibitors (gliflozins)
Insulin
13
Q
Hypoglycaemia in type 2 diabetics
A
• Type 2 diabetics on sulphonylureas/insulin are at increased risk of hypoglycaemic events.
• Defined as a blood sugar level<4mmol/l.
• Symptoms:
-Headache and double vision
-Sweating
-Fatigue
-Dizziness
In severe cases can lead to coma and death
14
Q
Hyperosmolar hyperglycaemic state (HHS)
A
Type 2 diabetics
Insidious in onset – usually weeks
High blood sugars & resulting high osmolality without ketosis BG >30mmol , Osmolarity >320
Symptoms : dehydration ,weakness , leg cramps, confusion Triggered by example an infection , MI etc
15
Q
Diabetic hyperglycaemic crises
DKA vs HHS
A
Diabetic ketoacidosis:
Younger type 1 diabetes
No hyperosmolality
Volume depletion
Electrolyte disturbances
Acidosis
Hyperglycaemic hyperosmolar state (HHS)
Older, type 2 diabetes
Hyperosmality
Volume depletion
Electrolyte disturbances
No acidosis
16
Q
Diabetic foot infections
Which bacteria?
Which antibiotics?
How long for?
A
• Which bacteria?
• Commonly Gram positive : Staphylococcus & Streptococcus
• Some Gram negative : pseudomonas , E coli, Klebsiella,
• Which antibiotics?
Depends on local guidelines
• Antibiotic formulary
• Oral or IV?
• Mild / Moderate / Severe
• Higher doses due to absorption
• How long for?
• Prolonged courses 7 days +
17
Q
Difference between type 1 and type 2 diabetes
A
Type 1:
• Absolute lack of insulin
• Insulin required at all stages of treatment
• Need insulin to prevent hyperglycaemia and ketoacidosis
Type 2:
• Relative insulin lack/insensitivity
• Diet control - oral hypoglycaemic agents - insulin
18
Q
What is checked in the regular diabetes review?
A
- HbA1c, cholesterol and BP
- Diet and lifestyle
- Eye checks
- Urine tests
- Foot checks
- Sensory tests
- Blood tests – FBC, U+Es, BMs
19
Q
Types of insulin
A
Animal
Beef (Bovine) – cattle pancreas
Pork (Porcine) –pig pancreas
Human
Most commonly used
Genetically engineered using either yeast or bacteria
Analogue insulin
• Both effectively obsolete but available for patients who have been using it for a long time
20
Q
Types of acting insulin
A
• Classed according to duration of action:
Types of Insulin
– Ultra fast acting analogue insulin
– Rapid acting analogue insulin
– Short acting human soluble insulin
– Intermediate acting human insulin
– Long-acting analogue basal insulin
– Ultra long-acting analogue basal insulin
– Biphasic insulin (mixture of rapid/short and intermediate acting insulin)
21
Q
Rapid acting insulin
A
• Onset: 10 - 20 minutes
• Peak: 1-3 hours
• Duration of action: up to 5 hours
• Clear (no need to suspend)
– E.g.Novorapid (insulinaspart), Humalog (insulin lispro), Apidra (insulin glulisine)
– Inject immediately before or just after meals
– FIASP (insulin aspart)–ultrafast within 2.5mins ! – quicker but shorter action
22
Q
Short acting insulin
A
• Onset: within 30 minutes (5mins if IV)
• Peak:1.5- 3.5hours
• Duration of action: Up to 8 hours
• Clear (no need to resuspend)
E.g Actrapid, Humulin S,
• Inject 15-30 mins before meals
• Advantage that it can be given IV, IM, SC,
23
Q
Intermediate acting insulin
A
• Onset: 1.5 hours
• Peak: 4 - 12 hours
• Duration of action: up to 24 hours
• May require twice daily
• Crystals in suspension (cloudy) needs re- suspending
Humulin I, Insulatard,Insuman Basal (NPH / Isophane)
24
Q
Long acting insulin
A
• Delayed and prolonged absorption from injection site
• Onset: 0 – 2 hours
• Peak: Levemir = 5 hrs, others = no peak
• Duration of action: up to 24 hours
• Clear - no need for re-suspension
– E.g. Lantus, Abasaglar ( both insulin
glargine*), Levemir (insulin detemir) (start with this one)
– Prolonged plateau, providing a fairly stable level of insulin for most of 24 hr period, reduced hypoglycaemia
25
Ultra long acting analogue insulin
• Duration of up to 42 hours
• Use once a day with rapid acting analogue insulin
• Steady state after 2-3 days
26
Biphasic insulin
Useful for district nurses visiting patients twice daily
– E.g.Novomix30,HumalogMix25, Humalog Mix 50, Mixtard 30, Humulin M3, etc
– Mixtureof:
• Short acting insulin plus intermediate acting insulin
• Rapid acting plus intermediate acting insulin
27
Soluble pre mixed insulin
• Premixed combinations of short and intermediate acting insulin (biphasic)
• Cloudy (needsre-suspending).Crystals in suspension
• Onset: within 30minutes
• Peak:2–8hours
• Duration of action: Upto24hours
Eg humulin M3, insuman comb 15, 25, 50
28
Analogue pre mixed insulin
• Pre mixed combinations of short and intermediate acting insulin (biphasic)
• Cloudy (needs re-suspending). Crystals in suspension
• Onset:10-20minutes
• Peak:1-4hours
• Duration of action:Upto24hours
Eg Novomix 30, Humalog Mix 25, Humalog Mix 50
29
Basal boils regime for T1 diabetics
Gold standard
Short acting/rapid acting insulin at meals (bolus)
• Long acting/intermediate acting insulin at bedtime (basal)
• E.g. Novorapid 8 units TDS (three times daily) with meals and Lantus 24 units at night
30
Basal Bolus Soluble / NPH Insulin
Once daily NPH with short acting soluble insulin cover for each main meal (onset, peak & duration as described previously)
Examples of basal bolus soluble / NPH combinations
Insulatard once daily NPH with Humulin S short acting insulin
Humulin I once daily NPH with Actrapid short acting insulin
31
Basal Bolus Analogue Insulins
• Once daily basal analogue with rapid acting analogue cover for each main meal (onset, peak and duration as described previously)
• Examples of basal bolus analogue combinations:
– Lantus, Abasagalar, Toujeo, Degludec or Levemir once daily basal analogue with Novorapid, Humalog or Apidra rapid acting analogue
32
Twice daily insulin
• Use biphasic e.g. Novomix 30, Mixtard 30, Humalog Mix 25
• Twice a day pre-breakfast and pre-evening meal
33
Carbohydrate counting for type 1 diabetics
• determining the dose of insulin from the amount of carbohydrate the patient is about to eat
• A long-acting insulin is given once a day
• Rapid acting insulin is given at meal times; the dose will vary depending on how carbohydrate will be consumed
• Should only be used in patients specifically trained to use such regimens
• Examples include:
DAFNE Dose Adjustment For Normal Eating.
