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203: Theme 1 - 304 - Endocrinology > Long and Short term effects of Diabetes + Psychology > Flashcards

Long and Short term effects of Diabetes + Psychology Flashcards

1
Q

What is Diabetic Keto-acidosis?

  • describe the pathogenesis
A
  • this is a diabetic emergency that presents with
    • hyperglycaemia
      • due to insulin deficiency –> glycogenolysis
    • Dehydration
      • osmotic diuresis - the osmotic force of unreabsorbed glucose holds water in tubules
    • high anion gap metabolic acidosis
      • due to the dissociation of ketone bodies into hydrogen ion and anions
    • and ketonaemia
      • hyperglucagonaemia –> decreases malonyl co A production and increases carnitine palmitoyltransferase I –> free fatty acids are converted to ketones rather than triglycerides
  • this is mostly associated with T1DM (increasing prevalence in T2DM)
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2
Q

What are the precipitating events that lead to a DKA?

A
  • Infection (30-40%)
  • New-onset diabetes (25%)
  • Inadequate insulin treatment or non-compliance (20%)
  • MI/ Stroke
  • Acute Pancreatitis
  • Trauma
  • Drugs: clozapine/olanzapine, cocaine, lithium, terbutaline
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3
Q

Describe the physiological effects insulin deficiency has on adipose tissue

A
  • Increased lipolysis and reduced esterification of fat due to
    • Insulin deficiency
    • Glucagon/adrenaline excess
    • Results in excess FFA and glycerol from breakdown triglycerides
  • FFA substrate are used for hepatic synthesis of ketone bodies
    • Acetoacetate/Hydroxybutyrate – strong organic acids (Acetone)
    • Rate of ketogenesis is linked to rate of gluconeogenesis
  • Muscle and brain can utilise ketones as main energy substrate
  • Ketoacidosis results when ketone body production exceeds rate of utilisation in peripheral tissues (brain and muscle) and renal clearance
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4
Q

What compensatory mechanisms does the body take to manage acidosis?

A
  • Intracellular buffering - H+ / K+ exchange
    • Potassium hydrogen ion pump
  • Respiratory compensation – hyperventilation
    • H+ stimulates respiratory centres
    • Breathe off CO2 (H+ + HCO3- H2O + CO2)
  • Renal excretion of H+ (slow response)
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5
Q

Give a clinical overview of DKA

  • Age:
  • Precipitating causes:
  • Serum sodium:
  • Blood glucose:
  • Serum bicarbonate/pH:
  • Serum ketones:
  • Mortality:
  • Subsequent course:
A
  • Age: Mostly young T1DM
  • Precipitating causes: Relative or absolute insulin deficiency
  • Serum sodium: Normal or low
  • Blood glucose: Usually <40mmol/l
  • Serum bicarbonate/pH: <14mmol/l / pH<7.3
  • Serum ketones: high +++++
  • Mortality: 5% depending on age
  • Subsequent course: Insulin dependent
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6
Q

What are some symptoms and signs of DKA?

  • what causes these?
A
  • Thirst and polyuria | Weakness and malaise | Drowsiness, confusion
    • caused by Hyperglycaemia + dehydration, seen via
      • Dry mouth, Sunken eyes, Postural or supine hypotension, Hypothermia & Coma
  • Nausea and vomiting | Abdominal pain | Breathlessness
    • caused by Acidosis seen via
      • Facial flush, Hyperventilation, Smell of ketones on breath and ketonuria
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7
Q

What is the management plan for DKA?

  • 5 steps
A
  1. Confirm diagnosis and check for precipitating causes
  2. Rehydrate & monitor fluid balance
    • Iv fluids - saline with added potassium
    • Consider urinary catheter
  3. Lower glucose
    • Intravenous insulin – fixed-rate 0.1Unit/kg/hr
  4. Monitor electrolytes
    • Potassium (and sodium)
  5. Prevent clots
    • Prophylactic low molecular weight heparin
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8
Q

Apart from the 5 management steps what else needs to be considered in treating DKA?

A
  • Is the patient conscious?
    • assess GCS –> potentially call ICU
  • Are they at risk of aspiration?
    • consider NG tube
  • Recovery needs to be monitored regularly
    • Glucose, ketones, pH, potassium - hourly
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9
Q

What is Hyperosmolar Hyperglycaemic State (HHS)?

-

A
  • similar to DKA caused by insulin deficiency and glucagon excess however there is
    • little or no ketoacid accumulation
    • serum glucose conc. often exceeds 50mmol/ L
    • plasma osmolality may reach 280mosmol/kg
    • neurological abnormalities are frequently present
  • there is enough insulin to present lipolysis but not enough to allow appropriate levels of glucose utilisation
    • hence no ketonacids accumulating
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10
Q

Give an overview of the clinical features for HHA (HONK)?

