diabetes type 1 Flashcards

1
Q

explain the pathology behind type 1 diabetes?

A
  • pancreas stops being able to produce adequate insulin
  • glucose isn’t taken up into cells so they think there’s no glucose available
  • however, glucose levels in blood keep rising causing hyperglycaemia
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2
Q

what does type 1 diabetes present with?

A
  • classical triad of symptoms of hyperglycaemia ( polyuria, polydipsia, weight loss)
  • diabetic ketoacidosis
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3
Q

whats the underlying cause of type 1 diabates?

A

unclear
certain viruses may trigger it

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4
Q

whats the ideal blood glucose concenration?

A

4.4-6.1mmol/L

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5
Q

what process does insulin cause?

A

glycogenesis

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6
Q

what process does glucagon cause?

A

gluconeogenesis

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7
Q

explain the role of glucagon in glucose metabolism?

A
  • alpha cells - islets of langerhans
  • catabolic
  • released in response to low blood glucose and stress
  • tells liver to break down glycogen and releases it into the blood as glucose - glycoenolysis
  • also tells liver to convert proteins and fats into glucose - gluconeogenesis
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8
Q

explain the role of insulin in glucose metabolism?

A
  • hormone
  • beta cells - islets of langerhans
  • anabolic
  • reduces blood sugar in 2 ways
  • causes bodily cells to absorb glucose
  • causes cells to store it as glycogen
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9
Q

explain the role of ketones in metabolism?

A
  • released when low glucose stores
  • made by the liver
  • made from long chain fatty acids
  • water soluble
  • can cross blood-brain barrier
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10
Q

how can ketone levels be measured?

A
  • urine - dipstick test
  • blood - ketone meter
  • acetone smell breath
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11
Q

what is the most common scanario for diabetic ketoacidosis to occur?

A
  • type 1 diabetes
  • type 1 diabetic with other illnesses eg infection
  • type 1 diabetic who isnt sticking to their insulin regeime
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12
Q

what are the 3 key features for diabetic ketoacidosis?

A
  • ketoacidosis
  • dehydration
  • potassium imbalance
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13
Q

the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the ketoacidosis is present?

A
  • without insulin body cells dont recognise glucose even tho its there in the blood
  • liver will then start to produce ketones
  • the kidney produces bicarb to buffer these but they get used up making the blood acidic
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14
Q

the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the dehydration is present?

A
  • hyperglycaemia overwhelmes the kidneys
  • glucose leaks into the urine
  • this pulls water with it
  • causes polyuria and polydipsia
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15
Q

the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the potassium imbalance is present?

A
  • insulin normally drives potassium into cells
  • no insulin so little potassium in cells
  • blood potassium can either be high or normal bc the kidneys balance it
  • however total body potassium is low because it isnt in cells
  • patients develop hypokallaemia v quickly qhich can lead to arrhythmias
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16
Q

what is the pathophysiology of diabetic ketoacidosis?

A
  • hyperglycaemia
  • dehydration
  • ketosis
  • diabetic acidosis (with a low bicarb)
  • potassium imbalance
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17
Q

what are the symptoms of diabetic ketoacidid?

A
  • polyuria
  • polydypsia
  • nausea and vomitting
  • acetone smelling breath
  • dehydration
  • weight loss
  • hypotension
  • altered consciousness
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18
Q

what is the diabetic ketoacidosis diagnosing criteria?

A
  • hyperglycaemia - blood glucose over 11mmol/L
  • ketosis - blood ketones above 3mmol/L
  • acidosis - PH below 7.3
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19
Q

what are the most dangerous parts of diabetic ketoacidosis and therefore what is the treatment priority?

A
  • dangerous - dehydration, potassium imbalance, acidosis
  • priority - fluid resuscitation - insulin infusion
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20
Q

what are the principles of management and whats the nemonic?

A

FIG-PICK
F - fluids - IV fluid with normal saline - 1L in the first hour followed by 1L every 2 hours)
I - insulin - fixed rate insulin infusion
G - glucose - add glucose when less than 14mmol/L
P - potassium - ass potassium to IV
I - infection - treat underlying infections
C - chart fluid balance
K - ketones - monitoe blood ketones, PH and bicarb

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21
Q

what must you ensure is true before stopping the insulin and fluid infusions?

