Diabetes Flashcards

1
Q

What is diabetes?

A

a chronic, metabolic disease of high glucose in the blood leading to damage to the heart, blood vessels, eye, kidneys and nerves

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2
Q

What is the epidemiology of diabetes?

A
  • 1 in 11 people have is
  • type 2 is most common
  • most likely in south asian population
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3
Q

What is the type of insufficiency in diabetes types?

A
  • absolute insufficient insulin = type 1

- relative insufficienti insulin = type 2

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4
Q

What are the main features of type 1 diabetes?

A
  • auto-immune
  • destructive insulitis
  • beta-cell failure with absolute insulin deficiency
  • specific antibodies aren’t helpful for childhood diagnosis
  • pre-school and peri-puberty
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5
Q

What are the main features of type 2 diabetes?

A
  • hyperinsulinaemia and insulin resistance
  • middle-aged or elderly and obese
  • can be microvascular disease at time of diagnosis
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6
Q

What is gestational diabetes?

A

diabetes diagnosed in the second or third trimester that wasn’t present before gestation

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7
Q

What are the other rarer types of diabetes?

A
  • MODY
  • pancreatic disease (CF)
  • endocrine disease (Cushing’s)
  • drug-induced diabetes
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8
Q

What is a normal blood glucose?

A

less than 6.1

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9
Q

What are the main symptoms of diabetes?

A
  • thirst
  • poluria
  • thrush
  • weakness fatigue
  • blurred vision
  • infections
  • signs of complications
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10
Q

What are the risk factors for type 2?

A
  • OBESITY
  • medications
  • PHx of MI/stroke
  • ethnicity
  • age
  • gestational diabetes
  • FHx
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11
Q

What is the criteria for testing for diabetes?

A

obesity and 2+ of

  • physical inactivity
  • PCOS
  • age
  • high HDL
  • CVD history
  • race
  • hypertension
  • 1st degrees relative
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12
Q

What does HbA1c measure?

A

glucose over the past 2-3 months

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13
Q

What are the main categories of complications in diabetes?

A
  • macrovascular: CVD and stroke

- microvascular: nephropathy, neuropathy and retinopathy

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14
Q

How is type 2 diabetes diagnosed?

A

by excluding type 1 and all other forms such as MODY

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15
Q

What is the risk of diabetes being in an affected patient’s children?

A

40%

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16
Q

What is ideal BMI?

A

23

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17
Q

What is the pathway from obesity to diabetes?

A

obesity and inactivity –> adiposity and increased free fatty acids –> insulin resistance

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18
Q

What happens to Beta cells in type 2 diabetes?

A

the vulnerable cells fail as they can’t respond and make more insulin

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19
Q

What is insulin resistance associated with?

A
  • hyperglycaemia
  • PCOS
  • hypertension
  • hyperlipidaemia
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20
Q

How does the presentation of diabetes differ between type 1 and 2?

A
  • type 1 is non-obese, all ages and DKA

- type 2 is slow onset (v occasionally DKA), middle-aged/elderly, obese

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21
Q

What is the ideal HbA1c?

A

less than 7% or 53mmol/mol

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22
Q

When are patients least likely to meet their HbA1c target?

A
  • female
  • young
  • obese
  • not at BP targets
  • many drug regimes
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23
Q

When is insulin given in T2DM?

A

when all other therapies fail and NPH insulin will be given to metformin

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24
Q

What is always done for patients with diabetes who are over 40 years?

A
  • prescribe a statin

- lower BP to 130/80

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25
Q

What are the nutrition aims for DM?

A
  • relieve acute symptoms
  • avoid extremes
  • maintain QoL
  • reduce micro and macrovascular complications
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26
Q

How much exercise is recommended?

A

150 minutes per week moderate to vigorous over 3 days

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27
Q

What are the main causes of hypo in T1DM patients?

A
  • missed meal
  • increased physical activity
  • too much insulin
  • alcohol
  • tight control
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28
Q

How can the risk of hypo be reduced?

A
  • carry emergency supply
  • check glucose regularly
  • don’t consume alcohol on an empty stomach
  • be aware of all the factors that affects blood glucose
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29
Q

What are the antibodies that are used in diagnosis of T1DM?

