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Year 3 > block 34 week 3 > Flashcards

block 34 week 3 Flashcards

1
Q

What is diabetes?

A

*Diabetes is a condition of chronic hyperglycaemia caused by an absolute or relative lack of insulin
*Symptoms include thirst, polydipsia, polyuria and weight loss

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2
Q

incidence of diabetes?

A

*More than 150 million people worldwide suffer from diabetes (WHO-2004)
*The incidence is estimated to double by 2025

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3
Q

types of diabetes?

A

–Type 1 (insulin dependent diabetes)
–Type 2 (non insulin dependent diabetes)

*MODY-Maturity onset diabetes of the young
*Gestational diabetes

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4
Q

secondary causes of diabetes?

A

– Chronic pancreatitis
– Endocrine disease: Cushings, Acromegaly
– Drugs: Steroids, thiazides, olanzapine

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5
Q

T1D presents in>?

A

*Presents mainly in childhood and early adult life and accounts for 20% of cases

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6
Q

types of type 1 diabetes?

A

–Type 1A: Proven autoimmune aetiology
–Type 1B: No demonstrable autoimmunity

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7
Q

what leads to the hyperglycaemia in T1D?

A

*Destruction of pancreatic b-cell, for example by:
–Islet cell antibodies (ICA), Anti Glutamic acid (GAD) antibodies
*When sufficient b-cell mass is destroyed hyperglycaemia occurs

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8
Q

in type 1 there is ? insulin def

A
  • In type 1 there is absolute insulin deficiency
  • abrupt onset of symptoms
  • prone to ketosis
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9
Q

what does T1D require?

A
  • Requires a genetic predisposition and interaction with environmental triggers that activate progressive b-cell destruction
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10
Q

T1D may occur w other autoimmune diseases like?

A

Addison’s, Hypothyroidism and Pernicious anaemia, coeliac

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11
Q

care for T1DM?

A
  • MDT approach
  • In primary care this is usually delivered by the general practitioner and the practice nurse
  • In secondary care this involves the diabetes consultants, diabetes specialist nurses, dieticians, podiatrists and the retinal screening team
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12
Q

Age of onset in diabetes?

A
  • type 1 usually occurs in childhood and young adults but can occur at any age
  • exclude special circumstances such as pregnancy which can cause glycosuria without having diabetes
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13
Q

ketones in urine levels?

A
  • 1+ of ketones can occur after starvation
  • 2+ indicates insulin deficiency
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14
Q

blood ketone levels?

A
  • blood ketones under 0.6 are normal
  • blood ketones above 1.5mmol/L are high
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15
Q

DKA - if on presentation the person is?

A

If on presentation the person is vomiting or unwell with sepsis then admit to hospital and exclude Diabetic Ketoacidosis (DKA)

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16
Q

diabetes - education on glucose monitoring?

A
  • teach home blood glucose monitoring and provide requisite kit
  • this education usually provided by diabetes specialist nurse
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17
Q

lipoatrophy and lipohypertrophy?

A
  • lipoatrophy - when ppl injec insulin into subcutaneous tissue which can lead to damage and cause lumps - hypertrophy or atrophy - dips in the tissue
  • liophypertrophy is more common - hypertrophied fat cells. Insulin absorbed in an irregular fashion
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18
Q

New ppt w T1D - initiate?

A
  • Initiate insulin therapy
  • If premixed insulin (ratio 30/70, of short and intermediate acting insulin) BD before breakfast and before the evening meal.
  • The insulin is injected S/C and a reasonable starting dose is 10 units morning and 6 evening
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19
Q

insulin advice/

A
  • Ppt given a supply of insulin and all the kit needed for injection and safe disposal of needles
  • The patient is given contact numbers to call for advise both during normal working hours and after
  • The DSN usually rings the patient after 24 hours and regularly thereafter for a few weeks to provide support and advise on insulin dose titration
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20
Q

DSN role?

A
  • The DSN educates the patient on how to use the devise and inject safely (this is done using ‘dummy’ injections of sterile water).
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21
Q

ppt whose diabetes is out of control?

A
  • If blood glucose (BG) is out of control, ketones are elevated and the patient is vomiting or septic then admit
  • If poor BG control is new then look for signs of infection and treat if needed
  • Enquire about new medication such as steroids which can cause temporary increase in BG - needs increased insulin dose
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22
Q

basal bolus insulin regime?

A
  • Insulin injection regimens therefore use short acting insulin to simulate normal meal time insulin levels and delayed acting insulin to provide background insulin levels. This is called the basal bolus regimen (involves 4 to 5 injections daily)
  • this allows the person to adjust their insulin e.g. if they’re skipping a meal or eating later on
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23
Q

twice daily insulin regimes?

A
  • Twice daily injection regimens use mixed or biphasic insulin (usually a mixture of 30% short acting and 70% long acting insulin) injected at breakfast and with evening meal
  • have to eat at relatively fixed times - rigid
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24
Q

insulin injection - subcutaneous vs IV?

A
  • insulin injected into subcutaneous tissue self associates to form a hexamer which is too large to be absorbed into the circulation
  • insulin injected IV does not form a hexamer - all insulin acts the same IV, but forms hexamers when injected subcutaneously
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25
Q

short acting insulin?

A
  • a.k.a regular or soluble insulin
  • Usually injected subcutaneously 30 minutes before a main meal.
  • The time of peak action is about 1-3 hours (so the peak of blood insulin corresponds to the blood glucose rise after the meal) and duration of action is 4-8 hours
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26
Q

delayed action insulin?

A
  • Such as isophane and lente insulin are insoluble suspensions of insulin mixed with protamine and /or zinc ions
  • The onset of action is 1-2 hours, the time of peak action is about 4-12 hours and duration of action is up to 24 hours thereby providing background insulin cover
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27
Q

biphasic insulin?

A
  • These have set ratios of short-acting and isophane insulin premixed in the insulin vial or cartridge
  • The most common mixture is 30% short-acting and 70% isophane which is then injected twice daily before breakfast and before the evening meal
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28
Q

insulin pumps?

A
  • Continuous subcutaneous insulin infusion (CSII) is an insulin delivery system where insulin is delivered subcutaneously at an adjustable constant (basal) rate (usually 1 unit/hour) and further boosts delivered at meal times
  • Mimics physiology most closely but requires high degree of training and motivation and is expensive.
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29
Q

benefits of a cont insulin infusion?

