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CCE2: Medicine Block > Abnormal blood sugar: includes ACI clinical diabetes > Flashcards

Abnormal blood sugar: includes ACI clinical diabetes Flashcards

1
Q

What percentage of patients are affected by:

1) type 1
2) type 2

A
  • Type 1- 15%
  • type 2- 85%
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2
Q

Define diabetes Mellitus:

A

A heterogeneous complex metabolic disorder characterised by elevated blood glucose secondary to either:

Resistance to the action of insulin

OR

Insufficient insulin secretion

OR both.

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3
Q

How is diabetes classified?

A
  • Diabetes is a continuum of disordered glucose metabolism
  • WHO classification encompasses 4 stages:
    • Normal
    • Impaired fasting glycaemia
    • Impaired glucose tolerance
    • Diabetes
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4
Q

How do we diagnose diabetes?

A
  • Clinical history PLUS
  • random blood glucose (> or equal to 11.1 mmol/L in T1DM) (normal less than 7.8 mmol/L)
  • Fasting plasma glucose tests
  • HbA1C (glycosylated haemoglobin)
  • oral glucose tolerance tests - normally inpatient test, fast overnight, take 75 grams of glucose, measure blood before and then 2 hrs later. Level of 2 hr mark can define diabetes.
  • Urine tests
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5
Q

What is the WHO diagnostic criteria for:

Normal glucose tolerance

Impaired fasting glycaemia

Impaired glucose tolerance

Diabetes

A

1) Normal - HbA1C: Less than 42 mmol/mol (less than 6%). Fasting plasma glucose (FPG) < 6.1 mmol/L

(Cannot use HbA1C in young patients, pregnant, acutely unwell, CKD, anaemia)

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6
Q

What is the WHO diagnostic criteria for:

Impaired fasting glycaemia

A

Impaired fasting glycaemia:

  • Fasting plasma glucose > 6.1 mmol/L but less than 7mmol/L. Need oral glucose tolerance test
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7
Q

What is the WHO diagnostic criteria for:

Impaired glucose tolerance

A
  • Impaired glucose tolerance: Oral glucose tolerance test 2hr glucose greater or equal to 7.8 mmol/L but less than 11.1 mmol/L
  • HbA1C of 42-47 mmol/mol = high risk of diabetes
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8
Q

What is the WHO diagnostic criteria for:

Diabetes

A
  • Diabetes:
    • HbA1C: 48 mmol/ mol and above (6.5%)
    • fasting plasma glucose (FPG) above 7 mmol/l
    • OR oral glucose tolerance test 2hrs greater than 11.1 mmol/L
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9
Q

Under what circumstances can you not use HbA1C to diagnose diabetes?

A

Cannot use HbA1C in:

young

pregnant

acutely unwwell

CKD

anaemic patients

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10
Q

What are the main classifications of diabetes?

A

Broadly divided into type 1 and type 2

Type 1: Juvenile or insulin dependent diabetes - pancreas does not produce sufficient insulin

Type 2: Adult onset diabetes - characterised by high blood sugar levels due to insulin resistance eventually leading to failure of production of insulin

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11
Q

What are the other types and causes of diabetes?

A
  • Gestational -
  • Drugs - steroids, thiazides, anti psychotics (class ii)
  • Pancreatic - pancreatitis, surgery, trauma, destruction e.g. heamochromatosis (condition of excess iron absorption), CF, cancer
  • Endocrine- Cushing’s disease (increase corticosteroids), acromegaly (too much GH), phaemochromocytoma (tumour of adrenal glands), hyperthyroidism
  • Genetic - Monogenic - NDM (neonatal diabetes mellitus) MODY (mature onset of diabetes of the young), glycogen storage disorder, congenital lipodystrophy with insulin receptor antibodies
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12
Q

What are the 4 common presenting symptoms of T1DM?

A

Polyuria

Polydipsia

Unintentional weight loss

Hyperglygaemia

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13
Q

T1DM

previous name

age of onset

condition that is part of T1DM

A
  • Insulin dependent diabetes mellitus
  • age of onset : usually younger, lean patients but can occur at any age
  • LADA- latent autoimmune diabetes of adults (form of T1DM) - slower progression to insulin dependence in later life
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14
Q

LO: underlying pathophysiology of T1DM?