A
  • GAD
  • IA-2
  • ZnT8
    when these are all used together they are effective
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30
Q

What is a main marker used in diabetes?

A

C peptide will be very low in those with type 1 diabetes after 3 years as one is made for every molecule of glucose and comes from insulin being cleaved

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31
Q

What are all the contributions to the near perfect test for diabetes?

A
  • genetics
  • antibodies
  • BMI
  • age
  • C peptide
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32
Q

What are the main features of MODY?

A
  • non-insulin dependant
  • autosomal dominant
  • age of onset usually before 25
  • beta cell works but there is no insulin sensing
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33
Q

What are the types of MODY?

A
  • glucokinase: higher glucose from birth but stable, diet, rare complications, no treatment
  • transcription factors: progressive so originally normal, complications
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34
Q

What is the best treatment for transcription factor related MODY?

A

sulphonylureas

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35
Q

What is neonatal diabetes?

A
  • rare
  • baby requires insulin for first 3 months of life
  • can be transient so resolves in 12 weeks and returns in teenage years
  • can be permanent and life-long
36
Q

What can neonatal diabetes be treated with?

A

a sulphonylurea to close the ATP channel to cause insulin to be released

37
Q

What are the BMI parameters?

A
Normal = 18.5-24.9
Overweight = 25-29.9
Obese I = 30-34.9
Obese II = 35-39.9
Obese III = 40+
38
Q

When is waist circumference used?

A

when the BMI is less than 35 which shows the amount of visceral fat

39
Q

What is the usual aim for HbA1c?

A

48-53(58?)

40
Q

What are the highest risk groups for annual diabetes testing?

A
  • impaired glucose tolerance
  • impaired fasting glycaemia
  • past history of gestational diabetes
41
Q

What are important aspects of diabetes treatment in primary care?

A
  • retinopathy screening
  • identifying other risk factors
  • managing cardiovascular risk
  • managing glycaemic control
  • foot screening and risk assessment
42
Q

How does diabetes cause complications?

A

hyperglycaemia and hyperlipidaemia –> hypoxia, oxidative stress, inflammation and mitochondrial dysfunction –> microvascular complications

43
Q

What are the essential screening tools for microvascular complications?

A
  • digital retinal
  • foot risk assessment
  • urine albumin:creatinine ratio
44
Q

What are the four types of neuropathy?

A
  • peripheral eg pain/lack of sensation in feet/hands
  • autonomic eg bowel, bladder, sweating, HR, BP, sexual responses
  • proximal eg thigh, hip, buttock pain so weakness in legs
  • focal eg sudden weakness in one nerve or group of nerves
45
Q

What are the features of peripheral neuropathy?

A
  • glove and stocking distribution
  • numbness, tingling, blurring, pain/cramp, sensitivity to touch and loss of balance and coordination
  • can lead to painless trauma, foot ulcer and charcot foot
46
Q

What are the common presentations of the diabetic foot?

A
  • ulcers
  • cold, pulseless feet
  • clawing of toes
  • charcot arthropathy
  • gangrene of toes
  • furring of blood vessels
  • occlusion of femoral artery
47
Q

What is charcot?

A

a destructive inflammation with a hot, swollen foot

48
Q

What is the treatment for charcot foot?

A
  • don’t weight bear
  • use total contact cast
  • aircast boot
49
Q

What are the medications that can be used for painful neuropathy?

A
  • amitriptyline
  • duloxetine
  • Gabapentin
  • if non, oral give Capsaicin cream
50
Q

What is diabetic amyotrophy?

A

pain in the thigh, hip, butt or leg on one side which regresses to weight loss

51
Q

What is a main result of autonomic neuropathy and what is it treated with?

A

gastroparesis which is treated with improving diabetes, changing diet, promotability drugs, anti-nausea drug, pain medication, botulinum toxin or pacemaker

52
Q

What are some cardiovascular neuropathies?

A
  • profuse sweating

- BP and HR changes which can cause postural hypotension

53
Q

what is nephropathy?

A

a progressive kidney disease which is caused by glomeruli damage so there is proteinuria and scarring leading to kidney failure

54
Q

What is the progression of nephropathy?

A

normal –> microalbuminuria (not detectable on dipstick) –> proteinuria (detectable on dipstick)

55
Q

How is the amount of protein excreted calculated?