• Either count in grams or as carb portions
• Identify your insulin-to-carbohydrate ratio
• Combining allows you to work out the number of units bolus need for the meal
• E.g. 70g carb meal, ration is 1:10 insulin to carb, you need 7 units of insulin
34
Starting doses of insulin for type 1 diabetics
Starting doses
An initial total daily dose of insulin in adults can be 0.2 to 0.4 units/kg/day.
• In children an initial daily dose will be 0.5 to 1.0 units/kg/day, and
• during puberty the requirements may increase to as much as 1.5 units/kg/day.
One half of the total dose is given as basal insulin and one half as bolus dosing
The simplest approach to covering mealtime insulin requirements is to suggest a range of doses, such as 4 units for a small meal, 6 units for a medium-sized meal, and 8 units for a larger meal.
For greater flexibility of carbohydrate content of meals can be calculated one unit of mealtime insulin for every 15 g of carbohydrate in the meal.
Using a food diary and 2-hour postprandial blood glucose measurements, the insulin-to- carbohydrate ratio can be adjusted.
35
Finding out a patients insulin dose
Finding out a patients insulin dose
• The most reliable source is the patient,so always ask them first
• If they are not able to tell you or don’t administer their insulin, ask the person who does (nursing home, family member, district nurses)
• District nurses notes on EMIS
• Community DSN notes via hospital DSNs
• Recent discharges/transfers/repats/clinicletters
• If all else fails, and you have no idea what dose a patient is on, prescribe a variable insulin after finding out blood sugar
36
Insulin devices
Vial and injection
Pre filled pen
Cartridges and re usable pen
Continuous subcutaneous insulin infusion (insulin pump)
37
Lypohypertrophies
Fatty lumps due to repeated insulin injections
Caused by bad technique
• Unsightly
• Painful
• Unpredictable insulin absorption
• To reduce risk:
• Rotate between sites
• Rotate within sites
• New needle for each injection
• Avoid injecting into lumps
38
Glycaemic targets for children and adults
• It is important that the blood glucose levels being aimed for are as near normal as possible. However, individual target levels must be agreed between the person and their diabetes team
• Children with Type 1 diabetes (NICE)
– On waking and before meals: 4-7mmol/l
– After meals: 5-9mmol/l
• Adults with Type 1 diabetes (NICE)
– On waking: 5-7mmol/l
– Before meals at other times of day: 4–7mmol/l
– 90 minutes after meals: 5-9mmol/l
39
Blood glucose monitoring targets
Monitor at least four times a day, including before each meal and before bed
Optimal targets are:
• - Fasting level of 5–7 mmol/L on waking
• - Level of 4–7 mmol/L before meals at other times of the day
For adults who choose to test after meals, level of 5–9 mmol/L at least 90 minutes after eating
• - Level of at least 5 mmol/L when driving
40
Continuous/flash glucose monitoring
(Pump in arm)
•all adults with type 1 diabetes should have access to either Flash or CGM
•all children with type 1 diabetes should have access to CGM and that
•some people with type 2 diabetes who use insulin intensive therapy (2 or more injections a day) should have access to Flash, for example if they experience recurrent or severe hypos, if they have a disability that means they cannot finger-prick test or if they would otherwise be advised to test 8 or more times a day.
41
What is hypoglycaemia?
Who is at risk?
Common causes
Symptoms
What is hypoglycaemia (a hypo)?
This occurs when the amount of glucose in the blood is below 4mmol/l.
Who is at risk?
People who treat their diabetes with insulin, sulphonylureas or prandial glucose regulators. (repaglinide , nateglinide)
Those who treat their diabetes with diet or metformin alone are generally not at risk
Common causes:
• Taking too much diabetes medication
• Delaying or missing a meal/snack
• Not eating enough carbohydrates
• Taking part in unplanned or strenuous physical activity
• Drinking too much alcohol or drinking alcohol without food
• Sometimes there are no obvious causes
Symptoms
Dizziness, sweating, blurred vision, looking pale, disorientation, tremor, hunger, Tingling of lips, fast pulse, confusion, irrational behavior, unconsciousness
42
Treatment for a mild hypo
15-20g of fast acting glucose
Eg 4-5 gluco tabs
Or if conscious and able to swallow 1x 60 ml bottle of gluco juice
43
Treatment of a severe hypo
Airway
Breathing
Circulation
Disability
Exposure
If patient is unconscious stop insulin infusion immediately if in situ
Administer at least 150mls of IV glucose
Or
Administer intramuscular injection of glucagon 1mg
Once patient is conscious administer 1 x 60ml bottle of gluco juice
44
Hyperglycaemia symptoms
Diabetic symptoms
Dry mouth
Increased thirst
Blurred vision
Weakness
Headache
Polyuria
45
Initial DKA management
Diagnose:
• CBG >11mmol/l OR known to have diabetes
• pH <7.3 and/or bicarbonate <15mmols Diagnose
• Ketones >3mmol/l
Fluids:
• Fluid resuscitate
• Restore volume
• Replace K+ (monitor K+)
Insulin:
• Fixed Rate Insulin Infusion (FRII) 0.1 units insulin per kg per hour
Monitor:
• Hourly monitoring • Senior review
46
Treating DKA (FIG PICK)
Follow local protocols carefully.