A
  • suitable for variable meal times and variable activity levels
  • insulin levels can be decreased/interested
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30
Q

diet and insulin?

A

*General principles are teaching the ability to estimate the carbohydrate content of meals and snacks and adjusting the dose of insulin to suit

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31
Q

the unconscious diabetic patient ?

A
  • ABCDE - check airway, breathing, circulation and disability, endocrinology - measure glucose
  • recovery position
  • measure capillary BG - finger prick
  • establish venous access by inserting cannula
  • glucose, U&Es, FBC, amylase
  • check arterial blood gas for pH and oxygen status
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32
Q

Hypoglycaemia?

A
  • usually when BG is below 4
  • Edinburgh Hypoglycaemia Scale
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33
Q

Tx of hypoglycaemia?

A
  • if concious administer oral glucose - 5 dextrosol tablets or 3 teaspoonfuls of sugar in a drink or 150ml lucozade
  • follow w starchy snack e.g. biscuit
  • recheck blood sugar in 10 mins
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34
Q

tx of hypoglycaemia - unconcious?

A

–100 ml of 20% or 200 ml of 10% glucose intravenous (IV) over 15 minutes followed by a saline flush
–1 mg intra-muscular (IM) glucagon can be given if IV access is delayed (the effect only lasts for 30 minutes and not always effective)
- Recheck blood sugar in 10 minutes and repeat IV glucose if < 4 mmol/L

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35
Q

when is glucagon given?

A

if IV access is delayed - effect only lasts 30 min

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36
Q

when should DKA be tested for?

A
  • If the BG is high then test for diabetic ketoacidosis (hyperglycaemia + ketones + arterial pH<7.3)
  • If this is not ketoacidosis, investigate for other causes of unconsciousness –e.g. alcohol intoxication, sepsis, stroke, deliberate/accidental drug overdose, etc
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37
Q

how should hyperglycaemia be treated?

A
  • Treat hyperglycaemia with IV insulin infusion and IV Normal Saline until able to eat and drink normally
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38
Q

what is DKA?

A

*State of severe uncontrolled diabetes due to insulin deficiency
*Diagnosed by presence of high blood sugars, ketone bodies (in blood and urine) and acidosis

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39
Q

DKA is usually precipitated by?

A
  • Usually precipitated by infection, missing or incorrect insulin injections and newly diagnosed diabetes
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40
Q

DKA symptoms?

A
  • medical emergency - needs admission for IV fluids and insulin replacement
  • Patients get nausea/vomiting, extremely dehydrated, hypotensive and hyperventilate
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41
Q

BP targets w diabetes?

A

*Tight BP control (<135/85 or <130/80 if microalbuminuria coexists)

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42
Q

HbA1C target in T1D?

A

< 53

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43
Q

when should aspirin be used in T1D?

A

*Aspirin if over 40 and have 1 other CV risk factor

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44
Q

When should statins be used in T1D?

A

*Atorvastatin 20 mg if over 40, nephropathy or additional CV risk factor

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45
Q

Lifestyle advice in T1D?

A
  • Stop smoking advise and encourage exercise and weight loss if needed
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46
Q

microvascular comps of diabetes?

A

– Diabetic retinopathy
– Diabetic renal disease nephropathy
– Diabetic neuropathy

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47
Q

macrovascular comps of diabetes

A

–Peripheral vascular disease
–Coronary heart disease
- Cerebrovascular disease

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48
Q

common presentation of T2D?

A
  • Hyperglycaemia -> polyuria and polydispsia
  • poor utilisation of glucose by cells which can lead to: weight loss (but less commonly than in T1DM) and fatigue
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49
Q

diagnosis of diabetes?

A
  • impaired glucose tolerance
  • impaired fasting glucose
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50
Q

T1 vs T2 - symptoms?

A
  • T1: symptoms appear more quickly
  • Type 2: develop more slowly, patient may not notice any symptoms
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51
Q

T1 vs T2 - age?

A
  • type 1: diagnosis more likely under 40
  • type 2: risk increases with age
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52
Q

T1 vs T2 - ethnicity?

A
  • risk increases with ethnicity: You’re more at risk of developing type 2 diabetes if you’re white and over 40
  • or over 25 if you’re African-Caribbean, Black African, Chinese or South Asian.
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53
Q

Main cause of morbidity from diabetes?

A
  • the main cause of morbidity/mortality is a 2-4x excess risk of cardiovascular disease
  • This is at least partly due to a higher prevalence of cardiovascular risk factors (e.g. hypertension, hyperlipidaemia) in diabetes patients
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54
Q

Excess cardiovascular risk has been shown to be reduced by treating:

A
  • Hypertension with antihypertensives
  • Hyperlipidaemia with lipid lowering agents e.g. statins
  • Prothrombotic tendency with anti-platelets.
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55
Q

Prevention of T2D?

A

*Since obesity is a major contributory factor to the development of type 2 diabetes, ways of preventing/treating obesity
- Lifestyle changes are likely to be the most effective treatments

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56
Q

Impacts of obesity?

A
  • Increases the risk of developing a range of serious diseases, including heart disease and cancers.
  • Associated with the development of long-term health conditions, placing demands on social care services.
  • Significant economic impact on the NHS and wider economy.
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57
Q
A
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58
Q

Management of obesity?

A
  • Multicomponent interventions including community settings
  • Dietary intervention
  • Physical activity
  • Behavioral change strategies
  • Medications
  • Bariatric surgery
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59
Q

Possible clinical features of type 2 diabetes include:

A
  • Symptoms such as polydipsia, polyuria, blurred vision, unexplained weight loss, recurrent infections, and tiredness
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60
Q

insulin resistance

signs of diabetes?

A
  • Signs such as acanthosis nigricans (a skin condition causing dark pigmentation of skin folds, typically the axillae, groin, and neck), which suggests insulin resistance.
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61
Q

Persistent hyperglycaemia is defined as?

A
  • HbA1c of 48mmol/mol
  • fasting glucose level of 7
  • random plasma glucose of 11.1mmol in the presence of symptoms or signs
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62
Q

how should diabetes be diagnosed in an asymptomatic person?