  • Age:
  • Precipitating causes:
  • Serum sodium:
  • Blood glucose:
  • Serum bicarbonate/pH:
  • Serum ketones:
  • Mortality:
  • Subsequent course:
A
  • Age: usually >40yrs
  • Precipitating causes: previously undiagnosed, steroids, diuretics, sugar
  • Serum sodium: usually high
  • Blood glucose: often >40mmol/l
  • Serum bicarbonate/pH: normal/ pH 7.4
  • Serum ketones: 0
  • Mortality: 30% (thromboses)
  • Subsequent course: Diet/tablet controlled
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11
Q

What is the management plan for HHS?

  • 5 key points
A

Correct the profound dehydration

  1. Confirm diagnosis and check for precipitating causes
  2. Rehydrate & monitor fluid balance
    • Iv fluids - saline with added potassium
    • Consider urinary catheter
  3. Lower glucose (once glucose not improving with fluids)
    • Intravenous insulin – fixed rate 0.05Unit/kg/hr
  4. Monitor electrolytes
    • Potassium (and sodium)
  5. Prevent clots
    • Treatment low molecular weight heparin
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12
Q

What is Hypoglycaemia?

A
  • Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but is often used to describe a clinical state.
  • The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopenic’.
  • Can be classified as
    • Asymptomatic: awake, sleeping
    • Mild symptomatic
    • Severw symptomatic
    • Coma and convulsions
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13
Q

What are symptoms of Hypoglycaemia?

  • autonomic
  • neuroglycopenic
A
  • Autonomic – sympathomedullary activation
    • Sweating, feeling hot
    • Trembling or shakiness
    • Anxiety
    • palpitations
  • Neuroglycopenic
    • Dizziness, light-headedness
    • Tiredness
    • Hunger, nausea
    • Headache
    • Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism
    • Coma and convulsions, hemiplegia
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14
Q

What are the causes of Hypoglycaemia?

A
  • Insulin
    • excessive doses
    • not eating or insufficient CHO
  • Sulfonylureas (diabetes medication)
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15
Q

What is the treatment for minor hypoglycaemic episodes?

A
  • 20g CHO as a sugary drink, fruit juice, glucose tablets, glucose gels
    • followed by something ‘starchy’ to eat
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16
Q

What is the treatment of a hypoglycaemic coma?

A
  • IM or IV glucagon 1mg
  • IV dextrose 25g (150ml 10% glucose)
17
Q

What are the types of long term complications that accompany diabetes?

  • Microvascular
  • Macrovascular
A

Microvascular

  • Retinopathy
  • Nephropathy
  • Neuropathy

Macrovascular

  • IHD
  • CVD
  • PVD
18
Q

What can be seen through pathological investigations in those presenting with Diabetic retinopathies?

A
  • Loss of pericytes
  • Basement membrane thickening
  • Capillary closure
  • Ischaemia
    • Vascular endothelial growth factor (VEGF) production
    • Increased capillary permeability, due to hyperglycaemia increasing mean arterial pressure
19
Q

What are the clinical stages of Retinopathy?

A
  • Non-proliferative
    • background
    • pre-proliferative
  • Proliferative
  • Macular Oedema
    • sight-threatening
    • non-sight threatening
20
Q

Explain Background Retinopathy (R1)

A
  • death of retina pericytes, thickening of the retinal basement membrane –> impairment of function
  • this is associated with the formation of microaneurysms and increased vascular permeability
    • leads to the leakage of hard exudate (proteinaceous material)
  • vascular occlusion and rupture may be caused by preceding cycles of cell death and renewal involving
    • intraluminal proliferation
    • changes in platelet function
    • erythrocyte aggregation
    • high plasma fibrinogen levels
21
Q

Explain Preproliferative Retionpathy (R2)

A
  • Intraretinal microvascular abnormalities (IRMAs): these are dilated capillaries that occur in response to retinal ischaemia
  • This is the occurrence of intraretinal infarcts - cotton wool spots or soft exudate - distal to the microvascular occlusion
  • further growth of the endothelial cells of retinal veins –> venous calibre abnormalities
    • venous bleeding
    • loops and dilation
22
Q

Explain Proliferative Retinopathy (R3)

A
  • continuous microvascular occlusion and retinal ischaemia –> increased release of vaso-proliferative substances
    • IGF-1 and VEGF (vascular endothelial growth factor)
  • ​these factor promote neo-vascularization, forming mesh of fibrous tissue connecting them.
  • New vessel formation is associated with the following risk
    • ​Pre-retinal or vitreous haemorrhage: due to fragility
    • Retinal detachment: with new vessel maturation the fibrous component becomes more prominent resulting in contraction/ detachment from the choroid
  • new vessel formation can also occur on the surface of the iris or the interior chamber –> glaucoma by blocking the outflow of the virtuous humour
23
Q

What pathology is this?

A
  • Vitreous haemorrhage
  • due to new arteries and veins being fragile and prone to rupture
24
Q

What pathology is this?

A

diabetic maculopathy with haemorrhages and circinate exudates

  • associated with a best visual acuity of 6/12 or less
25
Q

Explain what Maculopathy is

A
  • this is when there are exudates within one disc diameter of the centre of the fovea
  • microaneurysms or haemorrhage within one disc diameter of the centre of the fovea associated with visual acuity of 6/12 or less
  • retinal thickening within one disc diameter of the centre of the fovea
26
Q

What is Macular Oedema?