•F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
•I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
•G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a
certain level (e.g. 14 mmol/l)
•P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
•I – Infection – Treat underlying triggers such as infection
•C – Chart fluid balance
•K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is
unavailable)
Establish the patient on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.
Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.
47
DKA diagnosis requirements:
Capillary blood glucose > 11 mol/L
Capillary ketones > 3 mol/L and
Venous pH <7.3 and/or bicarbonate <15 mol/L
48
Managing diabetes when unwell
When a person with diabetes is unwell they should be encouraged to:
• Continue taking their diabetes medication.
• If they're unable to take solid food and are at risk of hypos, sipping sugary or milky drinks or sucking boiled sweets or glucose tablets will help prevent hypos.
• Aim to drink plenty of sugar-free fluids.
• Continue blood glucose testing, and if it rises above 15mmol/l, those
with Type 1 diabetes should test for ketones.
• Increase their medication if their blood glucose level rises above 13mmol/l (people need to be educated on how to manage this).
• Contact their healthcare team if their blood glucose levels remain high or they are unable to keep food down.
Sugar - check your blood glucose level every 2 to 3 hours
Insulin - always continue to take your insulin even when you are sick to avoid DKA
Carbs - make sure you take enough carbs and drink enough fluids
Ketones - check your blood or urine ketones every 4 hours, take rapid acting insulin if ketones are present and drink plenty of water to flush them out of your system.
49
• Lucy is 19 years old and has type 1 diabetes. She presents to your surgery with erratic blood glucose readings varying between 3.1 mmol/l and 25.6 mmol/l. Her body mass index is 18.2 kg/m2. She uses a multiple injection regimen with 8 mm needles.
Which one of the following may help to improve her erratic blood sugar control?
• 1. Change to a shorter needle for injecting insulin (correct)
• 2. Encourage her to use the same injection site in a place where you know the insulin will be absorbed quickly (eg the abdomen)
• Change to a longer needle for injecting insulin
50
You see a 19 year old woman during a home visit. She has had type 1 diabetes for three years and is being treated with premixed 30/70 insulin twice daily.
She has not attended a diabetes clinic since her initial diagnosis.
She has had diarrhoea and vomiting for the last three days
She has not been able to tolerate food or fluid for the last 48 hours, and has not been taking her insulin for that time because she was worried about hypoglycaemia.
She is drowsy (Glasgow coma scale 14/15) and appears dehydrated.
Her pulse is 110 bpm and her blood pressure is 85/50 mm Hg. Her respiratory rate is 30 breaths per minute.
Her abdomen is soft and there is some epigastric tenderness. You can’t find any other physical abnormalities.
Diabetic ketoacidosis
51
BP targets for diabetics
Diabetes
• Type 2 DM SIGN : 130/80 or ABPM 125/85 NICE 140/90 if end organ damage 130/80
• Type 1 DM / Renal disease Depends on Albumin / CR
<70 : 140/90
>70 : 130/80
52
• You see an adult patient with known diabetes who is sweating and shaking slightly. You believe these are symptoms of hypoglycaemia. They are conscious and cooperative.
What is the first step in the management of these symptoms?
1. Give 15 g to 20 g of quick acting carbohydrate
53
A 29-year-old woman is referred to a diabetic clinic for poor diabetes management. Recently, the patient has been suffering fluctuations in her plasma glucose levels and her previously well-controlled glycated haemoglobin has risen to 8.1%. The patient admits she has recently been avoiding using her injections. On examination, the patient has a raised, smooth lump that is firm on palpation at the lower abdomen. The most likely diagnosis is:
Lypohypertrophy
54
A 29-year-old woman is found unconscious by her partner and rushed to accident and emergency. She is a type 1 diabetic and has maintained excellent glucose control using insulin injections. Blood biochemistry results demonstrate a moderately raised level of insulin, and very low blood glucose. Her partner mentions she is a lawyer and has been working particularly hard in the last week, eating quick meals and occasionally missing meals. The most likely diagnosis is:
• Hypoglycaemic coma
Answer
The history indicates that the patient has been missing meals but adheres to her insulin regime. The patient has therefore not eaten sufficiently to maintain an adequate glucose level despite taking a recommended dose of insulin.
55
According to diabetes UK, what is the peak age for the diagnosis of type 1 diabetes?
10-14
56
Management of diabetic nephropathy
Management of Nephropathy
• ACE-I/A2RB should be started ideally (even without HTN)
• Control BP
• ACE-i/A2RB
• Optimise glycaemic control
• Reduce dietary protein intake to <0.7-1.0g/kg/day
• Manage other RFs
• Referral to nephrologist when eGFR<45 or Creatinine >150; increasing proteinuria without retinopathy (could be a sign of other cause), uncontrolled HTN, rapid decline in GFR, unexplained anaemia and abnormal bone function
• CKD management
57
• 40 year old Type 1 Diabetic
• Developed age 16
• Numbness and burning pain in both feet
• Sometimes wakes her up at night
• OE- Reduced sensation in both feet up to ankle
• What is the diagnosis?