A
  • If the person is asymptomatic, do not diagnose diabetes on the basis of a single abnormal HbA1c or plasma glucose result.
  • Arrange repeat testing, preferably with the same test, to confirm the diagnosis. If the repeat test result is normal, arrange tomonitorthe person for the development of diabetes, the frequency depending on clinical judgement.
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63
Q

how many tests need to be done to prove hyperglycaemia for diabetes?

A
  • at least 2 and both need to show hyperglycaemia - 1 can’t be normal
  • one abn result needed if symptomatic, two needed if asymptomatic
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64
Q

when HbA1c should not be used:

A
  • under 18
  • ppts of any age suspected of having type 1 diabetes
  • symptoms of diabetes for less than 2 months
  • People taking medication that may cause hyperglycaemia (for example long-term corticosteroid treatment).
  • People with acute pancreatic damage, including pancreatic surgery.
  • end stage renal disease
  • HIV
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65
Q

Causes of T1D?

A
  • autoimmunity is the main factor in the destruction of beta cells
  • It is thought that genetically susceptible individuals may develop autoantibodies that target the beta-cells in response to an external trigger (e.g. viral infection). Up to 85% of patients with T1DM are found to have circulating autoantibodies.
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66
Q

ab found in T1D?

A
  • The anti-glutamic acid decarboxylase (anti-GAD) antibody, an enzyme found within beta cells of the pancreas, is most commonly identified.
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67
Q

Causes of T2D

A
  • obesity and inactivity accounts for over 80% of the risk
  • poor diet - low fibre, high glycaemic index
  • low birth weight
  • meds
  • PCOS
  • history of GDM
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68
Q

diabetes care consumed ? of all NHS resources

A

10%

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69
Q

rare causes of diabetes?

A
  • chronic panc
  • monogenic diabetes
  • cushings
  • drugs - steroids, antidepressants
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70
Q

T1D typical patient?

A
  • Usually younger, lean, european
  • not generally inherited
  • autoimmune condition
  • insulin deficient, always need insulin
  • presence of ketosis more likely
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71
Q

genetic factors in T1D?

A
  • genetic factors - HLA-DQ
  • autoimmunity: autoantibodies to glutamic acid decarboxylase
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72
Q

Envir factors in t1d?

A
  • environmental@ e.g. exposure to cows milk, enteroviruses, vitamin D deficiency
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73
Q

pathology of t2d

A
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74
Q

typical type 2 ppt?

A
  • mostly older, overweight, all racial groups
  • strong familial tendency
  • no autoimmunity
  • partial insulin def, insulin resistance
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75
Q

Lifestyle factors cont to type 2?

A

sedentary lifestyle, excessive food intake

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76
Q

intrauterine factors cont to t2?

A

decreased birth weight, thrifty phenotype

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77
Q

genetic factors in t2?

A

strong familial tendency

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78
Q

epidemiology of T1?

A
  • prev of 0.25% in the UK
  • usually occurs in children but can present at any age
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79
Q

why is there inc risk of ketoacidosis in t1?

A
  • insulin deficiency
  • high stress increases glucagon and cortisol levels -> decrease action of insulin
  • increased hepatic glucose production
  • inc ketogenesis
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80
Q

ketone bodies ->

A
  • ketone bodies -> vomiting and acidosis
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81
Q

hyperglycaemia ->

A

osmotic diuresis

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82
Q

T1 sx tends to come on rapidly over ?

A

a few eeks

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83
Q

How is insuslin secreted?

A
  • secreted in response to glucose
  • glucose picked up by GLUT2 receptors
  • leads to release of stored insulin granules
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84
Q

primary effects of insulin on blood glucose?

A
  • decreases hepatic glucose production
  • increases peripheral glucose uptake by muscles
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85
Q

dietary aspects in diabetes management?

A
  • Lifestyle advice can help patients achieve sustained weight loss, better physical fitness, improved diet and ultimately improved glycaemic control.
  • high fibre, low-index carbohydate and controlling intake of high fat foods
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86
Q

exercise aspects in diabetes management?

A
  • exercise - exercise daily with at least 150 minutes of moderate intensity activity over a weekly period.al
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87
Q

other lifestyle advice 4 diabetes?

A
  • Patients should be encouraged to reduce alcohol consumption and stop smoking.
  • Alcohol increases weight and may exacerbate or prolong hypoglycaemia induced by antidiabetic medications.
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88
Q

steps of diabetes home testing techniques?

A
  • Wash your hands.
  • Put a lancet into the lancet device so that it’s ready to go.
  • Place a new test strip into the meter.
  • Prick your finger with the lancet in the protective lancing device.
  • Carefully place the subsequent drop of blood onto the test strip and wait for the results.
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89
Q

Flash glucose monitoring?

A
  • placed on the back of the upper arm
  • worn externally by the user, allowing glucose information to be monitored using a mobile app
  • offered to all people with T1D or insulin treated type 2 diabetes who are living with a learning disability and are recorded on their GP learning disability register.
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90
Q

CGM?

A
  • CGM is a small device that sticks to the skin. It measures glucose levels continuously throughout the day and night and can show trends in glucose levels over time.
  • The information is available instantly when a patient looks at the reader. Importantly, it can alert the user if the glucose goes too high or too low.
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91
Q

first line in T2D?

A

standard release metformin

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92
Q

when should an SGLT2 inhibitor be added to metformin?

A
  • if they have chronic HF or established atherosclerotic CV disease offer an SGLT2 inhibitor
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93
Q

how should metformin be dosed?

A
  • Gradually increase the dose of standard-release metformin over several weeks to minimise the risk of gastrointestinal side effects in adults with type2 diabetes.
  • If an adult with type2 diabetes experiences gastrointestinal side effects with standard‑release metformin, consider a trial of modified‑release metformin
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94
Q

first line when metformin is not tolerated/ is CI?

A
  • CVD/ atherosclerosis: SGLT2 inhibitor
  • if not, use DPP4 inhibitor, pioglitazone, sulfonurea, SGLT2 inhib
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95
Q

Before starting an SGLT2 inhibitor, check whether the person may be at increased risk of diabetic ketoacidosis (DKA), for example if:

A
  • they have had a previous episode of DKA
  • they are unwell with intercurrent illness
  • they are following avery low carbohydrate or ketogenic diet.
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96
Q

DSN?

A
  • doctors can work with DSN to provide education and training to patients
  • medication manegement - monitoring adherence, assessing for side effects
  • patient support
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97
Q

podiatrists?

