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FINALS > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are the symptoms of diabetes mellitus

A

polyuria polydipsia weight loss

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2
Q

At what age does diabetes mellitus usually present

A

5 – 15 but can prison at any stage of life

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3
Q

pathophysiology of diabetes mellitus

A

and autoimmune disease of beta islets of langerhan, becoming symptomatic 180 – 90% of cells have been destroyed this causes an insulin deficiency which leads to the inability to use glucose in peripheral muscles and adipose tissue this causes an increase in glucagon adrenaline cortisol and growth hormone to be released these hormones especially glucagon promote gluconeogenesis glyconolysis and ketohgenesis (liver) causing an increasing glucose and ketones

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4
Q

what symptoms should make you suspect DKA

A

abdominal pain and nausea and vomiting tachyopnea lethargy

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5
Q

a patient presents with a three week history of polyuria severely weight loss polydipsia and some abdominal pain and lethargy what should be your next step in the management of this patient

A

start immediate insulin treatment

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6
Q

what are the indications of starting immediate insulin treatment at any age

A

a short history (weeks of severe symptoms) fame/anorexia moderate/high plasma or urine glucose levels

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7
Q

when taking the history of a diabetic patient what should you include?

A

type and duration of diabetes/insulin treated/if so type of insulin number injections and dose/do they get key ptosis or hypoglycaemic often/what treatment of a following and what is the compliance/are they matching lifestyle requirements: type I1 carohydrate counting and matched insulin type to eating less and avoiding refined carbohydrates/ CVS RF

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8
Q

how would you diagnose diabetes if the patient is symptomatic

A

random plasma glucose >11.1 or fasting plasma glucose >7.1

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9
Q

how would you diagnose diabetes if patient is asymptomatic

A

mainly in type II found on screening fasting glucose >7.1 on two occasions glucose tolerance test with two hour blood glucose >11.1 + HbA1c: if >48 then repeat again and if elevated once more it is diagnostic if it is not elevated then they are high risk and test should be repeated within six months or they become symptomatic

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10
Q

how would you monitor Type II diabetes

A

HbA1c

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11
Q

what is HbA1c a marker of

A

reflects hypoglycaemic levels over the last three months

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12
Q

what routine lab investigations apart from blood glucose should be performed in diabetes mellitus

A

HbA1c U+E lipids LFT (T2) urinary albumin (+glucose)

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13
Q

what is HbA1c target in diabetic patients

A

around 48

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14
Q

what is a normal value for HbA1c

A

31 – 37

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15
Q

why should you check liver function in type II diabetics

A

check for non-alcoholic fatty liver disease or non-alcoholic steatohepatitis

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16
Q

What are the aspects of an individual care plan in diabetes care?

A

Education including recofnising Sx and Mx of hypoglycaemia also give information oon suppor groups / insulin therapy and information on slef monitoring / Give special adice on glycaemic control for situations like fasting (ramadam eg) driving sporting activities / give contraceptive advice and pregnancy planning / give contacts of diabetic team and the details of next appointment

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17
Q

What should the targets of glycaemic control be?

A

fasting on waking - 5-7mol plasma BM before meals = 4-7 or after meals 5-9

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18
Q

how often should someone be checking their BMs?

A

before meals and before bead (total 4xd)

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19
Q

what are the sick day rules?

A

measure BMs more often / have easily digestive foods or drinks / oral rehydration sachets glucose tablets / gels / additional insulin / blood ketone strips

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20
Q

what are complications of poorly controlled diabetes mellitus?

A

can be microvascular : retinopathy nephropathy neuropathy inc. autonomic neuropathy

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21
Q

what sare signs nephropathy is occuring in DM?

A

frothy urine from proteinurea and increased BP

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22
Q

what drug can cause nephropathy esp. in those with DM?

A

ACEi (used for BP control)

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23
Q

what are the manifestations of autonomic neuropathy?

A

postural dizzyness, nocturnal diuresis, vomiting, change in taste, sweating

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24
Q

on examination of a foot of a patient with DM you notice 3 signs which makes you suspect Diabetic neuropathy, what are these?

A

clawed toes, callused heels and metatarsel heads, possible an ulcer if severe

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25
Q

where do ulcers most commonly occur in diabetic neuropathy?

A

metatarsel heads, between toead and dorsa of toes and heel

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26
Q

what two tests should you do to check sensation in the diabetic foot exam?

A
  1. vibration with tuning fork 2. 10g microfilament test
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27
Q

wht signs on fundoscopy would incucate diabetic retinopathy?

A

cotton wool haemorrages / hard exudats / extra proliferationn of the blood vessels

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28
Q

what is the pathpphysiology of diabetes mellitus type 2?

A

characterised by insulin resistance there is deficits in insulin action and production leading abnormal glucos metabolism to a hypergkycaemic state - much like DMT1

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29
Q

what HBa1c values are caracterised as pre - diabetes?