Distal symmetrical neuropathy
58
Classification of diabetic neuropathy
Acute reversible:
Hyperglycaemic neuropathy
Persistent:
Symmetrical
Distal symmetrical neuropathy
(Peripheral neuropathy)
Acute painful neuropathy
Focal and multi focal
Pressure palsies
Carpal tunnel syndrome (median nerve)
Ulnar nerve compressions at the elbow
Mononeuropathies:
Diabetic amyotrophy (femoral nerve)
Autonomic
59
Diabetic neuropathy types
Distal Symmetrical Polyneuropathy:
•Axon tips of long nerves, therefore glove and stocking distribution
•Joint position and vibration sense 1st
•Numbness, pain (burning), altered sensation, neuropathic ulcers, joint abnormality
Mononeuropathy:
•Pressure palsies- carpal tunnel syndrome, ulnar nerve palsy etc.
•Other neuropathy e.g. cranial nerves
• Mononeuritis multiplex= multiple individual nerves
•Radiculopathy e.g. femoral amyotrophy
Autonomic Neuropathy:
•Postural hypotension
•Neuropathic bladder, erectile dysfunction (men), sexual dysfunction (female)
• Gastroparesis, gustatory sweats, diarrhoea
60
Diabetic neuropathy management
Diabetic Neuropathy Management
• Avoid touching limb (protective films)
• Duloxetine, Amitriptyline, Pregabalin- NICE says no one drug is
• Duloxetine was 1st line, then switch to Amitriptyline (if duloxetine not helpful) + add Pregabalin (if further control needed)
• Basic analgesia- Paracetamol, Opiates
• Improve glycaemic control
• Mononeuropathies may be self limiting
• Various treatment depending on site
• E.g. carpal tunnel syndrome: steroids, splint etc.
• Peripheral neuropathy= good foot care
61
30 year old type 1 diabetic presents with numbness and tingling in outer 3 and a 1⁄2 fingers. Wakes her at night time
What type of diabetic neuropathy is this?
Mononeuropathy
62
50 year old type 2 diabetic develops new onset double vision when looks to the right. You notice then when eyes look towards the right, the right eye does not fully abduct
Which diabetic neuropathy is this?
Mononeuropathy
63
69 year old with type 1 diabetes develops a foot ulcer. On examination there is reduced sensation up to the ankle in both legs and the ankle reflex is absent
Which diabetic neuropathy is this?
Polyneuropathy- distal symmetrical polyneuropathy
64
How is a diabetic foot examined?
• Inspection- ulcer, ischaemia, amputation, necrosis, clawing, Charcots, temperature, CRT etc.
• Sensation- Monofilament
• Vibration sense
• Reflexes
• Pedal pulses
65
Management of diabetic foot disease
PREVENTION!
• Annual foot screening- foot pulses, sensation (10g monofilaments), inspect for abnormalities, foot pulses
• EDUCATION!
• Wash feet daily
• Check feet regular
• Regular chiropody involvement
• Well fitting shoes; don’t walk barefoot
Foot Ulcer
• Relieve pressure (rest, total contact casting)
• Treat infection (r/o osteomyelitis)
• Severe involvement: surgical debridement/amputation
66
Macro vascular disease diabetic complication examples
• Cerebrovascular disease, peripheral vascular disease and coronary artery disease
• Cardiovascular disease accounting for 60-75% of all deaths in diabetics
• Enhanced atherosclerosis
• Endothelial Dysfunction
• Less vasodilatation
• Enhanced haemostasis
67
Management of macro vascular disease
Management of Macrovascular Disease –
Control Risk Factors
Hyperlipidaemia
Hypertension- aim <130/80
Stop smoking
Treat obesity
Healthy diet
Optimise glycaemic control
68
Diabetic annual review
Education & Self Management
Diabetic Annual Review
• How are they coping
• Diet (appropriate for diabetes)
• Do they need further education about self-management: DAFNE, DESMOND, dietetics, exercise/activity programmes
• Smoker- smoking cessation advice
Treatment
•What they take
•Are they coping well with this regimen
•Are they compliant
•Side effects
Monitoring
•How often and when do they monitor •Review BM diary
Pregnancy and Pre-pregnancy
•Are they pregnant or planning to have children (are they aware of advice re: pregnancy and diabetes)
Complications
• Hypo episodes- how often, signs/symptoms
• Hospital admissions: how often, what for (DKA, HHS, hypo), severity
• CVS: MI, CVA, PVD
• Neuro: peripheral neuropathy
• Feet disease- have they seen podiatrist
• Eyes disease- have they had annual screening
• Kidney disease
• Erectile dysfunction
• Mood
• Other general illnesses
69
Diabetic annual review examination and investigations
Examination:
•Weight, height, BMI
•Urinanalysis: ketones, protein
•Inspect injection sites
•CVS: BP, heart sounds, peripheral pulses, bruits
•Eyes: Cataracts, eye movements, acuity, inspect retina (should be done as part of annual
screening)
•Neuropathy: Foot examination
Investigations:
•HbA1c
•BM measurements
•Lipid profile
•Kidneys: eGFR and urine albumin:creatinine ratio
70
Diabetic ketoacidosis pathophysiology
Lack of insulin:
• Hyperglycaemia -> osmotic diuresis and electrolyte loss
• Lipolysis (insulin inhibits hormone-sensitive lipase)
• Free-fatty acids are oxidised to ketone bodies
• Ketone bodies are acids, cause nausea
• N+V -> further dehydration and K loss
• Acidosis + insulin deficiency -> Hyperkalaemia
71
Signs and symptoms and triggers of diabetic ketoacidosis
Signs and Symptoms
•Hyperosmolar: thirst, polyuria and polydipsia
•Blurred vision
•Abdominal pain
•N+V
•Sweet, ketone smell to breath
•Kussmaul breathing
•Confusion and lethargy
Triggers
•Infection
•Omitting insulin/not taking to much
•NEVER STOP INSULIN
•Stressful injury: Trauma, surgery, MI •Binge drinking
72
Diabetic ketoacidosis management
FLUIDS = first line treatment
• Management
• IV fluid hydration (1hr-2-2-4-4-6)
• Replace Potassium if low/give with Sliding scale or treat is significant hyperkalaemia • Fixed rate insulin (0.1units/kg/hr)- start IV 10% Glucose when BM<14mmol/L
• Keep giving long acting insulin whilst on IV insulin
• Hourly ketones (if possible) and BMs
• Monitor urine output
• If fails to improve increase rate of sliding scale; IV Bicarbonate if persistent acidosis
(pH<7.0)
• Complications
• Cerebral oedema (higher risk if child)
• VTE
• Aspiration of vomitus (especially if GCS low)
73
78 year old man with Type 2 Diabetes.
