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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what is OGTT?

A

oral glucose tolerance test

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2
Q

what is normal fasting glucose levels?

A

4-6mmol/L

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3
Q

what is normal post -prandial adult blood glucose?

A

<7.8mmol/L

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4
Q

what is normal HbA1c in adults?

A

<53mmol/L

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5
Q

what do you do if someone has borderline levels?

A

clinical judgement to decide what is most appropriate for patient

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6
Q

what glucose levels would be deemed as impaired?

A

5.6-6.9mmol/L
not failed but are failing

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7
Q

what is the majority of the pancreas’ function?

A

digestive makes up 95%

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8
Q

where is the pancreas in respect to the stomach?

A

retroperitoneal and lies deep to greater curvature of the stomach

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9
Q

what do the duct cells secrete?

A

aqueous NaHCo3 solution

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10
Q

what do acinar cells secrete?

A

digestive enzymes

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11
Q

what two ducts form the main bile duct?

A

common bile duct and common hepatic duct

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12
Q

why is having 2 hormones important for control of blood glucose?

A

allow for tighter regulation - insulin and glucagon

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13
Q

how do negative feedback systems work?

A

if one increases it will work to decrease back to normal?

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14
Q

how does positive feedback mechanisms work?

A

responses increases deviation

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15
Q

do the Islets of Langherhans equate to a large % of pancreatic mass?

A

no about 2%

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16
Q

how mnay Islets of Langherhans are there within pancreas?

A

1.5 million and spread out throughout

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17
Q

what do alpha cells secrete?

A

glucagon

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18
Q

what cells secrete insulin?

A

beta cells of pancreas

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19
Q

what secretes somatostatin cells?

A

delta cells of pancreas

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20
Q

what is the role of somatostatin cells?

A

inhibit insulin and glucagon

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21
Q

what do epsilon cells do?

A

increase appetite

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22
Q

what do pancreatic polypeptides do?

A

promotes GI fluid secretion and feeling full

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23
Q

what is satiety?

A

feeling of fullness

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24
Q

what is glycogenesis?

A

glycogen to glucose

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25
Q

what is gluconeogenesis?

A

using amino acids/ glycerol to make glucose

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26
Q

can you store amino acids well in the body?

A

not very well

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27
Q

what occurs duirng periods of hyperglycaemia (following meals)?

A

beta cells are stimulated and they release insulin into blood
insulin triggers glucose absorption into cells
then will be converted into glycogen

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28
Q

what is HbA1c?

A

test to measure glycation of RBC over past 2-3months

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29
Q

why is HbA1c measuring past 2-3mths?

A

RBC lifespan is 120 days

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30
Q

what is T1DM aetiology?

A

genetic, auto-immune mechanisms, can be environmental linked

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31
Q

what is the pathophysiology of T1DM?

A

pancreas function suddenly declines - no insulin produced
results in hyperglycaemia - hence symptoms

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32
Q

when is common onset of T1DM?

A

early
10-14yrs for diagnosis
more common in europeans

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33
Q

what are symptoms of T1DM?

A

weight loss
polydipsia, polyuria, glycosuria
first presentation may be a DKA

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34
Q

what are symptoms of DKA?

A

dehydration and acidosis
nausea, abdo pain, tachypnoea, tachycardia, acetone breath

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35
Q

what is T2DM aetiology?

A

higher genetic deposition than T1
lifestyle and exercise
obesity

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36
Q

what is T2DM pathophysiology?

A

due to prolonged hyperglycaemia, peripheral tissues stop responding to insulin
pancreas works harder to produce more insulin
vicious circle
results in desentisation
less insulin secreted, less receptors

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37
Q

what is HHS or HONK?

A

hyperosmolar hyperglycaemia state
very high glucose result sin dehydration - water follows glucose that needs to be excreted by urine as no other way
there are no ketones as there is some insulin

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38
Q

what is diabetes insipidus?

A

not diabetes
lack of ADH - causing polyuria hence got similar name

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39
Q

what tissues get priority for glucose during fasting periods?

A

glucose -requiring - CNS has a huge glucose need
degradation of liver glycogen first to get glucose

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40
Q

which hormones promote glycogen degradation?

A

adrenaline and glucagon

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41
Q

which receptor is responsible for bringing in glucose?

A

GLUT-4 - when insulin binds the transporter is moved to membrane to allow for glucose to be brought in

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42
Q

what is the role of incretins?

A

released following a meal - stimulates insulin release
makes you feel full, promotes gastric emptying
reduce glucose synthesis

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43
Q

in diabetics what is the lowest BM result you want?