A
  • ketones and acidosis should have resolved
  • they should be eating and drinking
  • they should have started their regular subcutaneous insulin
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22
Q

what are the key complications during treatment?

A
  • hypoglycaemia
  • hypokalaemmia
  • cerebral oedema
  • pulmonary oedema
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23
Q

what can be used to assess if a patient has type 1 or type 2 diabetes?

A

autoantibodies and serum-c peptide

autoantibodies present in a type 1 diabetic are:
- anti-islet cell antibodies
- anti-GAD antibodies
- anti-insulin antibodies

serum-c peptode is a measure of insulin production - if lots then lots

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24
Q

what components are involved in the long-term management of type 1 diabetes?

A
  • subcutaneous insulin
  • monitoring dietary carbohydrate intake
  • monitoring blood sugar levels upon waking, at each meal, and before bed
  • monitoring for and managing complications, both short and long term
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25
Q

what are the different ways of managing insulin artificially?

A
  • basal-bolus reegime
  • insulin pumps
  • pancreas/islet transplant
  • monitoring
  • closed-loop system
26
Q

explain what the basal-bolus regime is?

A

combo of:
- background, long acting insulin injected once a day
- short-acting insulin inhjected 30 mins before consuming carbs

27
Q

what is the issue with always injecting into the same spot?

A
  • lipodystrophy - subcutaneous fat hardens and dont absorb insulin properly
  • cycle the injection sites
28
Q

explain what an insulin pump is and list the different types?

A
  • pumps that continuously infuse insulin at diff rates to control sugar levels
  • pushes insulin through a cannula
  • cannula replaced every 2-3 days

types:
tethered pump
patch pump

29
Q

what are the advantages and disadvantages of insulin pumps?

A

advantages:
- better blood sugar control than basal-bolus
- more flexibility with eating
- less injections

disadvantages:
- difficulties learning to use the pump
- having it attached all the time
- blockage of infusion set
- small risk of infection

30
Q

describe the differences between tethered and patch pumps?

A

tethered pumps:
- replacable infusion sets and insulin
- attached to patients belt
- controls of pump itself

patch pumps:
- on skin with no tubes visible
- replaced when insulin runs out
- remote controlled

31
Q

what does a pancreas transplant involve?

A
  • implanting a donor pancreas to produce insulin
  • original pancreas is left in place to produce digestive enzymes
  • carries significant risks and life -long immunosuppressio is required to prevent rejection
32
Q

what does islet transplantation involve?

A
  • donor islet cells into patients LIVER
  • cells will then produce insulin
  • patients still usually need insulin therapy after
33
Q

whats the role of HbA1c in measuring?

A
  • measures glycated haemoglobin
  • this is how much glucose is attached to the haemoglobin molecule
  • reflects the average glucose level over previous 2-3 months
  • measured every 3-6 months
34
Q

what are the different methods of glucose monitoring?

A
  • capillary blood glucose
  • flash glucose monitors
  • continuous glucose monitor
35
Q

what is a capillary blood glucose monitor?

A
  • finger prick test
  • can be measured using a blood glucose monitor
  • gives an immediate result
  • patients with type 1 and type 2 diabetes rely on these
  • self-monitoring
36
Q

what is the flash glucose monitor?

A
  • sensor on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue
  • 5-min lag
  • records at short intervals over time
  • need to swipe mobile phone over sensor
  • sensor needs replacing every 2 weeks
37
Q

what is the continuous glucose monitor?

A
  • similar to flash glucose monitor
  • don’t need to scan sensor - the results are sent over via bluetooth
38
Q

what is the closed loop system / artificial pancreas?

A
  • combo of continuous glucose monitor and insulin pump
  • the devices communicate to automatically adjust insulin based off the glucose readings
  • patients still need to input carb intake and adjust the system for exersize
39
Q

what are the short-term complications to immediate insulin and blood glucose management?

A
  • hyperglycaemia and diabetic ketoacidosis
  • hypoglycaemia
40
Q

what are the causes of hypoglycaemia?

A
  • too much insulin
  • not enough carbs
41
Q

what are the symptoms of hypoglycaemia?