He is insulin dependent and takes: Metformin,
Sitagliptin and Humilin I- 40units, bd.
Also suffers from hypertension, LVSD, had a stroke and has residual right sided weakness.
Has been unwell over the past week with a chest infection and progressively become confused and drowsy over the past 24 days, with reduced urine output and poor oral intake. He has no had any of his diabetic medications in the past 24 hours and not been given his Humulin
Clinically he is dehydrated, BM= 21.5mmol/L; BP= 85/50, capillary ketones= 1.6mmol/L
What is the likely diagnosis?
Hyperosomolar hyperglyaemic state
74
Hyperosomolar hyperglyaemic state
• Previously known as HONK (hyperosmolar non-ketotic state)
• Consequence of hyperosmolar effects of hyperglycaemia
• More common in type 2 diabetics and elderly
• Hyperglycaemia, dehydration and uraemia without significant ketosis or acidosis
• Causes: Infection, MI, diuretics, steroids, omission of anti-diabetic medications
• Management: Similar to DKA (variable rate insulin)
75
A 46-year-old woman develops and infected foot ulcer after dancing at a wedding. She has had diabetes for 7 years and is being treated with Metformin-500mg, TDS; Gliclazide- 90mg, bd. Her HbA1c is 75mmol/mol
How would you manage the foot ulcer?
What are the complications?
Take a foot swap
Keep elevated
Don’t walk around bare foot
Keep clean
Give fluloxcyclin
Osteomyelitis
Necrosis
Septic
76
• A 30 year old man with type 1 diabetes presents with lethargy, weakness and confusion. He is acidotic, ketotic and has raised BMs. He has been unwell with a productive cough and has reduced a/e at the R.base
• BP= 100/80, P= 110, RR= 24, SATs= 96% (RA), T= 38.9 degrees C
• Which is the most important treatment to start first?
What is a likely diagnosis?
A. 1L N.Saline over one hour
DKA caused by infection, likely right basal pneumonia
77
• A 67 year old man with type 2 diabetes for 12 months is treated with Gliclazide-160mg,bd; Pioglitazone- 30mg, od as he was intolerant of Metformin.
• He had an MI 2 years ago.
• Recent tests show evidence of micro albuminuria.
• Retinal screening showed a few areas of hard exudate with 3 small dots and blots.
• He has normal foot sensation and normal pulses I’m his feet
• How should this patient be managed?
• Weight=120kg;Height=1.73m
• BP=150/100
• SerumChol=5.1mmolL;HDL=0.7mmol’L;TG=2.0mmol/L
• HbA1c=69mmol/mol
Aspirin for MI
• Recent tests show evidence of micro albuminuria. Therefore could be diabetic nephropathy so do kidney function test
Retinal screening showed a few areas of hard exudate with 3 small dots and blots. Suggests background retinopathy so refer 1-3 months
Control blood pressure with ACE/ARB
Statins for cholesterol
Improve glycaemic control
Lifestyle changes to improve BMI
78
A 14 year old girl presents with 2 weeks of general malaise and thirst. Over the past 24 hours she has had a low grade temperature, is vomiting and has central abdominal pain
• BP= 100/75, P= 130, RR= 30, SATs= 99% (RA), T= 37.3degreesC, Blood sugar is 28.1mmol/L
• What would you expect her arterial blood gas to show
A. pH= 7.53, pO2= 14.5kPa; pCO2= 2.4kPa; Bicarb= 24mmol/L
B. pH= 7.39, pO2= 11.9kPa; pCO2= 3.1kPa; Bicarb= 20mmol/L
C. pH= 7.27, pO2= 9.6kPa; pCO2= 8.1kPa; Bicarb= 27mmol/L
D. pH= 7.16, pO2= 14.5kPa; pCO2= 2.1kPa; Bicarb= 11mmol/L
E. pH= 7.57, pO2= 12.0kPa; pCO2= 4.9kPa; Bicarb= 37mmol/L
D (DKA)
79
A 65 year old type 2 diabetic is complaining of intermittent episodes of nausea with dizziness and sweating almost every other day in the morning. He started Gliclazide 2 weeks ago for his diabetes
What is the most likely cause of his symptoms?
Hypoglycaemia
Side effect of medication
80
What would you expect to see if the thyroid wasn’t responding to TSH?
High TSH but low T3 and T4
81
What would you expect to see if the thyroid was overactive?
Low TSH
High T3 and T4
82
What would you expect to see in hypothalamic/ pituitary dysfunction?