A

4mmol/L
4 is the floor

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44
Q

at 3mmol/L what symptoms are likely?

A

mild neurological and cognitive impairment slightly

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45
Q

what lifestyle advice is given to T1DM?

A
  • Health balanced diet – low fat/ sugar. Lots of fibre/ fruit and veg
  • Specialist diabetes dietician referral
  • Smoking cessation
  • Reduce alcohol intake
  • Physical exercise – 30mins 5xweek
  • Manage weight to healthy BMI
  • Regular diabetes check ups: most GP surgeries have a special diabetes clinic – can detect and treat complications. They check HbA1c, cholesterol, BP. Diet/ lifestyle. Eye, urine, foot, sensory and blood tests
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46
Q

how long is the onset on rapid acting insulin?

A

10-20mins

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47
Q

how long does rapid acting last?

A

2-3hrs

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48
Q

give examples of rapid acting insulin?

A

vovorapid
aspira

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49
Q

how long does short acting insulin take to work?

A

<20mins

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50
Q

what examples of short acting insulin?

A

actrapid
Humulin S

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51
Q

which insulins are clear suspension?

A

short acting - no zinc crystals

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52
Q

name some examples of intermediate acting inuslin?

A

HUmulin I
Insulatard
Insuman basal

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53
Q

how long does intermediate insulin last?

A

4-12hrs

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54
Q

give some examples of long acting insulin?

A

Lantas
levemir
abagalar

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55
Q

how long does ultra long analogue insulin last?

A

steady state after 2-3 days

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56
Q

how can long acting insulin prevent hypos?

A

basal control in biphasic therapy
prolonged plateau that is fairly stable

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57
Q

how do you prepare cloudy mixtures?

A

invert 10x to resuspend

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58
Q

what analogue insulin?

A

more like human

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59
Q

what is soluble insulin?

A

modified insulin - better absoption

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60
Q

why is basal bolus regime the gold standard?

A

short acting/ rapid acting at meal times
long acting is during other periods of the day to provide basal control

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61
Q

how does carb counting work?

A
  • Determining dose of insulin from amountof carbs that you eat – more freedom and can not having to restrict as much
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62
Q

in carb counting what is the ration between carbs and insulin?

A

1:10 insulin to carb
eg for 70g of carbs, you would need 7 units of insulin

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63
Q

what can DAFNE do?

A

dose adjustment for normal eating
- support group in T1DM

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64
Q

what is the initial dose of starting insulin?

A

0.2-0.4 units/kg/ day

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65
Q

how many units of insulin is needed for a small meal?

A

4 units

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66
Q

how many units of insulin are needed for a large meal?

A

8 units

67
Q

name some examples of devices used to administer inuslin?

A
  • Vial and injection – hospital care
  • Pre-filled pen – patient own
  • Cartridges and re-usable pen – patient own
  • Continuous subcutaneous insulin infusion pump
68
Q

when might a continuous subcutaneous insulin pump be used?

A

recommended in those 12+ that will require multiple injections a day or have disabling hypos or if their BM remains high despite continuous injections. Children may be eligible if they require many injections through the day or injections are inappropriate

69
Q

what are the advantages of using insulin pumps?

A

better control of BM (less high and lows)
- Less injections
- More flexibility in what you eat
- Better accuracy when bringing BM down

70
Q

what disadvantages are using insulin pumps?

A

pump is attached all the time except for small breaks eg swimming/ showering
- Infusion can sometimes get blocked – might need to change at short notice
- Lots of education required about pump
- Small risk of infection – cannula inserted at all times
- Always need to know which insulin – still need to finger prick

71
Q

how do you store insulin?

A

in the fridge
can be in room air for 30 days

72
Q

where on the body do you inject insulin?

A

– in stomach in subcutaneous fat layer (thigh, buttock can be used).
never through clothes

73
Q

where on the body do you never want to inject insulin?

A

avoid back of arm - risk of getting into muscle - unpredictable absorption - hypo risk

74
Q

what needle sized should be used for injecting insulin?

A

4-5mm needle to ensure it goes into subcutaneous fat

75
Q

what are lipotrophies caused by?

A

caused by poor administering technique

76
Q

what are lipotrophies?

A

fatty lumps die to repeated insulin injections - unsightly, painful and unpredictable absorption

77
Q

how do you reduce lipotrophies?

A

rotate between sites and within sites - new needle for each injection and avoid injecting into lumps

78
Q

why does a reused needle have less accurate penetration?

A

microscopic changes - less sharp

79
Q

why is there no need for 24hr basal insulin in T2DM?