A
  • Doctors can refer patients to podiatrists for regular foot screenings, risk assessments, and preventive interventions.
  • patient education
  • collaboratiev care to address both medical and podiatric concerns
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98
Q

dieticians

A
  • nutritional assessments - provide individualized dietary recommendations for individuals with diabetes, taking into account their medical history, lifestyle, and treatment goals.
  • meal planning
  • nutrition education
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99
Q

doctors and dieticians - collaborative care?

A

Doctors and dietitians collaborate to integrate nutrition therapy into the overall diabetes management plan

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100
Q

2 major acute complications of t2?

A

hypoglycaemiaandhyperosmolar hyperglycaemic state (HHS).

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101
Q

Microvascular comps - retinopathy?

A
  • diabetic retinopathy
  • Other disorders include cataracts and ocular palsies.
  • When diagnosed with T2DM, GPs should immediately refer for eye screening.
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102
Q

mechanism behind diabetic retinopathy?

A
  • Persistent damage to the retina leads to areas of ischaemia and release of angiogenetic factors such as vascular endothelial growth factor (VEGF).
  • This promotes new formation of vessels that are weak and friable.
  • This leads to complications including haemorrhage, fibrosis and retinal detachment.
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103
Q

how is retinopathy managed?

A
  • Photocoagulation is used to manage proliferative disease.
  • The aim of photocoagulation is to burn holes within the ischaemic retina to prevent the release angiogenesis factors (e.g. VEGF), which stimulate new vessel formation.
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104
Q

How is it measured?

diabetic nephropathy?

A
  • The earliest sign of diabetic nephropathy is the presence of microalbuminuria, which can be assessed with an albumin:creatinine ratio (ACR).
  • An ACR 3 - 30 mg/mmol is suggestive of microalbuminuria
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105
Q

Staging of nephropathy?

A
  • A1:< 3 mg/mmol, normal or mild increase
  • A2:3 - 30 mg/mmol, moderately increased
  • A3:> 30 mg/mmol, severely increased
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106
Q

microalbumuria - Tx?

A
  • microalbuminuria is a marker of systemic microvascular damage and patients shoild be treated w an ACEi or ARB even in the presence of normotension
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107
Q

CKD in diabetes?

A
  • Chronic kidney disease (CKD) in diabetes is evidenced by a persistently low eGFR < 60 mmol/L and/or an ACR persistently > 3 mg/mmol/L.
  • Offer an SGLT2 if ACR > 30 mg/mmol
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108
Q

types of diabetic neuropathy?

A
  • symmetrical poluyneuropathy
  • mononeuropathy
  • diabetic amyotrophy
  • autonomic neuropathy
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109
Q

Symmetrical polyneuropathy?

A

typically a peripheral neuropathy that occurs in the leg secondary to loss of vibration, pain and temperature sensation.

110
Q

Mononeuropathy?

A

damage to a single cranial or peripheral nerve (e.g. third nerve palsy).

111
Q

diabetic amyotrophy?

A

a spectrum of disease affecting the lumbosacral plexus leading to symmetrical pain, weakness and wasting of the proximal muscles of the leg.

112
Q

autonomic neuropathy?

A
  • a spectrum of conditions related to damage of the autonomic nervous system
  • Some of the major autonomic neuropathies include postural hypotension, gastroparesis (delayed gastric emptying leading to vomiting), diarrhoea, bladder dysfunction and erectile dysfunction.
113
Q

diabetic foot?

A
  • secondary to the combination of peripheral neuropathy and poor vascular supply.
  • Due to loss of sensation and poor blood supply, patients are at risk of a number of complications including diabetic ulcers, secondary infection (e.g. cellulitis, osteomyelitis), skin necrosis and eventually amputation.
114
Q

charcot’s joint?

A
  • results from loss of sensation and subsequent repeated micro-trama to the foot - traditionally mid foot
  • Microtrauma in the presence of poor peripheral blood flow leads to remodelling, swelling and distortion of the whole joint.
115
Q

macrovascular comps from t2?

A
  • diabetes is a major RF for atherosclerosis
116
Q

diagnosis of hypoglycaemia is based on ? triad?

A
  • diagnosis based on Whipple’s triad
  • Low blood glucose concentration
  • Symptoms of hypoglycaemia
  • Reversal of symptoms when blood glucose concentration is restored to normal
117
Q

ppts treated w ? are at inc risk of hypoglycaemia?

A

insulin and sulphonylureas

118
Q

hyperosmolar hyperglyacaemic state ?

A
  • acute diabetic emergency that occurs in patients with type 2 diabetes - life threatening
  • HHS occurs insidiously over several days with dehydration and metabolic disturbances that are more extreme than diabetic ketoacidosis (DKA).
119
Q

HHS is characterised by?

A
  • Hypovolaemia
  • Hyperglycaemia(> 30 mmol/L)
  • Mild or absent ketonaemia(blood ketones < 3 mmol/L)
  • High osmolality(> 320 mOsm/kg)
120
Q

HSS ppts tend to be?

A
  • Patients are usually elderly with multiple co-morbidities, and as a result may be very unwell.
  • HSS usually occurs in the elderly but is increasingly recognised in younger ppts
121
Q

What happens in HHS?

A
  • In HHS, therelative lack of insulin is coupled with a rise in counter-regulatory hormones(e.g. cortisol, growth hormone, glucagon) that leads to a profound rise in glucose.
  • bc a certain level of insulin is retained, this prevents the development of ketosis that epitomises DKA
  • However, the level of insulinis inadequate to prevent profound hyperglycaemia.
  • The excessive glucose leads tomassive osmotic diuresis within the kidneys with the loss of essential electrolytes such as sodium and potassium.
  • As water is lost, there is profound dehydration and reduced circulating volume, resulting in hyperosmolarity and marked hyperglycaemia
  • The increase in osmolality increases compensatory mechanisms such as release of anti-diuretic hormone (ADH) and stimulation of thirst.
122
Q

If the patient can’t compensate for the water loss (HHS)

A
  • However, if this cannot compensate for the renal water loss (e.g. elderly patients with co-morbidities) then hypovolaemia develops with progression to acute kidney injury, electrolyte disturbances, hypotension and coma.
123
Q

complication wise

HHS - the hyperosmolar state leads to?

A
  • The hyperosmolar state of the condition leads to hyperviscosity that increases the risk of arterial and venous thrombosis(e.g. stroke, DVT).
124
Q

Precipitants of HHS?