A

39-48

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30
Q

what HBa1c values are characterised as diabetes?

A

> 48

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31
Q

what BM values are characterised as pre diabetes ?

A

5.6-6.9

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32
Q

what BM values are characterised as diabetes ?

A

> 6.9

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33
Q

when would you start pharmacy therapy in the management of DMT2?

A

HBa1c > 53

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34
Q

What drugs (non diabetes drugs) are used in the management of DMT2?

A

Hanti-hypertensives / statins / antiplatekets

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35
Q

what are the indications of starting antiplatelets drugs in the management of DMt2?

A

have existing CVD / 50-70y and at risk of CVD

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36
Q

describe the stepwise diabetes drug management of DMT2?

A

metformin –> dual therpay of metformin + other agent –> triple therapy of metformin + 2 other agents OR starting an insulin based therapy –> metformin + insulin basal therapy —? Metformin + long and short acting insulins

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37
Q

do Bm’s need to be checked in DMT2?

A

not needed unless: on insulin frequently having hypoglycaemic episodes or Sx of hypoglycaemia taking medication which predisposes to hypos - using heavy machienery - pregnant or trying to concieve

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38
Q

what are the additional drugs which can be added to metformin in dual or triple therpay of DMT2?

A

gliptin / pioglithazone / sulfonyurea / sodium glucose co transporter 2 inhibitors

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39
Q

why is insulin ‘controversial’ In the mamagent on DMT2?

A

insulin causes weight gain, in T2 diabetes mellitus this can cause a viscious cycle unless you actively counteract CVD RF

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40
Q

what are side effects of metformin?

A

GI upset which can be intolerable / renal impairment (do not use if renal function is poor)

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41
Q

what are gliptins and how to they work in DMT2 management?

A

a DPP-4 inhibitor DPP-4 breaks down incretin a hormone which helps the body produce more insulin. Blocking DPP-4 means increasing incretin and increasing insulin so decreasing glucagon

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42
Q

what are pioglithiazones and how to they work in DMT2 management?

A

increases senstivity to insulin

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43
Q

what are sulfynureas and how to they work in DMT2 management?

A

ey cholorpomide. Cause increased secretion of insulin by binding to ATP-sensitive potassium channels

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44
Q

what are sodium glucose co transporter 2 inhibitors and how to they work in DMT2 management?

A

eg dopaglioflozin reduces the ampunt of glucose being absorbed in the kidneys

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45
Q

what are side effects of sodium glucose co transporter 2 inhibitors

A

GU infections as renal function changed from the medicine

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46
Q

how does metformin work?

A

reduced hepatic glucose production and increases insulin sensitivity by increasing AMPK in skeletal muscle causing Glut 4 deposition increase and thus an insulin independent glucose uptake

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47
Q

what is meant by basal insulin?

A

either long or intermediate acting insulin types

48
Q

descibe the basal bolus phenomenon found in on diabetic patients?

A

in non diabteics there is a basal bolus phenomenon by which there is always an underlying insulin level which then raises at/just after meal times

49
Q

why do DMT2 patients eventually require insulin therapy?

A

because as condition progresses the body stops producing its own insulin, this is a gradual process so at the start just basal insulin is required but as it progresses it needs short and long acting insulin

50
Q

what is the onset time + peak of rapid insulins?

A

10-20mins peaking at 30-90

51
Q

what is the onset time + peak time + duration of human basal insulin ?

A

aka nph, onset of 90min, peak at 4h lasting 18-20 h

52
Q

describe the action of basal analogue isulins

A

don’t peak at all - this is very similar to normal insulin but takes a few days to reach a steady onset

53
Q

who tensds to use mixed insulin?

A

those who struggle with control and may get recurrent infections

54
Q

what are the pros and cons of mixed insulin

A

easy to use - one mixed dose covers daily insulin requirements con: not a physiological match increasing risks of nocurnal hypo’s and increases risks of fasting hypers uf basal doesn’t last for long enough so will generally have a higher HBa1c

55
Q

why does subcut insulin take longer to get into the system than normal insulin roduced by the body

A

normal human insulin is just secreted into the digestive tract

56
Q

does the DVLA need to be informed about diabetes

A

if on insulin the yes

57
Q

what two things should be on person in someone with diabetes?