A

managed by insulin secretion in the B cells

80
Q

which antidiabetic medication with insulin has a risk of hypos?

A

sulfonylureas

81
Q

insulin and glitazonees have a risk of what condition?

A

heart failure

82
Q

how often should a diabetic check their insulin?

A

4x a daily - before each meal and bed

83
Q

what is continuous flash glucose monitoring?

A

the circle on people arms
all T1DM have should have access or T2DM who require lots of injections daily

84
Q

what is defined as hypoglycaemia?

A

<4mmol/L

85
Q

what can cause hypos?

A
  • Causes: too much diabetes medication, delaying/ missing meal/ snack. Not eating enough carbs, taking part in too much unplanned/ strenuous activity. too much alcohol or drinking alcohol without food
86
Q

what BM is seen in a DKA?

A

> 11mmol/L

87
Q

what capillary ketones is seen in DKA?

A

≥ 3mmol/L

88
Q

what pH is seen in DKA?

A

≤7.3

89
Q

what are symptoms of DKA?

A

acetone breath, tachycardia, hypotension, acidosis, hyperglycaemia, hyperkalaemia, polyuria

90
Q

how do you manage DKA?

A

: fluids, replace K+, fixed rate insulin (0.1 units insulin/ kg/hr), hourly monitoring and senior input, needs glucose potentially

91
Q

why do you replace fluids first in DKA management?

A

as the fluid dehydration will kill first

92
Q

what is VRIII?

A

variable rate insulin?

93
Q

when would be VRIII be indicated?

A

hyperglycaemia, vomiting (no DKA), NBM, severe illness to achieve good glycaemic control

94
Q

what do you do with a patients normal insulin during hypo/ HHS/ DKA?

A

keep going with normal insulin regimes

95
Q

would you give glucose if someone has DKA?

A

yes later in management - to stop ketones being created by burning fat

96
Q

what are SICK day rules?

A

management in HHS/ DKA/ hypo
S: sugar – check Bm every 2-3hrs – even more if children/ pregnant
I: Insulin – continue to take meds even when unwell to prevent DKA
C: carbs: make sure you take enough carbs in and rink enough fluids – not all sugary
K: ketones – check blood or urine ketones every 4hrs, take rapid insulin if ketones are present. Drink lots of fluids to flush out ketones in system

97
Q

when should you inform the DVLA?

A
  • Inform DVLA if taking insulin/ have had 2+ hypos in last year/ if hypos are disabling or unable to recognise start
98
Q

what is recommended for diabetics to do with driving?

A
  • Check BM before driving and every 2hrs on long journeys.
  • Eat some carbs before driving
  • Have hypo treatment in car
  • Have snacks incase of delays
99
Q

what is T2DM characterised by?

A

insulin resistance - impaired secretion, receptor resistance

100
Q

how much of the cases does T2DM account for?

A

90-95%

101
Q

what HbA1c do you aim for in T2DM?

A

48mmol/L

102
Q

if 48mmol/L is not achievable what HbA1c should be aimed for?

A

53mmol/L

103
Q

what should BM be before meals?

A

4-7mmol/L

104
Q

what should BM be 2hrs after eating?

A

<8.5mmol/L

105
Q

how often should HbA1c be measured?

A

checked every 3-6mths until it is stable than 6mths following

106
Q

what is the DESMOND programme?

A
  • Diabetes, Education, Self Management for Ongoing and Newly Diagnosed
    supportive and patient education
107
Q

what BP should be aimed for in T2DM?

A

<140/90

108
Q

what BP should be aimed for in T2DM in those with albuminuria or other features of metabolic disease?

A

<135/85

109
Q

what does hyperglycaemia do to the body?

A
  • Neurotransmitter dysfunction
  • Increased lipolysis and reduced glucose uptake
  • Increased glucose reabsorption in kidneys
  • Decreased incretin effect- released after eating and signal for insulin to be released
  • Increased hepatic glucagon secretion in liver
  • Impaired insulin secretion in pancreas
110
Q

what medication is the gold standard in T2DM?

A

metformin

111
Q

what is the action of metformin?

A

reducing hepatic glucose production, intestinal absorption of glucose, increasing glucose utilisation by enhancing the action of insulin at peripheral receptors
- Needs to be taken with meals

112
Q

when does metformin need to be taken?

A

with meals

113
Q

what are the advantages of metformin?

A

: no weight gain, has CVD protective effects -reduce risk of MI and stroke, do not cause hypoglycaemia, cost effective and long term evidence

114
Q

what are the disadvantages of metformin?