A
  • Most cases are from a new diagnosis of type 2 diabetes
  • Infection
  • High-dose steroids
  • Myocardial infarction
  • Vomiting
  • Stroke
  • Poor treatment concordance
125
Q

Sx of HHS?

A
  • Polydipsia
  • Polyuria
  • Nausea
  • Vomiting
  • Muscle cramps
  • Weakness
  • Altered mental status
  • Seizures
  • Coma
126
Q

signs of HHS?

A
  • dehydration
  • hypotension & tachycardia
  • decreased urine output
  • decreased concious level and coma
  • focal neurology signs
127
Q

diagnosis of HHS?

A

The diagnosis of HHS is based on identification of characteristic features including marked hyperglycaemia, raised serum osmolality, and mild/absent ketonaemia.

128
Q

main goals of tx in HHS?

A
  • Normalise osmolality
  • Normalise blood glucose
  • Replace fluid and electrolytes
  • Prevention of arterial/venous thrombosis
  • Prevention of complications & foot ulceration
129
Q

When is DKA more common?

A
  • more common w T1D but can also occur w T2D
130
Q

DKA results from a ?

A
  • DKA results from an absolute or relative deficiency of insulin, leading to increased hepatic glucose production, decreased peripheral glucose utilization, and enhanced lipolysis with subsequent ketone body formation
131
Q

Causes of DKA?

A
  • Driven by insulin deficiency which can be caused by inadequate insulin therapy, illness, or stress.
  • The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.
132
Q

Insulin deficiency leads to:

A
  • hyperglycaemia
  • ketosis
  • metabolic acidosis
133
Q

DKA - hyperglycaemia?

A
  • hyperglycaemia: Increased gluconeogenesis and glycogenolysis in the liver, combined with decreased glucose utilization in peripheral tissues, result in hyperglycemia.
134
Q

DKA - ketosis?

A
  • ketosis: Insulin deficiency promotes lipolysis, releasing free fatty acids that are converted to ketone bodies (β-hydroxybutyrate and acetoacetate) in the liver
  • High levels of ketone bodies lead to ketonemia and ketonuria.
135
Q

DKA - metabolic acidosis?

A
  • metabolic acidosis: Accumulation of ketone bodies causes an increase in the anion gap metabolic acidosis.
136
Q

DKA - how does ketosis ?

A
  • ketosis presents as characteristic sweet, fruity, or acetone odour on the breath.
137
Q

management of DKA - emergency team?

A

fluid resus, begin insulin therapy

138
Q

endocrinologist?

A
  • endocrinologists - They provide expertise in adjusting insulin therapy, managing electrolyte imbalances, and addressing underlying factors contributing to DKA.
139
Q

DSN?

A
  • diabetic specialist nurses - DSNs play a crucial role in educating patients about diabetes self-management, including insulin administration, blood glucose monitoring, and lifestyle modifications. They also provide support and guidance during hospitalization and after discharge.
140
Q

GP in diabetes management?

A
  • GP - ongoing diabetes management, preventative care, regular monitoring of blood glucose levels
141
Q

how does DKA present?

A
  • Patients classically exhibit polyuria, polydipsia, and profound weakness, with notable signs including
  • Kussmaul breathing, dehydration, and a distinct acetone odour on the breath.
142
Q

management of DKA?

A
  • fluid replacement - isotonic saline
  • insulin - IV infusion
  • correction of electrolyte disturbance - potassium
  • long-acting insulin should be continued, short-acting insulin should be stopped
143
Q

Ketonaemia and acidosis should resolve within?

A
  • ketonaemia and acidosis should have been resolved within 24 hours
  • If this hasn’t happened the patient requires senior review from an endocrinologist
  • patient should be reviewed by diabetes specialist nurse prior to discharge
144
Q

psychological impact of T1D?

A
  • shock and denial
  • fear and anxiety - prospect of managing a chronic condition
  • stress - managing the demands of diabetes care such as monitoring blood glucose levels. adhering treatment regimes, making lifestyle adjustments
  • grief and a sense of loss of their pre-diagnosis lifestyle
  • increased risk of depression
  • anger and frustration - resentful towards their body or towards others who don’t understand their challenges
145
Q

social impacts of a diabetes diagnosis - family dynamics and peer relationships?

A
  • family dynamics - as it can often require adjustments in daily routine, meal planning and lifestyle habits
  • peer relationships - Individuals with type 1 diabetes may face social challenges in peer interactions, such as concerns about disclosing their condition, managing blood glucose levels in social settings, and addressing misconceptions or stigma related to diabetes
146
Q

social effects of diabetes diagnosis?

A
  • school/ work envir - concerns around accomodations. stigma, discrimination
  • social activities e.g. sports might need planning and consideration of diabetes
  • emotional wellbeing - isolation, depression, low self esteem
  • stigma and discrimination
147
Q

Hypoglycaemia is a level below?

A
  • glucose level of below 3.3mmol
148
Q

causes of hypoglycaemia?

A
  • excess insulin
  • sulfonylureas
  • hypoglycaemia
149
Q

Excess of insulin?

A
  • excess of insulin - Most commonly this is from exogenous, injectable insulin used in the management of type I or type II diabetes mellitus.
  • Levels of insulin may be higher than necessary if the patient has taken too much insulin, or has used the same amount of insulin whilst not eating enough or skipping a meal or snack
150
Q

sulfonylureas side effects

A
  • Sulfonylureas (e.g. gliclazide) act by increasing the secretion of insulin from β-cells. ]
  • Hypoglycaemia is a common adverse effect, especially when starting this medication or increasing dose.
151
Q

hypoglycaemia is more likely to occur in?

A
  • Hypoglycaemia is more likely to occur in diabetics who have a viral illness, have drunk alcohol, exercised more than usual or have just started or changed dosage of a new medication.
152
Q

iatrogenic causes of hypoglyc?

A

IGF-1, lithium, pentamidine

153
Q

what is the most common non-iatrogenic cause of hypo?