  • presenting
  • exams to confirm
A
  • retinal thickening due to leaky blood vessels - can develop at any stage of retinopathy
  • presents with gradual onset of blurring of near and distant vision
  • referred to an ophthalmologist for
    • slit-lamp examination: detects thickening
    • fluorescein angiography: detects local leakage associated with oedema
27
Q

What measures can be taken to reduce the risk and progression of Retinopathies?

A
  • Glycaemic control
    • lowering HbA1c: 1% decreases reduces risk by 37%
  • Controlling blood pressure
    • Lisinopril (ACE inhibitor): used in normotensive T1DM patients was seen to be effective in reducing the progression of retinopathy
  • Multifactorial lifestyle change (diet, therapy, exercise, smoking cessation etc.)
  • Fenofibrate therapy + Antiplate agents show some efficacy, further study needed
  • Regular screening needed in pregnancy due to increased risk
28
Q

What treatment is there for established retinopathy?

A
  • Laser Photocoagulation
    • only advised for more advanced retinopathy except in treating macular oedema
    • reduces the risk of visual loss, needs aggressive monitoring and treatment
  • Inravetriol steroids
    • used to treat macular oedema, repeated injections usually necessary
  • Vitrectomy
    • used to preserve useful vision
    • followed by removal of the vitreous humour and photocoagulation can restore some functional vision
  • Growth factor inhibitors
    • VEGF inhibitors
29
Q

What is Diabetic Neuropathy?

  • types of neuropathy
A
  • this is caused by the loss of myelinated and unmyelinated nerve fibres due to vascular and metabolic factors that impair nerve repair mechanisms

They include

  • Peripheral neuropathy
  • Mononeurotherapy
  • Autonomic neuropathy
30
Q

How does Peripheral neuropathy present?

  • what are other signs it presents with
A
  • distal sensory loss or paraesthesia
    • a sensation of numbness, tingling, burning, or sharpness
    • this starts at the feet and spreads proximally
  • some patients experience neuropathic pain,
    • usually at night and in the lower extremities
  • Signs: loss of the following sensations
    • pinprick sensations
    • temperature
    • vibration
    • joint position
    • with diminished ankle reflexes
31
Q

What is the presentation of Mononeuropathy

A
  • motor weakness in a single cranial or peripheral nerve
    • III, IV, VI, VII,
    • median, ulnar, peroneal nerve
  • most common is ptosis and ophthalmoplegia
    • due to cranial nerve III palsy
  • may present with mononeuropathy multiplex
32
Q

How does Autonomic Neuropathy present itself?

A
  • due to longstanding diabetes that leads to dysfunction involving the cholinergic, noradrenergic and peptidergic system
  • Cardiovascular
    • postural hypotension
    • resting tachycardia
  • Gastrointestinal
    • gastroparesis (delayed gastric emptying)
      • may present with anorexia, N&V early satiety, bloating
    • diarrhoea or constipation
    • gustatory sweating
  • ​​Genitourinary
    • bladder dysfunction, incontinence
    • recurrent UTI
    • erectile & female dysfunction, reduced libido
  • Hyperhidrosis & anhidrosis
33
Q

What are the pathological findings of those with Diabetic Nephropathy?

A
  • Basement membrane thickening
    • Loss of negative charge
  • Podocyte loss
    • Loss of integrity of the filtration barrier
  • Glomerular sclerosis
  • Mesangial expansion
34
Q

What are the clinical stages of Diabetic Nephropathy?

  • dipstick tests
35
Q

How can Diabetic nephropathy be treated or it’s progression reduced?

  • ABCD
A
  • ACE inhibitor and ARBs
    • ACE inhibitors decrease microalbuminuria and hence risk of developing proteinuria in T1 +2 DM
  • Blood pressure control
  • Control of glycaemia
  • Diet: protein restriction
36
Q

What is Diabulimia?

  • aetiology
A
  • Insulin omission
    • seen in 40% of T1 adolescents
  • poorer outcomes fro diabulimia
  • due to secondary and scute risk of DKA
  • can be hours away from fatality even if they don’t appear obviously unwell
37
Q

What are the signs of Diabulimia?

A
  • Symptoms of untreated diabetes
  • Severe Fluctuations in weight/ Severe weight loss/Rapid weight gain/anorexic BMI
  • Fear of injecting or extreme distress at injecting
  • Co-occurrence of depression, anxiety or other psychological disturbance such as Borderline Personality Disorder
  • Anxiety/ distress over being weighed at appointments
  • Frequent Requests to switch meal plans
  • Encyclopaedic knowledge of carbs

in serious conditions, they should be handled by a MDT + MH services

38
Q

What is the physical and psychological effect of diabetes on sex?

A
  • Due to microvascular damage there is
    • loss of sensation
    • vaginal dryness & erectile dysfunction
      • 35-70% of men, 33% of women
  • Psychological damage
    • fear of hypos during sex
    • body image & devices
    • shame

203: Theme 1 - 304 - Endocrinology (15 decks)

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