Low TSH and low T3 and T4
83
Common presentation of excess thyroid hormones
Eg hyperthyroidism, thyrotoxicosis, Graves’ disease
• Heat intolerance (moist/warm skin)
• Anxiety
• Tremor
• Weight loss (despite increased appetite)
• Tachycardia >90 BPM (reporting palpitations)
• Eyelid retraction, eyelid lag
84
What are common presentations of lack of thyroid hormones:
Hypothyroidism
• Cold intolerance
• Cool, dry & coarse skin
• Fatigue and depression
• Constipation
• Low pitched voice
• Muscle weakness
85
Mrs Edna Wilson presented complaining of feeling unusually tired. She initially put it down to age but has noticed that she is also more constipated recently and had gained weight over the last year.
• You note:
• Bradycardia (62 bpm)
• ‘puffy face’
• BP 128/88
• Dry, cracking skin
• Hoarseness of voice
• Periorbital oedema
• No palpable thyroid
What is the diagnosis and treatment?
Hypothyroidism
• Treatment: Levothyroxine (synthetic T4)
• Start at 1.6 μg/kg (od)
• Or 25 μg daily in older adults of
CHF
• Titrate dose as required (monitor TH profile using TFT results)
86
What are the hormones and what are their roles which are produced in the hypothalamus/ pituitary gland?
■ Anti-diuretic hormone (ADH) - stimulates kidneys to increase water absorption into the blood
■ Oxytocin - "bonding hormone" - involved in breast milk production, orgasm, the ability to trust, social bonding, body temp regulation and sleep cycles
■ Thyrotropin releasing hormone (TRH) - triggers release of TSH which then triggers thyroid gland
■ Prolactin inhibiting hormone and prolactin releasing hormone – stimulates anterior pituitary to do something with prolactin (breast milk production)
■ Corticotropin releasing hormone (CRH) - stimuilates anterior pituitary to furthermore stimulate adrenal glands and corticosteroids
■ Gonadotropin releasing hormone (GnRH) - stimulates anterior pituitary to release FSH and LH for normal function of sex glands
■ Growth hormone releasing/inhibiting hormone – prompts AP to release or inhibit growth hormone
87
What is Acromegaly?
■ Acromegaly is the result of too much growth hormone
■ Rare – approx 3-4 people in every million
Most often caused by a benign pituitary tumour, but can in rare cases be caused by a non-endocrine tumour secreting GH
Further divided into micro and macroadenomas (macros most common)
■ Acro – extremities, mega – large
■ Some genetic link
88
Acromegaly signs and symptoms
Onset often slow and insiduous, most often diagnosed in middle age. Men and women are equally affected.
Growth of hands and feet
Change in facial features – widening bridge of nose, thick lips, protruding jaw and brow, macroglossia, teeth seperation
Headaches and visual disturbance due to tumour
Deeper voice
Skin tags, excessive sweating.
Mild hirsuitism in women.
Joint pain and carpal tunnel syndrome.
Hypertension and diabetes
Organomegaly (liver/spleen/goitre)
89
Investigations and treatment for acromegaly
Investigations:
■ Routine bloods – glucose, lipids, bone profile (may all be raised)
■ IGF-1 excludes acromegaly if normal
■ OGTT to confirm raised IGF-1
■ Check thryoid, prolactin, gonadal and adrenal hormones
■ MRI scan to assess for tumour
■ CT if non-endocrine tumour suspected
■ Cardiac work up: ECG and echo
■ Thyroid ultrasound (inc risk of Ca)
Treatment:
Nothing is 100% so normally a combination
Endoscopic trans-sphnoidal surgery first line
Radiotherapy as adjuvant
Somatostatin analogues first line drug treatment (ie octreotide)
Dopamine agonists such as bromocriptine sometimes used
90
Prolactinoma
Benign brain tumour
■ Classified as microprolactinoma (<1cm), macroprolactinoma (1-4cm) and giant. Rarely malignant.
■ Usual presentation is of raised prolactin (but caution – raised in lots of other states!)
■Women commonly present with irregular or absent menstruation, galactorrhoea, reduced libido and hirsutism
■ Men are more subtle – erectile dysfunction, galctorrhoea, reduced beard growth, reduced libido. Often present late with osteoporosis.
Can also get effects of tumour – headache, visual disturbance etc espically if large
Treatment is usually medical with cabergoline (dopmaine agonist). Can cause issues with impulse control and sleepiness.
If patient becomes pregnant, must be under specialist team
Prevent osteoporosis as around 30% lose bone density
91
Which disease is a result from too much cortisol production?
Cushing syndrome
92
What is cortisol stimulated by and what does cortisol cause?
• Cortisol-
– Stimulated by: stress, hypoglycaemia,
– Causes: Insulin resistance, central adiposity, raised cholesterol (high TG and low HDL), muscle catabolism, reduced bone density, Sodium retention and potassium loss (affinity for minnerocorticoid receptor), HTN (various mechanisms including increased sensitivity to caetacholamines), emotional changes, growth (important for growth but too much inhbits growth), anti-inflammatory effects
93
What is LH an FSH stimulated by and what does it regulate?
LH + FSH-
– Secretion stimulated by GnRH
– Secretion inhibited by Prolactin
– Regulate testosterone (males), oestrogen and progesterone (females) synthesis
– Libido, erectile/sexual function, secondary sexual characteristics (breast and penile development, hairs, testicular size and muscle mass in males)
94
What is anti diuretic hormone stimulated by and what is its effect?