What autoimmune diseases are associated and which specific antibodies?

Is it all genetics?

What % of patients w t1dm?

A
  • Autoimmune T cell destruction of Beta cells in the islets of langerhans
  • Pancreatic Beta cells do not release insulin, cannot act on insulin receptors
  • Blood glucose remains elevated - no blood glucose transported to liver, brain, muscle or adipose tissue
  • glucagon becomes activated
  • Associated conditions:
    • Coeliac disease
    • Thyroid disease
    • 80% of patients carry HLADR3 +/- DR4 (gene complex found on chromosome 6 - part of immune response system)
    • concordance of only 30% of identical twins - indicating environmental trigger
  • T1DM - accoutns for approx 10% of all cases
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15
Q

How does T1DM commonly present?

A
  • Asymptomatic = rare!
  • Mild - moderate disease - present 70% –> fatigue, polyuria, polydipsia and weight loss
  • severe (30%) : diabetic ketoacidosis
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16
Q

What are the NICE diagnostic guidelines for T1DM?

A
  • Adults presenting with hyperglycaemia (random venous plasma glucose concentration > equal to 11.1 mmol/l) and typical presentation of:
    • ketosis (raised ketone bodies in tissues)
    • rapid weight loss
    • age below 50 yrs
    • BMI below 25kg/m2
    • personal +/- FH of autoimmune disease
  • Do not discount a diagnosis of T1DM if an adult presents with a BMI of 25kg/m2 or above OR 50 years and above
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17
Q

What leads to the signs and symptoms of T1DM?

A
  • Loss of insulin secretion
  • Cannot uptake glucose into cells
  • Cannot store glucose as glycogen
  • Unopposed glucagon action (physiological fasted state)
  • Glycogenolysis and gluconeogenesis (e.g. from free fatty acids)
  • Unopposed hyperglycaemia
  • Metabolic derangement –> signs and symptoms
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18
Q

Explain the pathphysiology underlying the common symptoms of T1DM

A
  • Polyuria:
    • hyperglycaemia leads to glycosuria (excretion of glucose within the urine, filtered load excess capacity for reabsorption of glucose)
    • Glucose in urine inhibits the kidne’s concentrating ability
  • Polydipsia:
    • Physiological response to dehydration to maintain fluid balance
    • High blood glucose also stimulates thirst response directly
  • Weight loss:
    • unopposed lipolysis and proteolysis for gluconeogenesis precursors
    • Starvation in the face of plenty
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19
Q

How can we manage T1DM?

A
  1. Conservative
    • MDT
    • monitoring - 4 c’s
    • lifestyle modifications
  2. medical - insulin
  3. surgical
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20
Q

Who is part of the MDT for diabetes care? what roles

A

GP: monitoring in community, medication review, patient education especially on alcohol (calorific) and precontraception (risk to mother and fetus), hypoawareness and response, DVLA advice

Endocrinologist and diabetic specialist nurse: outpatinet monitoring, review for complications (DKA, podiatry, opthalmologist, foot ulcers) medication review

Psychologist - need phobia, fear of wieght gain, transition clinics for adolescents –> adult

dietician - DAFNE (dose adjustment for normal eating) - motivated patients can self manage theur dose, structured programme to stabilist blood glucose and lower complications.

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21
Q

Monitoring T1DM

A

1) Control (glycaemic)

  • Capillary blood glucose monitoring
  • HbA1C (control over 2-3 months)
  • hypoawareness
  • BP control, lipids

2) Competency

  • with insulin injections
  • checking insulin sites - Lipodystrophy (abnormal accumulation of fat tissue- both fat loss and abnormal accumulation)
  • checking their own BM

3) Coping

  • Psychosocial - depression
  • Occupation - driver?

4) Coping

  • Of treatment
  • Of unopposed hyperglycaemia
22
Q

What is the underlying pathophysiology that can lead to complications in DM?

A
  • Unopposed hyperglycaemia –> metabolic derangement —> signs and symptoms –> Complications:
  • 1) microvascular: retinopathy, nephropathy, neuropathy
  • 2) macrovascular: cardiovascular, CAD, cerebrovascular - stroke, peripheral vascular disease
23
Q

How do we monitor for complications of diabetes?