A
  • hunger
  • tremor
  • sweating
  • irritability
  • dizziness
  • pallor
    severe:
  • reduced consciousness
  • coma
  • death
42
Q

how is hypoglycaemia treated?

A
  • rapid acting glucose
  • once it improves they consume slow acting carbs
  • severe: - IV dextrose and intramuscular glucagon
43
Q

how is hyperglycaemia treated?

A
  • doesnt acc nessasarily need treating
  • insulin takes a while to take effect and too much can cause hypoglycaemia
44
Q

what are the 3 main catagories of long term complications of chronic high blood sugar and why does this happen?

A
  • chronic high blood glucose causes damage to endothelial cells of blood vessels
  • causes them to become leaky
  • makes them unable to regenerate

catagories:
- macrovascular
- microvascular
- infection - related

45
Q

what are the macrovascular long-term complications?

A
  • coronary artery disease
  • peripheral ischemia
  • stroke
  • hypertension
46
Q

what are the microvascular long term complications?

A
  • peripheral neuropathy
  • retinopathy
  • kidney disease - nephropathy
47
Q

what are the infection-related long term complications?

A
  • urinary tract infections
  • pnemonia
  • skin and soft tissue infections, particularly in feet
  • fungal infections, particularly oral and vaginal candidiasis
48
Q

At what level of Beta cell destruction does hyperglycaemia develop?

A

80-90%

49
Q

At what level of blood glucose can it no longer be absorbed?

A

10mmol/L

Thirsty and develop polyuria - body attempts to remove excess glucose

50
Q

Diagnosis of T1DM (3)

A

Random blood glucose ≥11.1mmol/L
Fasting blood glucose ≥7mmol/L
HbA1c ≥ 48mmol/mol

  • One abnormal result in symptomatic patients is sufficient
  • Two abnormal results needed in asymptomatic patients on 2 different days
51
Q

Environmental factors that can increase the risk of developing T1DM (4)

A
  • Diet
  • Vitamin D deficiency
  • Early-life exposure to viruses associated with islet inflammation (eg: enteroviruses)
  • Decreased gut-microbiome diversity
52
Q

Epidemiology of T1DM (4)

A
  • Young (usually between 5-15 years)
  • Lean
  • North European descent
  • 10% of diabetes is type 1
53
Q

First line treatment for T1DM (2)

A

Basal-Bolus regimen of Insulin

Basal - Long acting (either given twice or once daily)
Bolus - Short acting before meals

54
Q

How can T1DM be differentiated from Latent Autoimmine Diabetes in Adults (LADA)? (2)

A
  • In LADA age of onset is >30 yrs
  • Low to normal C-peptide
55
Q

how does type 1 diabetes differ from monogenic diabetes?

A

In type 1 diabetes:
- C-peptide present
- Autoantibodies absent

56
Q

How can T1DM be differentiated from Neonatal diabetes?

A

neonatal occurs in first 6 months of life
due to genetic mutation - testing

57
Q

NICE diagnostic criteria for T1DM (6)

A
  • Clinical features and evidence of hyperglycaemia
  • Ketosis
  • Rapid weight loss
  • < 50 years
  • BMI < 25 kg/m2
  • Personal and/or family history of autoimmune disease
58
Q

Other autoimmune conditions that can result from T1DM (most to least common) (6)

A
  • Thyroid disease
  • Autoimmune gastritis
  • Pernicious anemia
  • Coeliac disease
  • Vitiligo
  • Addison’s disease
59
Q

Signs of T1DM (6)

A
  • BMI < 25kg/m2
  • Failure to thrive in children
  • Glove and stocking sensory loss
  • Reduced visual acuity
  • Diabetic retinopathy
  • Diabetic foot disease
60
Q

What is a Mixed insulin regimen? (3)

A
  • A mixture of short or rapid acting and intermediate-acting insulin
  • Twice daily
  • For those who can’t tolerate multiple injections for basal bollus
61
Q

what is continuous insulin for?

A
  • If patient has disabling hypoglycaemia
  • or persistently hyperglycaemic (HbA1c > 69mmol/mol) on multiple injection insulin therapy
62
Q

Which genes are linked with increased risk of developing T1DM? (4)

A

HLA-DR2 and HLA-DQ3
or
HLA-DR4 and HLA-DQ8