Anti-diuretic Hormone aka ADH (Vasopressin)-
– Stimulated by, hyperosmolality, reduced perfusion of
hypothalamus (e.g. from low BP), angiotensin II – Effect- Increases aquaporin 2 at collecting
tubulesàenhanced H20 re-absorption (ie. anti-diuresis)
95
Role of oxytocin
Oxytocin-
– Uterine contractions during childbirth – Bonding
– Mild ejection
96
Prolactin
Prolactin-
– Dopamine inhibits secretion
– Suckling, sleep and stress (and TRH) stimulates secretion
– Lactation- following childbirth
– Prolactin inhibits LH and FSH secretion (hence ammenorrhoea and other symptoms associated with low FSH and LH levels)
97
55 year old man. 3 months of weight gain, generalized weakness and fatigue.
Difficulty getting up from sitting position without using arms
Reduced libido
BP= 153/83
• Na= 143mmol/L (135-145) • K= 3.6mmol/L (3.5-5.0)
• Urea= 5.6mmol/L (3.5-6.7) • Creatinine= 95 (60-100)
• Glucose= 11.3mmol/L
• pH= 7.52
• pO2= 12.1kPa (11-13)
• pCO2= 4.8kPa (4.5-6.0)
• HCO3= 37mmol/L (22-28)
• BE= +7.3 (0+/- 2)
Describe symptoms, results and suspected diagnosis?
Weakness around hip/shoulders/central muscles = proximal myopathy
Metabolic alkalosis (due to excess aldosterone causing a reduction in H+)
High BP
High glucose (insulin resistance from excess cortisol)
CUSHINGS SYNDROME:
Appearance is likely to be-
Rounded face
Stretch marks
Central adiposity
Thin legs and arms
Flushing of cheeks
98
Symptoms of Cushing’s syndrome
Upper body obesity with thin arms and legs
Dorsal fat pad (Bufallo hump)
Flushed and round face
Hirutism in women
Primal myopathy
Bruising/ thin skin
High blood pressure
High blood glucose
Acne
Water retention
Mentrual irregularities
99
Cushing’s syndrome causes:
Ectopic ACTH
Adrenal adenoma
Cushing disease
Latrogenic (ie long term steroids)
100
56 year old man with Cushing’s Syndrome undergoes bilateral adrenelectomy.
• Over the next few weeks develops headache and skin changes.
Why does he have an adrenelectomy, explain the symptoms and what is the suspected diagnosis?
Cushing syndrome causes adrenal hyperplasia therefore needs removal of the adrenal glands
Headache is caused by pituitary gland increasing in size
Diagnosis = Nelson’s Syndrome (rapid increase in ACTH following removal of adrenals due to lack of –ve feedback)
101
Acromegaly complications
- Bitemporal heminopia (and other CN palsy)
- CVS- Hypertension, cardiomyopathy
- Peripheral neuropathy
- Impaired glucose tolerance
- Colo-rectal Cancer
- OA
102
What is acromegaly?
Symptoms
Investigations
Management
• Excess GH from pituitary tumour
• Symptoms:
– Pressure symptoms and GH excess
– Ammenorhoea, reduced libido, headache, sweating, snoring, arthritis, shoes and rings don’t fit, curly hair, wait gain (excess muscle mass), physical features change
• Investigations:
– GH and IGF-1 levels
– Oral Glucose Tolerance Test
– MRI pituitary
– Other pituitary hormones (pressure effectàhypopituitism of other hormones)
• Management:
– Control complications
– Trans-sphenoidal hypophysectomy (first line)
– 2nd line: Somatostain analogues (Octreotide); radiotherapy, GH antagonists
103
What is Addisons disease and what are common causes?
Adrenal insufficiency
Causes:
• Addison’s Disease (autoimmune, TB, HIV, metastasis, lymphoma, haemorrhage)
• Other causes: chronic steroid use, pituitary disease (ACTH def.)
104
Investigations for Addisons disease
Investigations:
• Hyponatraemia and hyperkalaemia
• Hypoglycaemia
• Short SynACTHen Test (gold standard test for diagnosing adrenal insufficiency)
• ACTH level, renin-aldosterone levels
• 21 Hydroxylase Adrenal Autoantibodies
105
Management of Addisons disease
Management
• Hydrocortisone (STAT IV in crisis), oral (glucocorticoid)
• Fludrocortisone (mineralcorticoid)
106
A 45 year old woman with Addisons disease goes to the GP surgery because of a sore throat, fever Ned feeling run down over the ast 24 hours. She is taking regular hydrocortisone and flurocortisone.
T=37.8 degrees, inflamed pharynx on examination.
What should you recommend about how she commences taking her hydrocortisone?
Should double the one during the illness
107
Causes of secondary hypertension
Cushing syndrome
Acromegaly
Conns syndrome
Pheochromocytoma
Hyperthyroidism
Carcinoid syndrome
Chronic kidney disease
Renal artery stenosis
Coarctation of aorta
Aortic dissection
Aortic stenosis
Renin secreting tumour
Iatrogenic- steroids, adrenaline, COCP
Anxiety
White coat HTN
Pregnancy
108
What is prolactinoma?
Symptoms, investigations and management.
Prolactinoma
• Prolactin secreting pituitary adenoma
• Causes symptoms of:
– Pressure effect (headache, bitemporal heminopia, cranial nerve
palsy etc.)
– Hyperprolactinaemia:
• Galactorrhoea,Amenorrhoea,erectiledysfunction
• Inhibits gonadotropin release (infertility,hypogonadism,osteoporosis)
• Investigations:
– Prolactin Levels= significantly raised – MRI Pituitary
• Management
– Dopamine agonists e.g. Bromocriptine or Cabergoline – Surgery
109
What is hypopituitarism and what are some causes?