A
  • BP control - aim for tighter control of 135/80
  • renal disease - urine dip for proteinuria (use ACE-i inhibit RAAS regardless of BP - renoprotective)
  • cholesterol checks
  • eye checks (retinopathy, cataracts)
  • foot checks - ulcer, sensory neuropathy
24
Q

What lifestyle modifications can be made in diabetes?

A

DELAYS

Dietary changes - calorie intake

Exercise

Lipids

reduce Alcohol intake

Yearly check up (if stable with clinician)

Smoking cessation

25
Q

What is the medical management of diabetes?

A
  1. Basal Bolus regime
    • 2 metabolic states –> Absorptive state -store energy (insulin) and Post absorptive states –> use energy (glucagon)
    • Goal of insulin is to mimic physiological changes - 3 meals a day, insulin after a meal peaks
    • hence give a basal regime and then bolus during a meal
26
Q

How is insulin administered?

A
  • Subcutaneously usually - basal bolus regime is preferred (peptide hormone therefore would be broken up by stomach acid)
  • Many types and delivery devices vary - can be difficult to prescribe
27
Q

What are the different types of insulin that could be prescribed?

A
  • Rapid-acting:
    • (Lispro, novorapid) reaches the blood within 15 minutes after injection
    • Peaks 0-30 minutes later and may last as long as 5 hours
    • given as bolus pre meal
  • Short acting:
    • ​(Actrapid) insulin reaches blood w/in 30 mins post injection. Peaks 2-4 hrs later, remains in blood 4-8 hrs
  • Intermediate acting:
    • ​(NPH/ isophane insulin) reach the blood 2-6 hours afer injection. peaks 4-14 hours later and stay in the blood for 14-20 hours.
  • Long acting:
    • (Glargine-Lantus, Levemir) insulin takes 6-14 hours to start working. It has no peak or a very small peak 10-16 hours after injection. It stays in the blood between 20-24 hours.
    • Pre-mixed- Humalog Mix 50:50
    • given as basal insulin in basal bolus regime
  • Note –> can give IV insulin if soluble. (Actrapid)
28
Q

What is an insulin pump and when is it indicated?

A

Insulin pump is an insulin resevoir and provides continuous subcutaneous insulin infusion therapy. (Rapid acting insulin)

It is indicated in patients who have poorly controlled blood glucose despite optimum medical treatment.

6% of adults with T1DM

19% of children with T1DM

Is offered to T2DM on case-case basis (specialist review)

29
Q

What is the medical management for a type 1 diabetic patient that is feeling unwell and eating less?

A
  • Regime of choice for T1DM: ultiple daily injection basal- bolus insulin regimens, rather than twice-daily mixed insulin regimens
  • sick day rules:
    • ​Illness increases insulin requirements despite a reduced food intake
    • stress response leads to increased release corticosteroids –> hyperglycaemic state
    • check BM more often –> may need to increase insulin
    • Consider admitting if vomitng, dehydrated, pregnant or young
30
Q

Outline the medical management of T1DM patients

A

Aim: support adults with T1DM to aim for a target HbA1c level of 48 mmol/mol or lower, AND to minimise the risk of long term vascular complications

Regimen of choice: multiple daily injection basal-bolus insulin regimen

follow sick day rules previously described

patient alert cards

Look out for associated illness: markers of coeliac disease, autoimmune disease (pernicious anaemia, addisons, thyroid disease)

31
Q

What are the surgical options for T1DM?

in which patients is this indicated?

A
  • Islet and or pancreas transplantation
  • Surgical management indicated for patients with:
    • recurrent severe hypoglycaemia that has not responded to other treatments
    • Suboptimal diabetes control who have had a renal transplant and are currently on immunosuppressive therapy.
32
Q

Patient case: 3 months after a patient has been diagnosed with T1DM they present to ED unwell and “sleepy”.

HPC: Abdominal pain and vomiting over last 24 hours

Just started university, been drinking this weekend

PMH: Newly diagnosed T1DM

Meds: Insulin: basal- bolus regime, Lantus 12 units, Novorapid 3 units w each meal.

Obs: BP 100/72, HR 118 bpm, regular, RR 32 with kussmaul breathing, spo2 97% on RA, T = 36.9.