A
  • alcohol consumption - most commmon non iatrogenic cause of hypo
  • This is due to its inhibitory effect on gluconeogenesis and glycogenolysis.
154
Q

blood glucose conc of under 3.3. can cause autonomic symptoms due to release of glucagon and adrenaline:

A
  • sweating
  • shaking
  • hunger
  • anx
  • nausea
  • tremor
  • palpitations
155
Q

Blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:

A
  • Weakness
  • Vision changes
  • Confusion
  • Dizziness
156
Q

the diabetes control and complications trial (DCCT trial)

A
  • landmark clinical trial
  • demonstrated the importance of intensive glycemic control in preventing or delaying the development of diabetes-related complications in individuals with type 1 diabetes.
  • The DCCT provided robust evidence that maintaining blood glucose levels as close to normal as possible significantly reduces the risk of long-term complications of diabetes, such as retinopathy, nephropathy, and neuropathy.
157
Q

what did the DCCT trial demonstrate?

A
  • The trial demonstrated that achieving lower hemoglobin A1c (HbA1c) levels through intensive insulin therapy was associated with better outcomes.
158
Q

establishment of HbA1c targets?

A
  • DCCT established HbA1c targets for individuals with type 1 diabetes, with the goal of reducing levels to below 7% to minimize the risk of complications.
  • This set a benchmark for glycemic control that has since been widely adopted in clinical practice
159
Q

metformin dual therapy

A
160
Q

Discuss with patients the dietary recommendations in Type 1 diabetes?

A
  • A diet that includes carbohydrates from fruits, vegetables, whole grains, legumes, and low-fat milk is encouraged.
  • People with diabetes are advised to avoid sugar-sweetened beverages (including fruit juice).
  • carb counting
161
Q

Which grps of ppl have inc risk of T2D?

A
  • The risk of developing the condition is as high as 75% if both parents have suffered from the condition.
  • Certain ethnicities (e.g. Asian/African) have a 2-4x increased risk of developing the condition.
162
Q

Envir causes of T2?

A
  • inactivity and obesity account for the majority of the risk
  • Poor dietary habit(low fibre, high glycemic index diet)
  • Low birth weight
  • Medications
  • Polycystic ovarian syndrome
  • History of GDM
163
Q

what is impaired glucose tolerance?

A
  • An inability of peripheral tissue to respond to insulin leads to hyperglycaemia, which in turn causes hyperinsulinaemia.
  • In the early stages of insulin resistance, abnormal regulation of glucose occurs following a meal in the post-prandial state.
  • This is termed impaired glucose tolerance (IGT).
  • IGT is a major risk for the future development of frank diabetes and cardiovascular disease.
164
Q

impairef fasting glucose?

A
  • High levels of glucose during the fasting state (between meals) can also occur with insulin resistance, which is termed impaired fasting glucose (IFG).
  • IFG itself is another risk factor for the development of frank diabetes.
165
Q

pre-diabetes?

A
  • hba1c 42-47
  • IFG and IGT are often collectively referred to as ‘pre-diabetes’ as they are significant markers for the future development of the condition if no intervention occurs to reduce risk (e.g. lifestyle and diet modifications).
166
Q

glucotoxicity?

A
  • As hyperglycaemia develops, the beta cells within the Islets of Langerhans must secrete more insulin to deal with the increase in glucose leading to hyperinsulinaemia.
  • These high levels of insulin are still inadequate to restore glucose homeostasis. It is thought that high glucose levels (and lipids) are toxic to beta cells leading to a depletion in their cellular mass. This is termed glucotoxicity
167
Q

HBA1C?

A
  • reflects the average blood glucose concentration over a three month period (the average survival time of an erythrocyte)
  • increases as blood glucose levels increase
  • diabetes >48mmol
  • 42-47mmol = pre-diabets
168
Q

what can impact hba1c level?

A
  • conditions interrupting erythryopotein like (e.g. EPO use, iron-deficiency), haemoglobin structure (e.g. haemoglobinopathies), glycation (e.g. CKD, alcoholism), or red cell survival (e.g. haemolysis, splenectomy) will effect the level of HbA1c.
169
Q

normal fasting plasma glucose levels?

A
  • should be approx 4-6mmol
170
Q

diabetic fasting plasma glucose levels?

A
  • diabetes can be made if the fasting glucose levels are ≥ 7 mmol/L on two separate readings in a patient who is asymptomatic or a single reading if the patient is symptomatic
171
Q

fasting glucose level that suggests IFG?

A
  • fasting glucose level between 6-6.9 mmol/L are said to have impaired fasting glucose (IFG), which is a marker of pre-diabetes and increases the risk of developing overt diabetes.
172
Q

Plasma glucose levels?

A
  • not used for diagnosis
  • A random blood glucose level ≥ 11.1 mmol/L is indicative of diabetes
173
Q

ppts w high random plasma glucose levels?

A
  • Patients with a high random plasma glucose should be assessed for potential complications (e.g. HHS, DKA) and concurrent illness.
174
Q

what can also inc random plasma glucose?

A
  • Concurrent illnesses can increase plasma glucose levels as part of the normal physiological stress response.
  • Patients with high levels should undergo further testing (e.g. HbA1c or fasting glucose levels).
175
Q

oral glucose tolerance test?

A
  • The oral glucose tolerance test (OGTT) measures the ability of the body to deal with a glucose load over a two hour period.
  • use has largely been replaced by Hba1c
176
Q

OGTT that indicates diabetes?

A

Levels greater than 11 mmol/L at 2 hours are suggestive of diabetes.

177
Q

OGTT that shows IGT?

A

Levels ≥ 7.8 mmol/L but < 11.1 mmol/L are suggestive of impaired glucose tolerance (IGT)

178
Q

OGTT is usually reserved for?

A
  • the oral glucose tolerance test is usually reserved for assessment of gestational diabetes
179
Q
A
179
Q
A
179
Q
A
180
Q

management of diabetes involves

A
  • education
  • lifestyle advice
  • medication
  • monitoring for complications
180
Q

mechanism of metformin

A
  • Biguanide
  • lowers blood glucose levels through inhibition of hepatic gluconeogenesis whilst increasing peripheral insulin sensitivity and enhancing peripheral uptake of glucose.
181
Q

step 1 of diabetes management?

A
  • Standard release metformin
  • Aim for HbA1c < 48 mmol/mol, increasing dose as needed
182
Q

all ppts w t2 should be started on?

A
  • All patients with T2DM should be started on metformin unless contraindicated (e.g. CKD, those at risk of lactic acidosis, poorly tolerated).
183
Q

what should be monitored w metformin?

A
  • Monitor renal function, consider modified-release preparations if develop adverse GI effects
184
Q

step 2 of diabetes management?