Hypopituitism
• Reduced production of anterior pituitary hormones:
– GH -> Gonadotropins ->FSH ->LH ->PRL ->TSH -> ACTH
• Panphypopituitism= Reduction in all anterior pituitary hormones
• Causes (disease of hypothalmus-stalk and pituitary)
– Irradiation, Surgery, pituitary tumour, ischaemia or bleed, infiltration (amyloidosis, haemochromatosis), infections (TB, meningitis)
– Specific Causes:
• Kallman’ Syndrome
• Craniopharyngioma
• Apoplexy (pituitary haemorrhage or infarct)
• Sheehan’s Syndrome (apoplexy due to ischaemia from maternal haemorrhage)
110
Investigations of hypopituitarism
• Investigations
– Reduced LH, FSH, Testosterone, Oestrogen, TSH, T4+T3, Prolactin (may be raised due to loss of
–ve feedback from Dopamine), IGF-1+Cortisol
– Insulin Tolerance Test
– Short SynACTHen Test
– MRI of hypothalamic-pit
111
Signs and symtoms of hypopituitarism
Specific to the reduced pituitary hormone:
– GH Lack- Central obesity, atherosclerosis, dry skin, weakness, osteoporosis, hypoglycaemia
– LH and FSH- Oligo-/ammenorhoea, reduced libido, infertility, breast atrophy and painful intercourse (females), males= reduced hair, small testes, erectile dysfunction
– Prolactin- Lack of lactation
– Thyroid- Hypothyroid symptoms
– Cortisol- Adrenal Insufficiency Symptoms WITHOUT pigmentation
112
Hypopituitarism treatment:
Hypopituitism
• Treatment
– Treat underlying cause
– Replace deficient hormones:
• Hydrocortisone (most important to give)
• Levothyroxine
• Sex Hormones- Testosterone, Oestrogen
• Growth Hormone (Somatropin)
113
• 46 year old man presents with 3 months of fatigue, weight loss and has a car accident
• Past 4 weeks had a headache, worse when lying down and relieved when sitting up.
• Had a car crash because failed to see a driver coming around the corner
• Worried because of the fatigue, has difficulty with erections and has lost weight around arms and legs.
• On examination BP= 100/67, P= 55bpm, his skin is very dry and hair is very thin
• Prolactin= 3,719mU/L (<400)
Random cortisol = 791
What is the most likely diagnosis
Prolactinoma
Not Addisons disease as cortisol needs to be less than 400
114
Pituitary tumours:
Signs and symptoms
Management
Pituitary Tumours
• Most are non-secreting adenomas (cause symptoms by their pressure effects)
– Microadenoma <1cm – Macroadenoma >1cm
• Secreting tumours are usually: PRL, GH, ACTH (cushings disease)
• Signs and Symptoms:
– Headaches, Bitemporal heminopia, cranial nerve palsy
– Symptoms of hormone secretion (secreting adenoma)
– Features of hypopituitism (PRL can go up as compression of pituitary stalk prevent Dopamine stimulating anterior pituitary)
– Symptoms of hormone secreting (if secreting a hormone)
• Management:
– Hormone replacement
– Trans-phenoidal pituitary surgery (goes through nose to remove tumour)
– Radiotherapy
– Specific therapies
115
• 40 year old, headache
• BP 190/110
• Already on Ramipril- 10mg, od and Amlodipine- 5mg, od but no improvement in BP
• Na= 145 (low), K= 3.0 (low)
• pH= 7.63, pCO2= 3.7, pO2= 12.5, HCO3= 35.5, BE=+5.6
Describe the results and
What is the likely diagnosis?
Low sodium and potassium
Metabolic acidosis
Secondary cause of HTN
Diagnosis = conns syndrome
116
Primary hyperaldosteronsim
What is it?
Signs
Causes
Investigations
Management
Conns syndrome- benign tumour of adrenal gland which secretes lots of aldosterone
• Excess production of Aldosterone
• Signs:
– Hypernatraemia and thus water retention
– Reduced renin stimulation (due to water retention and hypernatraemia)
– Hypokalaemia
– Metabolic alkalosis
– Hypertension
– Usually asymptomatic of signs of hypokalaemia
• Causes:
– 2/3rd due to Conns Syndrome (aldosterone adrenal secreting tumour)
– 1/3 due to B/L adrenocortical hyperplasia
• Investigations – U+E
– Raised Aldosterone levels, low Renin and Angiotensin II levels
– Adrenal Imaging
• Management
– Adrenalectomy (Conn’s Syndrome)
– Potassium sparing diuretic: Spironalactone, Eplenerone, Amiloride
117
Phaeochromocytoma
What is it?
Symptoms
Investigations
Management
• Catecholamine producing tumours (usually from sympathetic paraganglion cells in adrenal medulla)
• 10% are malignant, 10% are extra-adrenal, 10% are bilateral and 10% are familial
• Symptoms: Tachycardia, sweating, headache, hypertension, D+V, Anxiety, Psychosis, heat intolerance and flushing
• Investigations:
– Plasma+3x24hrurinarymetadrenalineand
normetadrenaline
– Abdominal CT or MRI (to detect adrenal tumours)
• Management:
– Alpha blockade and beta blockade
– Surgery, if malignant then chemotherapy and radiotherapy may be helpful
118
Diabetes insipidus
What is it?
Symptoms?
Causes?
Diagnosis?
Diabetes Insipidus
• Inadequate vasopressin/ADH secretionàReduced water re-absorption, thus plasma becomes more concentrated and a hypernatraemia occurs
Symptoms
• Polyuria, Polydipsia, Dehydration
Causes
• Nephrogenic:
– Inherited
– Drugs such as Lithium,Democycline
• Cranial:
– Idiopathic
– Tumor:craniopharyngioma,metastasis,primarypituitarytumor
– Trauma/Hypophysectomy
– Infiltration:Autoimmune,sarcoidosis
– Haemorrhage
– Infection(menino-encephalitis)
Diagnosis:
Water deprivation test demonstrates failure of urine to concentrate