A

starting dose is 500mg daily and needs to be titrated upwards over period of weeks, often limited bu GI side effects. Care is eGFR <45

115
Q

does elective surgery effect metformin?

A

stop 48hrs prior to surgery
continue 48hrs following

116
Q

name some sulfonylurea examples?

A

glictazide - short acting
glimepride - long acting

117
Q

what is the action of sulfonylureas?

A

stimulates insulin secretion by acting directly on pancreatic beta cells
- Increase tissue sensitivity to insulin
- Requires residual beta cell function

118
Q

what can sulfonylureas cause?

A

hypos in T2DM

119
Q

name DDP-4 inhibitors

A

gliptins

120
Q

what are the actions of DDP-4 inhibitors?

A

inhibiting DDp-4 which acts on GLP1 pathway to increase insulin secretion and lower glucagon secretion

121
Q

name some GLP-1 agonists

A

exenatide, semaglutinade

122
Q

which is the action of GLP-1 agonist?

A

: binds to and activates the GLP-1 receptor: increase insulin secretion, decrease glucagon secretion, slow gastric emptying

123
Q

what are thiazolididiones?

A

glitazones

124
Q

what is the action of thiazolidiones?

A

: agonist of receptor called PPAR-gamma which enhances the action of insulin on liver, fat and skeletal muscle by increasing glucose uptake into muscle cells, reducing insulin resistance, decreasing hepatic glucose production

125
Q

name some SGLT-2 inhibitors?

A

dapaglifloxin

126
Q

what is the action of SGLT-2 inhibs

A

reversibly inhibits sodium – glucose co transporter (SGLT-2). Reduces glucose re-absorbtion and increases urinary glucose excretion. It is an osmotic diuretic

127
Q

what is the difference between DKA and HHS?

A

DKA - T1DM and ketones present
HHS - T2DM and no ketones

128
Q

what can be triggers for hypos?

A
  • Infection, over exercise, undereating, missed eating, delayed meals, gastroparesis (delayed gastric emptying), hypo unawareness, too much insulin (self harm, admin error), lipohypertrophy, renal failure, medications (sulfonylureas – stimulates insulin release from B cells – T2DM have some insulin secretion anyway)
129
Q

which type of symptoms appear first in a hypo?

A

autonomic - general - sweating, confusion, pale

130
Q

when would neuro symptoms appear in a hypo and what symptoms?

A

persistent - difficulty in speaking, loss in conc, drowiness, dizziness, hemiplegia, fits, coma, death

131
Q

what are macrovascular complications of diabetes?

A

: affects larger blood vessels
- Hypertension
- Arterial stiffness
- CKD
- Stroke
- MI

132
Q

what are microvascular complications of diabetes?

A

as smaller vessels experience atherosclerosis – causing ischaemia
- Retinopathy
- Nephropathy
- Neuropathy

133
Q

how many diabetic patients experience microvascular complications?

A

> 80%

134
Q

how many newly diagnosed diabetics have microvascular complications?

A

20-50%

135
Q

what is retinopathy?

A
  • Damage to blood vessels in retina due to hyperglycaemia
136
Q

what are the stages of retinopathy?

A

background diabetic retinopathy
pre proliferative retinopathy
proliferative retinopathy
advanced diabetic retinopathy

137
Q

what is seen in background diabetic retinopathy?

A

dots (micro-aneurysms) and blots ( small haemorrhages). Hard exudates – lipid that collect in circle around leaking blood vessel – yellowing deposits with sharp margins

138
Q

what is seen in pre proliferative diabetic retinopathy?

A

: cotton wool spots – fluffy opaque areas that result from retinal ischaemia. Venous changes – bleeding in segmental dilators

139
Q

what is seen in proliferative retinopathy?

A

: cotton wool spots – fluffy opaque areas that result from retinal ischaemia. Venous changes – bleeding in segmental dilators

140
Q

what is seen in advanced diabetic retinopathy?

A

– areas of neo-vascularisation lead to recurrent vitreous haemorrhage. The neo-vascularisation is usually on surface of iris and retina becomes ischaemic. The ischaemic retina releases VEGF – stimulating angiogenesis – new blood vessels grow in abnormal areas eg iris. It eventually becomes fibrotic, closing the normal angle of the eye and prevents fluid from leaving which increases intraocular pressure – neovascular glaucoma

141
Q

why is lens swelling common in newly diagnosed diabetics?

A
  • The hyperglycaemia causes the movement of water into the wrong places which results in lens swelling
142
Q

apart from retinopathy, what other eye complications can occur in diabetics?