A

Treat A-E approach: A (speaking but drowsy) B (equal air entry, RR32, kussmaul breathing as attempt to blow off C02 )

C - BP 100/72, heart sounds norm, HR 118, dry mucous membranes, cool peripheries

D- Alert to voice, BM: Hi urine ketones +++

E- no rash, trauma, abdo exam tender throughout no focal tenderness, guarding, soft

ABG shown - metabolic acidosis with respiratory compensation. Glucose and lactate also elevated- some damage to end organs.

33
Q

What are the three requirements for diagnosis of Diabetic ketoacidosis?

A

D - diabetic - BM > 11.1 (can be normal in pregnancy or alcoholics)

K- ketonaemia (blood ketones >= 3 or urine ketones >= 3+

A- acidosis pH < 7.3 or bicarb <=15

34
Q

What investigations would be done for a patient with suspected DKA?

A

Bedside:

  • Capillary glucose, capillary ketones
  • ABG (if Spo2 < 94% on RA) but VBG is preferable for monitoring
  • ECG: tachyarrhythmias (K+ can be deranged), exclude MI (can precipate DKA)
  • Urine dip: ketones +++ (do bHCG in females)
  • Bloods: FBC, U&E, LFTs, CRP, lab glucose, amylase
  • Hourly glucose, ketones monitoring
  • 4 hrs lab glucose and U&E
  • Imaging: CXR to exclude source of infection
  • Blood cultures if febrile
35
Q

What is the pathophysiology behind ketoacidosis?

A
  • Ketones are produced as an alternative energy source (due to lack of insulin action, body’s response is increased glucagon action thinking it is in starvation)
    • ​product of fatty acid metabolism
    • 3 main ketone bodies: Acetone (pear drop breath), acetoacetate, B hydroxybutryrate (is what is measured)
  • This can lead to acidaemia –> Diabetic ketoacidosis
  • A medical emergency almost exclusively in T1DM
36
Q

How does ketoacidosis present?

A
  • Presents with:
    • Signs of shock from severe dehydration
    • high RR - to blow off acid
    • Abdominal pain - can be severe
    • can be first presentation of patient without known T1DM (25%)
    • often preceded by other acute illness or insulin omission e.g. with alcohol intake
37
Q

What is the management of DKA?

A
  • Cardiac monitor on high dependency unit
  • Fluid resucitation - fluids bolus of 0.9% normal saline if BP < 90 mmHG, 1L in 1hr, 1L in 2 hrs x 2, 1L in 4 hours x 2
  • Fixed rate insulin infusion (FRII) : depends on weight - 0.1 units of soluble insulin per kg/hr IV
  • potassium replacement (as insulin drives K+ into cells)
  • continue long acting insulin (levemire, Lantus)
  • Look for precipitants:
    • Infection
    • Infarction
    • Iatrogenic: omitting insulin, surgery/ trauma
    • undiagnosed T1DM
38
Q

What is the AIM of treatment of DKA?

A
  • Reduction of ketones and BM/ glucose
  • Correction of acidosis
  • Restore volume deficit
  • Treat precipitants
  • If not improving - check equipment, increase insulin rate, review diagnosis or escalate
39
Q

Who are high risk patients with DKA?

When should you involve ITU?

When is DKA resolved?

A
  • extremes of age - young 18-25 yrs, elderly (young are prone to cerebral oedema)
  • pregnancy
  • clinical shock
  • renal and cardiac patients
  • consider involving ITU: if high risk patient e.g. shock, ketones > 6, pH< 7.1, GCS < 12, initial K < 3.5 mmol/L
  • DKA is resolved if ketons < 0.6 and pH > 7.3
40
Q

For the previous patient case explain the A-E approach - what treatments would you start?

A
41
Q

What are causes of recurrent DKA?

A
  • Insulin technique and sites
  • carb counting
  • alcohol
  • pregnancy
  • psychological and psychsocial difficulties - body image, needle phobia
  • nature of lifestyle
  • possible organic causes -gastroaparesis (not absorbing food properly)
  • iatrogenic causes e.g. surgery
  • manage in MDT- educate and negotiate care plan
42
Q

Define T2DM:

previous name

age of onset

genetic type of T2DM

who does it commonly affect?