A

the protein:creatinine ratio times by 10

56
Q

What is the treatment for nephropathy?

A

the first line is an ACEI/ARB which relaxes constriction of efferent arteriole and decreases proteinuria and GFR

57
Q

What are the possible pathologies related to retinopathy?

A
  • macular oedema
  • retinopathy
  • cataracts
  • glaucoma
  • visual blurring caused by acute hyperglycaemia
58
Q

What are the stages of retinopathy?

A

background –> moderate non-proliferative –> severe non-proliferative –> proliferative

59
Q

What is maculopathy determined by?

A

how close the issues are to the macula

60
Q

What is the treatment for retinopathy?

A

laser burning around the periphery and vitrectomy

61
Q

What is the normal pattern of secretion of insulin?

A
  • normal low basal rate

- post-prandial insulin is secreted in relation to post-meal glucose

62
Q

What does basal bolus insulin regimen do?

A

mimics normal endogenous insulin

63
Q

When is premixed insulin used?

A

in elderly who live steady lives with stable diet and little exercise

64
Q

What does insulin need to be matched to?

A

amount of carbohydrates eaten and amount of exercise

65
Q

What do insulin pumps administer?

A

short-acting insulin (so long-acting must also be injected)

66
Q

What is the device that is used to constantly monitor glucose?

A

Libre in the arm

67
Q

When is islet autotransplantation surgery done?

A
  • severe hypos

- severe complications despite maximum treatment

68
Q

What is the hormone used in a pregnancy test?

A

HCG hormone (comes from an implanted fertilised egg)

69
Q

What are the types of diabetes in pregnancy?

A
  • Type 1
  • Type 2
  • Gestational
70
Q

What happens in gestational diabetes?

A

progesterones and hPL lead to insulin resistance in mother so there is an increased blood glucose

71
Q

When does foetal organogenesis begin?

A

at 5 weeks

72
Q

What are the complications from diabetes in pregnancy?

A

Type 1 and 2

  • congenital malformation
  • prematurity
  • intra-uterine growth retardation

Type 1 and 2 and gestational

  • macrosomia
  • death in utero
  • excess amniotic fluid
73
Q

How does macrosomia occur?

A

the foetus produces its own insulin in the 3rd trimester which is a growth factor so macrosomia can occur

74
Q

What is the management of Type 1 and 2 diabetes in pregnancy?

A
  • pre-pregnancy counselling
  • good control at conception
  • folic acid 5mg 3 months before
  • stop all drugs accept metformin
  • aspirin
75
Q

When is gestational DM diagnosed?

A
  • in the third trimester

- if glucose is still high after 6 weeks then it is now T2DM

76
Q

What happens to hypothyroidism in pregnancy?

A

the demand is increased so there needs to be an increased dose of thyroxine

77
Q

What are the possible complications of hyperthyroidism in pregnancy?

A
  • infertility
  • miscarriage
  • stillbirth
  • thyroid crisis in labour
78
Q

What is the treatment for hyperthyroidism in pregnancy?

A

give beta blocker but only if the drugs are needed

79
Q

What is DKA?

A

the metabolic state that occurs in absolute or relative insulin deficiency and an increase in counter-regulatory hormones (GH, cortisol, adrenalin and glucagon)

80
Q

What happens in DKA?

A

without insulin, glucose can’t be uptaken and used by cells (except in the brain) so the liver takes fatty acids from lipolysis and makes them into ketone bodies for energy so the blood becomes acidic and K+ gets sent out of cells and into blood so there is hyperkalaemia

81
Q

What are the biochemistry parameters for DKA?

A

ketones > 3
blood glucose > 11
bicarbonate < 15

82
Q

What are the causes of DKA presenting?

A
  • not adhering to insulin
  • new presentation
  • infection
  • drug/alcohol abuse
83
Q

What is the classification of DKA symptoms?

A
  • osmotic: thirst, polyuria and dehydration

- ketone mediated: flushed, vomiting, abdominal pain and Kussmaul

84
Q

What is the treatment for DKA?

A
  • fluids
  • insulin
  • electrolyte replacement with K+
85
Q

What is the ideal blood ketone level?

A

<0.6

86
Q

What is euglycaemic ketoacidosis caused by?

A

SGLT2i