A
  • The hyperglycaemia causes the movement of water into the wrong places which results in lens swelling
143
Q

what management is used within diabetic retinopathy?

A

yearly eye screening, optimiase glycaemic control, manage BP, if later stages – laser photocoagulation can prevent angiogenesis, visual aids and DVLA regulations

144
Q

what is the first sign of diabetic nephropathy?

A

microalbuminuria

145
Q

what diagnostics can be involved in diabetic nephropathy?

A
  • Yearly eGFR and urinary albumin excretion (first pass morning urine specimen- albumin: creatinine ration of >3mg/mol) can help diagnose if tests are raised for >3mths
146
Q

why can you not diagnose diabetic nephropathy from one abnormal protein test?

A

levels may vary so need at least 3

147
Q

what management is used within nephropathy?

A
  • ACEi/ ARB should be started ideally before HTN to control BP
  • Optimiase glycaemic control
  • Reduce dietary protein to <0.7-1g/kg/day
148
Q

what can be seen in distal symmetrical polyneuropathy?

A

glove and stocking neuropathy
- Numbness, pain, altered sensation, pain, neuropathic ulcers, joint abnormality

149
Q

what is mononeuritis multiplex?

A

multiple individual nerves that cause issues in diabetic neuropathy

150
Q

what can be seen in autonomic neuropathy?

A

: postural hypotension, neuropathic bladder, erectile dysfunction and sexual dysfunction. Gastroparesis, gustatory sweats and diarrhoea

151
Q

what is the management within diabetic neuropathy?

A
  • Avoid touching limbs – they have loss of sensation if broken skin they have increases infection risk. The protective film has been disrupted
  • Duloxetine, amitriptyline, pregabalin – NICE says no drug is more superior
  • Basic analgesia (paracetamol, opiates)
  • Improve glycaemic control
152
Q

what do you do in a diabetic foot exam?

A

inspect for ulcers, ischaemic, amputation, necrosis, clawing, charcots, temps
- Check sensation – monofilament
- Vibration sense
- Reflexes
- They all have different nerves for these different responses
- Pedal pulses

153
Q

what is osteomyelitis?

A

infection that penetrates bone

154
Q

in diabetic neuropathy what occurs first?

A

peripheral neuropathy - loss in sensation
patients unaware of foot injury - can not feel it

155
Q

what symptoms would be seen in motor neuropathy?

A

: raised arch and clawed toes – pressure is mainly on pressure points and callus form – haemorrhage or necrosis can occur within callus and can ulcerate

156
Q

what symptoms are seen in autonomic neuropathy?

A

reduced sweating leads to dry and cracked skin - portal for infection

157
Q

what would peripheral vascular disease manifest as?

A

reduced blood supply to feet - ischaemia to peripheries

158
Q

what is diabetic neuropathy management?

A
  • Prevention – annual foot screening, education, wash feet daily, check feet regularly, well fitting shoes, do not walk barefoot
  • Foot ulcer- relieve pressure (rest, total contact casting), treat infection, if severe – surgical debridement/ amputation
159
Q

what accounts for 60-70% of deaths in diabetics?

A

cardio-vascular disease

160
Q

how do you manage macrovascular disease within diabetics?

A
  • Control RF: hyperlipidaemia, HTN, smoking cessation, treat obesity, healthy diet, optimise glycaemic control
161
Q

what is included within a diabetic annual review?

A

Education and self management:
- How they are coping, diet, exercise
- Further info/ education – DAFNE, DESMOND
- Smoking cessaion
Complications:
- Hypo episodes – how often, signs and symptoms
- Hosp admissions – why? Frequency
- Neuro, feet, eyes, kidney, CVD
- Mood
- Other general illnesses
Review BM diary, are they planning on getting pregnant – aware of pregnancy and diabetes advice

162
Q

what examinations would be included within diabetic annual review?

A

weight, height, BMI, urinalysis – ketones, protein. Inspect inject sites. CVS – BP, heart sounds, peripheral pulses and bruits. Eyes – cataracts, eye movements, inspect retina. Neuropathy – foot exam

163
Q

what investigations would be included within a diabetic annula review?

A

HbA1c, BM measurement, lipid profile, kidneys – eGFR and urine albumin: creatinine ratio

164
Q

why would ketones appear in DKA?

A

– when hyperglycaemic state and no insulin – body will run on stores of glycogen
- When stores run out – will turn to burn fats – the breakdown of fats produces ketones along side triglycerol
- Ketones are large acidic proteins

Endocrinology (6 decks)

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