A

medi-bracelet / card and insulin passport

58
Q

What is DKA

A

a biochemical triad of hyperglycaemia ketonaemia Metabolic acidosis with a rapid symptom onset

59
Q

what causes DKA

A

acute hyperglycaemia

60
Q

while the symptoms of DKA

A

increased thirst polyuria weight loss excess tiredness nausea vomiting dehydration abdominal pain hyperventilation and decreased consciousness

61
Q

if you suspect a patient has DKA what are the first tests you should perform

A

capillary blood glucose capillary blood ketones venous PH plus baseline assessment of: U+E especially sodium and potassium eGFR HCO3 lactate

62
Q

what factors can precipitate DKA

A

infections/stress non-compliance pregnancy steroid use alcohol use idiopathic

63
Q

what tests would you perform to find the underlying cause of DKA

A

MSU cultures ECG chest x-ray beta HCG stool sample CT head blood gases

64
Q

what level of capillary blood ketones is diagnostic for DKA

A

> 3

65
Q

what would DKA cause acidosis or alkalosis

A

acidosis it’s in the name

66
Q

what is the first step of the management of DKA if severe

A

500 mil 0.9 NaCl over 15 minutes and repeat once if necessary (is SBP <100) and call ICU

67
Q

what classes as severe DKA

A

patient in shock SBP <90 or criteria of severe DKA : ketones over six pH under 7.1 HCO3 under five potassium under 3.5 GCS and 12 SPO to under 92% heart rate over a hundred or less and 60

68
Q

what is a first step of the management of DKA if non-severe

A

1 L 0.9 NaCl over one hour

69
Q

what is the remaining Mx in the management of DKA after fluid has been given?

A

50 units to rapid insulin in 0.9 NaCl one units per mil if using .1 units per kilogram per hour/assess whether patient takes long acting insulin/replace potassium and reassess this

70
Q

why does potassium need to be so closely monitored in the management of DKA

A

life-threatening hypokalaemia can occur with incident infusions

71
Q

what is a contraindication to KCl infusion

A

anuria

72
Q

when would you need to replace potassium in the management of DKA

A

is < 5.5 (is <3.5 call for senior help!!)

73
Q

what additional management steps may you need to do in the management of DKA and why?

A

poor urine output = catheterisation/ persistent vomiting= ?NGT SPO to less than 94% on air = CXR+ABG persistent acidosis= look for other causes/ GCS less than 13 = heads a team

74
Q

what are the overall ongoing aims of in the management of DKA

A

a fall in capillary ketones of more than 0.5 mmol per litre per hour fall in capillary blood gas of greater than 3 mmol per litre arising HCO3 Gration 3 mmol per litre

75
Q

it during the infusion of insulin you notice that the patient is not responding what should you do

A

check infusion and line patency and then increase insulin by 1 to 2 units

76
Q

what is the definition of hypoglycaemia

A

blood glucose of less than 3.9

77
Q

how does hypoglycaemia causes symptoms

A

low plasma glucose causes an impaired brain function

78
Q

what are the features of hypoglycaemia

A

autonomic: trembling palpitations sweating anxiety hunger neuroglycopenic: decrease levels of consciousness confusion weakness drowsiness dizziness difficulty speaking non-specific symptoms: nausea headache

79
Q

what is Whipple’s triad

A

fasting hyperglycaemia levels less than 50 mg/dL symptoms of hypoglycaemia immediate relief of symptoms with IV glucose

80
Q

does hypoglycaemia more commonly occurring type I or type II and why

A

more commonly in type I as on insulin and there are no preservative mechanisms

81
Q

what are the risk factors for severe hypoglycaemia in type I diabetes

A

history of severe episodes HbA1c less than 48 long duration of diabetes renal impairment impaired awareness of hypoglycaemia extremities of age

82
Q

what are the risk factors for severe hypoglycaemia in type II diabetes

A

advanced age cognitive impairment depression aggressive treatment of glycaemia impaired awareness of hypoglycaemia duration of insulin therapy renal impairment and other comorbidities Solfinurea + insulin

83
Q

describe what occurs if blood glucose was below 3.8

A

as blood glucose falls hormones which inhibit insulin secretion are produced glucagon is produced at this stage causing glucogenesis and lysis and further decrease in insulinlevels of 3.2

84
Q

describe what occurs of blood glucose falls below 3.5

A

adrenaline is produced causing autonomic symptoms of glgenolysis and gluconeogenesis

85
Q

describe what occurs if blood glucose falls below 3.2/3.3

A

neuroglycopenic Sx occur

86
Q

what would get if blood glucose falls below 3

A

ECG changes

87
Q

what would occur if blood glucose falls to 3- 2.8

A

neurophysiological symptoms with decreased EEG waves and cognitive dysfunction

88
Q

how do you screen for hypoglycaemia

A

low HbA1c or high HP1 sees/long duration of diabetes/ask about history of hypoglycaemia/check if they get any aura symptoms before hypoglycaemia if not they will have impaired awareness of hypoglycaemia/recent episode of severe hypo/check daily insulin dose more at risk is greater than 0.85 units per kilogram per day/check physical activity/check renal function

89
Q

in which patients would you want to relax HbA1c target as well as the blood glucose level targets