A

T2DM: previously called NIDDM - prevalent and “epidemic” due to changes in lifestyle and improved longevity

Age of onset –> greater than 40 yrs, BUT teenagers are increasingly developing T2DM.

Genetic type: MODY - mature onset diabetes of the young, rare autosomal dominant T2DM affecting young with FH

Commonly affects men, especially asians (indian, pakistani, bangladeshi and sri lankan populations)

43
Q

What is the cause of T2DM?

A

Caused by an insulin resistance by the insulin receptors in the liver, muscle, brain and adipose tissue.

Beta cells initally raise insulin secretion in an attempt to compensate, this eventually reduces significantly and blood glucose remains elevated.

Eventually: Increased insulin resistance and reduced insulin secretion

44
Q

What patients may be affected by T2DM?

What is the genetic concordance like in T2DM?

A

Obese

sedentary

calorie excess

cushing’s

exogenous steroids, PCOS

Genetics: 80% concordance in identical twins, indicating stronger genetic influence than T1DM, heterogenous condition

45
Q

How does T2DM typically progress?

A

Typically progresses from preliminary phase of impaired fasting glucose or impaired glucose tolerance - window of opportunity.

46
Q

How does T2DM typically present?

A
  • Associated with complex metabolic derangement:
    • central/ visceral obesity
    • dyslipidaemia
    • other cardiac risk factors (HTN)
  • Asymptomatic: commonest - routine screening
  • mild-moderate: common: fatigue, vague symptoms, increased infections, poor wound healing, blurred vision
  • severe: 2% hyperosmolar hyperglycaemic state (HHS) (rare!)
47
Q

What is hyperosmolar hyperglycemic state?

A
  • Rare complication of T2DM
  • mortality rate of 8- 20%
  • hyperglycaemia is driving force (BM often > 40 mmol/l)
48
Q

How would a patient in hyperosmolar hyperglycaemic state present?

A
  • Fatigue and weight loss (unable to use glucose)
  • polyuria, thirst, signs of dehydration - osmotic diuresis secondary to hyperglycaemia
  • leads to increase in concentration of solutes
  • altered mental states- frequent, obtunded, COMA
  • T2DM’s version of starvation/ DKA, BUT insulin IS present- therefore ketone production is reduced.
  • TX –> ITU/Senior escalation, IV fluids, IV insulin
49
Q

What are the modifiable risk factors for T2DM?

A
  • Overweight or obese - BMI > 25kg/m2
  • Central obesity
  • Lack of physical activity/ exercise
  • smoking
  • poor diet
  • high saturated fat
  • low fibre
  • low SE status
50
Q

What are the non modifiable RF for T2DM?

A
  • Age . 40 yrs OR age > 25 yrs if south asian origin
  • Fam hx
  • ethnicity - black african or south asian
  • hx of gestational diabetes of baby . 4.5 kg at birth
  • Impaired glucose regulation - IGT, IFG (prediabetes) or non diabetic hyperglycaemia
  • hx of mental health conditions or use of antipsychotic medications
  • hx of HTN/CV disease or stroke
  • Low birth weight
  • PCOS
51
Q

What are the complications of T2DM? (same as t1dm)

A
  • Microvascular:
    • retinopathy
    • neuropathy
    • nephropathy
  • Macrovascular:
    • ischeamic heart disease
    • cerebrovascular disease
    • peripheral vascular disease
52
Q

What is the management of T2DM?

A
  • Conservative management same: lifestyle modification (DELAYS), MDT, monitoring (4C’s)
  • medical management:
    • oral hypoglycaemic agents:
      • decrease hepatic gluconeogenesis - BIGUANIDES (Metformin) (also increase insulin sensitivity and reduces glucagon effect)
      • increase insulin secretion - sulfonylureas (gliclazide) (work on K+ channels in pancreatic B cells, warning can cause hypoglycaemia)
      • reduce insulin resistance - thiazolidinediones
      • prevent breakdown of GLP - DPP4 inhibitors
      • promote glycosuria - SGLT2 inhibitors
      • decrease carbohydrate absorption - alpha glucosidase inhibitior
    • Injectable agents:
      • GLP1 analogues (Glucagon like peptide - enhances insulin secretion)
      • Insulin
  • Surgical management: often treat vascular complications e.g. amputations

CCE2: Medicine Block (20 decks)

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