A
  • Consider dual antidiabetic therapy if HbA1c rises > 58 mmol/L
  • Metformin in combination with a second antidiabetic agent:
  • Sulfonylurea (SU)
  • Dipeptidyl peptidase-4 inhibitor (DPP-4i)
  • Pioglitazone
  • Sodium–glucose cotransporter 2 inhibitor (SGLT-2i)
185
Q

goal in step 2 of diabetes management?

A
  • Aim for HbA1c < 53 mmol/mol
186
Q

step 3 of DM?

A
  • Consider triple antidiabetic therapy or an insulin-based regimen if HbA1c > 58 mmol/mol
  • Metformin, DPP-4i and SU
  • Metformin, pioglitazone and SU
  • Metformin, pioglitazone/SU, and SGLT-2i
187
Q

Step 4 of DM?

A
  • In patients on triple antidiabetic therapy and ongoing poor glucose control, consider further intensification
  • Consider combination treatment with metformin, SU and glucagon-like peptide-1 (GLP-1) mimetic
188
Q

If metformin not tolerated, alt step 1?

A
  • DPP-4i or pioglitazone or SU
  • Aim for HbA1c < 48 mmol/mol or < 53 mmol/mol if treatment with a SU
189
Q

if metformin not tolerated, alt step 2?

A
  • If HbA1c rises > 58 mmol/mol consider a combination of:
  • SU and pioglitazone
  • SU and DPP-4i or
  • Pioglitazone and DPP-4i
190
Q

if metformin not tolerated, alt step 3?

A
  • Consider an insulin-based regimen if HbA1c > 58 mmol/mol
191
Q

use of insulin in t2?

A
  • use should be considered early in the management of patients w T2DM
  • usually considered in patents with poor glycemic control despite dual antidiabetic with metformin and another agent.
  • not appropriate when there’s sig risk of hypogylacemia
192
Q

which type of insulin is used in t2?

A
  • In general, patients are offered an intermediate-acting insulin therapy such as NPH in the initial stages.
  • If glycemic control is particularly bad (e.g. HbA1c > 75 mmol/L) patients may be started on mixed insulin (intermediate and short-acting).
193
Q

t2 - long acting insulin?

A
  • Long-acting insulin is usually reserved for patients where hypoglycaemia is a problem with NPH insulin or the patients rely on carers for help with their injections.
194
Q

Management with lifestyle modifications only treatmetn target?

A

aim HbA1c < 48 mmol/mol

195
Q

Management with lifestyle and a single antidiabetic agent?

A

aim HbA1c < 48 mmol/mol

196
Q

Management with a drug associated with hypoglycaemia (e.g. SU)?

A

aim HbA1c < 53 mmol/mol

197
Q

Management with higher intensification regimes aim for?

A

aim HbA1c < 53 mmol/mol

198
Q

diabetic review?

A
  • patients should be regularly reviewed and complications assessed on at least an annual basis.
  • During each clinic review, patients should have their BMI checked, smoking status clarified and assessed for any psychosocial issues (e.g. anxiety/depression).
199
Q

HbA1c should be checked every ? in diabetics

A

Every 3-6 months, patients should have their HbA1c checked and management changed accordingly

200
Q

screening for retionopathy?

A

annual retinal screening and eye check

201
Q

screening for Nephropathy?

A

renal function (eGFR) and albumin:creatinine ratio (ACR)

202
Q

screening for neuropathy and diabetic foot?

A

assessment for peripheral neuropathy, autonomic neuropathy, full examination including footwear, monofilament assessment of neuropathy, vascular assessment +/- dopplers.

203
Q

screening for Cardiovascular risk factors?

A

primary/secondary prevention strategy with optimisation of blood pressure and lipids.

204
Q

Tx of HTN in diabetics?

A

ACE inhibitors/A2RBs are first-line regardless of age

205
Q

monitoring w amiodarone?

A
  • TFT, LFT, U&E, CXR prior to treatment
  • TFT, LFT every 6 months
206
Q

Pioglitazone may cause ?

A

fluid retention

207
Q

Pioglitazone - contraindicated by: ?

A

heart failure - Thiazolidinediones

208
Q

Thiazolidinediones are associated with an increased risk of ?

A

bladder cancer -

209
Q

SGLT2 inhibs side effects?

A

genital infections, diabetic ketoacidosis

210
Q

Biguanides e.g. metformin side effects?

A

GI upset, lactic acidosis

211
Q

GLP-1 mimetics side effects?

A

nausea, vomiting, pancreatitis

212
Q

insulin side effects?

A

weight gain, hypoglycaemia, lipodystrophy

213
Q

Secondary hyperparathyroidism shows a ?

A

high phosphate

214
Q

most common cause of tertiary hyperparathyroidism?

A

CKD

215
Q

Tertiary hyperparathyroidism?

A
  • Tertiary hyperparathyroidism usually occurs after prolonged secondary hyperparathyroidism - the glands become autonomous, and so produce excessive PTH even after the cause of hypocalcaemia has been corrected;
  • -this then causes the hypercalcaemia that typifies tertiary hyperparathyroidism.
216
Q

secondary hyperpara?

A
  • high PTH
  • Ca2+ normal or low
217
Q

what happens in secondary hyperpara?

A

In secondary hyperparathyroidism there in hyperplasia of the parathyroid glands in response to chronic hypocalcaemia (or hyperphosphataemia) and is a normal physiological response

218
Q

Primary hyperpara = P for?

A

P for primary, phosphate is low

219
Q

Secondary = C for?

A

seConDary for calcium, calcium is low, vitamin D is low

220
Q

tertiary = T for?

A

TerTiary = viTamin D and phosphaTe are low

221
Q

most common endgenous cause of cushings?

A

The most common endogenous cause of Cushing’s syndrome is a pituitary adenoma (also known as Cushing’s disease)

222
Q

what is the most common metabolic comp of cancer?

A

Hypercalcaemia is the most common metabolic complication in patients with cancer - treated w iV N saline

223
Q

what is typically low in t1?

A

C peptide levels, high in t2

224
Q

SGLT2 monotherapy - when?

A

T2DM initial therapy: if metformin is contraindicated + patient has a risk of CVD, established CVD or chronic heart failure → SGLT-2 monotherapy

225
Q

causes of raised prolactin - the ps?