A

those with frequent hypoglycaemic episodes want to find a balance

90
Q

what is the management of hypoglycaemia in a patient who is conscious and able to swallow

A

15 to 20 g or fast acting carbohydrate such as 3 to 4 heaped spoonfuls of sugar and water all 4/7 glucose tablets repeating again after 15 minutes as necessary up to 3 times once BM reaches full give a snack which has a long acting, hydrates such as a slice of bread

91
Q

what is the management of hypoglycaemia in a patient who is unresponsive or unconscious

A

IM glucagon or 10% glucose —> after 10% glucose do 20% glucose. Once BM is greater or equal to 4 give larger long acting carbohydrate such as two slices of toast however if they are nil by mouth and give a glucose 10% infusion

92
Q

when would glucagon not work

A

anyone with depleted liver glycogen stores such as those were fasting or malnourished and also may be less effective than those taking sulfonurea – SO GO STRAIGHT TO 10% GLUCOSE

93
Q

it hypo glycaemia has been caused by sulphonyurea or long acting insulin what should you be aware of

A

hypo may persist up to 24 – 36 hours

94
Q

what conditions can cause secondary hyper glycaemia or diabetes

A

cystic fibrosis haemochromatosis chronic pancreatitis PCOS Cushing’s pancreatic cancer glucagonoma pancreatectomy

95
Q

what drugs can cause secondary hypoglycaemia/diabetes

A

corticosteroids thiazide diuretics beta blockers and statins

96
Q

how does cystic fibrosis cause diabetes

A

the thick mucus blocks ducks in the pancreas causing scarring this leads to destruction of the islet cells and type I diabetes mellitus

97
Q

how does haemochromatosis cause diabetes

A

extra iron absorbed in the body is deposited into multiple organs including the pancreas this iron deposition causes scarring and damage to islet cells causing type I diabetes mellitus

98
Q

how does chronic pancreatitis cause diabetes

A

information of the pancreas causes scarring and damage –> DMT1

99
Q

how does PCOS cause diabetes

A

causes insulin resistance and an increase in circulating insulin which promotes an increase in testosterone and thus leading to increased weight has more type II diabetes picture

100
Q

how does cushings is cause diabetes

A

increase cortisol causes an increase in blood glucose and an increase blood pressure leading to type II diabetes

101
Q

how does pancreatic cancer lead to diabetes

A

causes insulin resistance

102
Q

what is a glucagonoma

A

tumour producing access glucagon causing an increase in blood sugars

103
Q

how do most drugs cause diabetes, which are exceptions to this

A

most increase blood glucose and cause insulin resistance giving a type II diabetes and it is picture beta-blockers however block insulin secretion causing a type I diabetes picture

104
Q

why are beta-blockers potentially dangerous in diabetes

A

they block insulin secretion (B1 blockers less lilely) also mask Sx of Hypo such as tachycardia

105
Q

what is mono genic diabetes

A

a raw form of diabetes caused by a single genetic mutation

106
Q

what feature in type I diabetes should be a red flag for mono genic diabetes

A

have very strong family history / onset before six months of life / -related conditions such as cysts in kidneys or gout

107
Q

what are the two types of mono genic diabetes

A

maturity onset of the young / neonatal diabetes

108
Q

what is a presentation of mono genic neonatal diabetes

A

low birth weight presenting before six months can be transient but then returned later in life

109
Q

how do you diagnose monogenic diabetes?

A

genetic testing is the only diagnostic factor and would be negative for auto antibodies present in type I diabetes but this is not very reliable

110
Q

what is the treatment of monogenic DM

A

treated like Type II with lifestyle –> but then add sulfynurea or insulin in neonated treat with sulfinuea unless v severe then add insulin

111
Q

What is charcots disease?

A

complication of neuropathy in the foot which can be caused by diabetes or other neurogenic conditions

112
Q

What is the pathophysiology of charcots disease?

A

and injury such as a break or dislocation occurs due to the neuropathy and individual doesn’t feel the injury so the injury goes untreated which can cause permanent deformity and other associated complications such as sources and pressure sores

113
Q

what is a presentation of charcots disease?

A

redness and swelling heat and can have pain depending on the extent of the neuropathy often looks similar to cellulitis

114
Q

what are the risk factors for charcots disease?

A

long-term duration of diabetes/diabetic neuropathy/injury to the foot/have existing ulceration

115
Q

how would you prevent charcots disease?

A

good diabetic control/regular diabetic foot checks/attend reviews and see podiatrist/if anyone does have neuropathy they should check their feet daily/ insoles specialised shoes which support the foot and allow for any changes to the foot

116
Q

what is the management of charcots disease?

A

needs immediate treatment immobilisation in a cast and non-weight-bearing for three months immobilised in a cast with weight-bearing for further months and then long-term use of foot aids / if it is very severe surgery may be required after eight months

FINALS (24 decks)

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