A
  • pregnancy
  • prolactinoma
  • physiological
  • polycystic ovarian syndrome
  • primary hypothyroidism
  • phenothiazines, metoclopramide, domperidone
226
Q

Endocrine parameters reduced in stress response:

A
  • Insulin
  • Testosterone
  • Oestrogen
227
Q

What is a spec feature of graves?

A

Exophthalmos is a specific feature of Grave’s disease rather than generic hyperthyroidism - diplopia

228
Q

hypercalcaemia and suppressed PTH?

A
  • Hypercalcaemia with suppressed PTH is highly suspicious for malignancy (e.g. solid organ, or myeloma).
  • Alternative diagnoses which can cause this pattern include thyrotoxicosis.
229
Q

Diabetes sick day rules?

A
  • when unwell, If a patient is on insulin, they must not stop it due to the risk of diabetic ketoacidosis.
  • They should continue their normal insulin regime but ensure that they are checking their blood sugars frequently
230
Q

comp of fluid resus in DKA?

A
  • Cerebral oedema
  • imp comp espec in young ppts
231
Q

cerebral oedema symptoms?

A
  • deteriorating mental status/ level of consciousness, incontinence unexpected for age,
  • abnormal neurogenic respiratory pattern (e.g. grunting, abnormal tachypnoea, apnoea) and vomiting.
232
Q

? disease is a cause of hypoglycaemia

A

addisons

233
Q

what can be used for symptom control in graves

A

propanolol - non cardioselectibe

234
Q

Patients with type I diabetes and a BMI > 25 should be considered for ?

A

metformin in addition to insulin

235
Q

triad in liver failure?

A

Liver failure = triad of encephalopathy, jaundice and coagulopathy

236
Q

what is a well recognised drug causing gallstones?

A

Co-amoxiclav is a well recognised cause of cholestasis - gallstones

237
Q

Thyrotoxicosis with tender goitre =

A

subacute (De Quervain’s) thyroiditis. Usually self limiting - conservative management + ibuprofen

238
Q

rf for c diff?

A

PPI

239
Q

What induces remission of graves?

A

Carbimazole induces remission of Graves’ disease and therefore is only needed for a period of 12-18 months usually.

240
Q

what can be used to manage diabetic neuropathy?

A

duloxetine

241
Q

what suggests alc hep?

A

AST: ALT > 2 suggests alcoholic hep

242
Q

AST: ALT ratio of under 1 suggests?

A

NAFLD

243
Q

what is used for hyperthyroidism in T1?

A
  • Propylthiouracil for pregnant women in the first trimtester w hyperthyroidism instead of carbimazole
  • When the woman reaches 12 weeks (second trimester), so would be switched to Carbimazole, as Propylthiouracil can cause severe hepatic injury.
244
Q

toxic multinodular goitre Tx?

A

radioactive iodine is the treatment of choice

245
Q

risk w SGTL2 inhibitors?

A

Closely monitor legs and feet of patients taking canagliflozin (SGLT2 inhibitors) for ulcers or infection - possible increased risk of amputation

246
Q

how is thyrotoxic storm Tx?

A

beta blockers, propylthiouracil and hydrocortisone

247
Q

precp events for thyroid storm?

A
  • thyroid or non-thyroidal surgery
  • trauma
  • infection
  • acute iodine load e.g.CT contrast media
248
Q

CF of thyrotoxic storm?

A
  • fever > 38.5ºC
  • tachycardia
  • confusion and agitation
  • nausea and vomiting
  • hypertension
  • heart failure
  • abnormal liver function test - jaundice may be seen clinically
249
Q

gold standard for coeliac?

A
  • Endoscopic intestinal biopsy, however, is the gold standard for the diagnosis of coeliac disease and should be offered to all adult patients if the diagnosis is suspected following serology.
  • Jejunal biopsy, as the duodenum and jejunum are the most affected portions of bowel in coeliac disease, while the ileum is not as affected (unlike in Crohn’s disease),
250
Q

Iron defiency anaemia vs. anaemia of chronic disease:

A

TIBC is high in IDA, and low/normal in anaemia of chronic disease

251
Q

what can mimic cushings disease?

A

Alcohol excess can mimic Cushing’s disease

252
Q

DKA management - FIG PICK?

A

F - Fluids
I - Insulin (Fixed rate 0.1u/kg/hr)
G - Monitor glucose
P - Monitor / give potassium
I - Treat any underlying infections / triggers
C - Monitor for signs of cerebral oedema
K - Monitor ketones & pH

253
Q

pretibial myxoedema?

A

Pretibial myxoedema is an uncommon but specific feature in Grave’s disease that is not seen in hyperthyroidism secondary to other causes

254
Q

Which diabetes meds are weight neutral?

A

DDP4i

255
Q

which drugs cause weight gain?

A

pioglitazone causes weight gan
sulfonureas cause weight gain

256
Q

which drugs cause weight loss?

A

SGLT2 inhibitors

257
Q

first-line for black TD2M patients who are diagnosed with hypertension?

A

An angiotensin II receptor blocker should be used first-line for black TD2M patients who are diagnosed with hypertension

258
Q

T2DM with abnormal LFTs ->

A

non-alcoholic fatty liver disease

259
Q

DM diagnosis?

A

fasting > 7.0, random > 11.1 - if asymptomatic need two readings

260
Q

ascites LTM?

A

stop drinking alcohol, and low sodium intake

261
Q

ferritin in IDA vs A of CD?

A

Ferritin is low in iron deficiency anaemia but high or normal in anaemia of chronic disease

262
Q

neuro features of perinicious anemia?

A

Neurological features of pernicious anaemia may include peripheral neuropathy, subacute combined degeneration of the spinal cord and neuropsychiatric disorders - more lkely w T1D bc both autoimmune

263
Q

autoimmune hep?

A

Antinuclear antibodies, anti-smooth muscle antibodies and raised IgG levels are characteristic of autoimmune hepatitis

264
Q

what can give a falsely low hba1c?

A

haemodialysis

265
Q

The Hba1c target for patients on a drug which may cause hypoglycaemia is?

A

The Hba1c target for patients on a drug which may cause hypoglycaemia (eg sulfonylurea) is 53 mmol/mol

266
Q

drugs to stop in AKI?

A

DAMN AKI?

Diuretics
Aminoglycosides and ACE inhibitors
Metformin
NSAIDs.

267
Q
A

Year 3 (45 decks)

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