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Diabetes Flashcards

Diabetic emergencies T1D T2D Diabetic complications Gestational, secondary, monogenic diabetes

1
Q

How is DKA defined in terms of measurable components in the blood?

A
  1. Glucose >11 or known diabetes
  2. Acidosis- pH<7.3 or bicarb <15
  3. Ketonaemia- >3 mmol/l or ++ on urine dip

DKA- D= diabetes K= ketonaemia A= acidosis

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2
Q

What does an increased anion gap indicate?

A

increased acid production or ingestion of acids

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3
Q

What are the causes of an increased anion gap?

A 
MUDPIES
M- methanol
U- uraemia
D- DKA
P- Paraldehyde
I- Isoniazid
L- lactic acidosis
E- ethylene glycol
S- Salicylates
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4
Q

What is the normal range for anion gap?

A

8-12 mEq/L (if without potassium)

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5
Q

What are the principles for the treatment of DKA?

A
  1. Fluid replacement
  2. Insulin therapy
  3. IV glucose therapy/IV dextrose
  4. Electrolyte replacement (K+)
  5. Treat underlying trigger
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6
Q

Which fluid would you administer in DKA and why?

A

IV 0.9% NaCl. IV dextrose not used until blood glucose has fallen to <14. Sodium bicarbonate is not routinely recommended.

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7
Q

Which insulin regimen would be commenced in DKA?

A

fixed rate IV insulin at 6 units/hr , independent of BM

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8
Q

What happens to potassium levels during DKA?

A

whole body potassium deficiency despite normal serum potassium results

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9
Q

What is the mechanism for potassium deficiency but normal potassium serum levels in DKA?

A

High levels of circulating H+ are shifted intracellularly at the expense of K+ which is shifted into the blood stream. Lack of insulin reduces action of NA+/K+ ATPase which would normally drive K+ into cells

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10
Q

Which electrolyte must be closely monitored during DKA treatment and why?

A

as insulin therapy is commenced, K+ will be transferred back into cells which can further worsen hypokalaemia

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11
Q

At what point should IV dextrose be halted in treatment of DKA?

A

until the patient is eating and drinking

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12
Q

Define anuric

A

failure of kidneys to produce urine

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13
Q

What are the four criteria to safely discontinue the DKA pathway?

A
  1. Eating and drinking (no n/v)
  2. Bicarbonate normal range/resolution of acidosis
  3. Ketones <0.3
  4. Restarted on normal insulin regime
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14
Q

What is the criteria for HHS?

A
  1. glucose >30mmol/L
  2. VBG H+ <50 mmol/L
  3. Vbicarb >15 mmol/L
  4. Ketones <3 mmol/L
  5. Serum osmolality >320 mosmol/Kg
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15
Q

What is the calculation for serum osmolality?

A

2(Na + K) + glu + urea

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16
Q

What is the initial management of HHS?

A

Start 0.9% normal saline, follow HHS pathway, insert a catheter to monitor urine output

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17
Q

Which conditions can precipitate HHS?

A

gastroenteritis, MI, medications, stroke, any infection, GI bleeding, hypo/hyperthermia, AKI etc etc

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18
Q

Does DKA or HHS have a higher risk of mortality/morbidity?

A

HHS

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19
Q

What a complication of HHS?

A

thromboembolism

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20
Q

What are less common types of diabetes?

A

gestational diabetes, MODY, pancreatic damage, steroid-induced

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21
Q

Which is the most common auto-antibody in T1D?

A

anti-GAD antibodies

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22
Q

How is T1D diagnosed?

A

clinical S&S + hyperglycaemia (random blood glu >11.1 or fasting blood glucose >7 mmol/l)

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23
Q

What are the investigations for T1D?

A

HbA1c, C-peptide, autoantibodies

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24
Q

What are the aspects of education in type 1 diabetes management?

A

insulin admin, blood glucose monitoring, sick day rules, driving, DAFNE programme (dose adjustment for normal eating)

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25
Q

What are complications of T1D?

A
  1. CVD
  2. Diabetic eye disease
  3. Nephropathy
  4. Neuropathy
  5. Diabetic foot disease
  6. Associated endocrine disease: thyroid, coeliac, addison’s
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26
Q

Does DKA only occur in T1D?

A

No, it can also occur in other types!!

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27
Q

How does ketogenesis result in acidosis?

A

ketones are weak acids

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28
Q

How come DKA doesn’t usually result in serious hyperkalaemia?

A

body has good mechanism for removing K+ from body by excretion by kidneys

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29
Q

What are the syx of DKA?

A

n/v, polydipsia, confusion, reduced GCS, dehydration, tachycardia, hypotension, dry mucus membranes, polyuria, glycosuria,, ketonuria

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30
Q

What are the complications of DKA?

A

mortality, VTE, arrhythmias (due to K), cerebral oedema, AKI

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31
Q

Name five differentials for hyperglycaemia

A

type 1, type 2, MODY, LADA, pre-diabetes, pancreatitis, haemochromatosis

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32
Q

Name five symptoms of T1DM

A

weight loss, lethargy, polyuria, polydipsia, abdo pain

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33
Q

What is the diagnostic criteria for DKA?

A

glu >11, bicarb <15, pH<7.3, ketones +++

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34
Q

Name three complications of DKAs

A

thromboembolism, AKI, arrhythmias

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35
Q

Is HHS or DKA more insidious?

A

HHS, therefore more difficult to treat

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36
Q

What are two criteria necessary to diagnose DKA?

A

BM >14 and Ketones (urinary or blood)

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37
Q

In which other conditions can you have ketosis aside from DKA?

A

vomiting, fasting, malnutrition

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38
Q

Which electrolyte disturbance can arise following IV insulin?

A

hypokalaemia, therefore monitor and treat with K+

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39
Q

Name two genetic associations of T1D?

A

HLA-D3 and HLA-D4

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40
Q

Name two abs present in T1D?

A

anti-islet, anti-GAD

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41
Q

Fasting and random glucose values for diabetes diagnosis?

A

 Fasting ≥7mM

 Random ≥11.1mM

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42
Q

When is oral glucose tolerance test required?

A

OGTT (75g) only needed if borderline fasting or random

glucose measurements.

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43
Q

List three secondary causes of diabetes

A

Drugs

Pancreatic pathologies: CF, chronic panceatitis, pancreatic cancer

Cushings
Phaeo
T4

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44
Q

Name two drugs that can induce DM

A

steroids
thiazides
anti-HIV

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45
Q

Aside from hypoglycaemic drugs, what is the management of diabetes?

A 
Diet
Exercise
Statins
BP control
Smoking cessation
Yearly/6 months check up
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46
Q

Define metabolic syndrome

A 
Central obesity (↑ waist circumference) and two of: 
  ↑ Triglycerides 
  ↓ HDL 
  HTN 
  Hyperglycaemia: DM, IGT, IFG
47
Q

Two contraindications to metformin?

A

GFR<30, tissue hypoxia (sepsis, MI), iodinated contrast media

48
Q

Two side effects of metformin?

A

nausea, diarrhoea, abdo pain, lactic acidosis

49
Q

Two SE of sulfonylurea?

A

hypoglycaemia, weight gain

50
Q

Discuss two insulin regimens

A
  1. BD biphasic regime (combination of rapid-acting and intermediate acting, taken 30 before breakfast and dinner)
  2. Basal-bolus regime (bedtime long acting and short acting before each meal)
51
Q

Which insulin regimen is most appropriate for someone who wants flexibility in their lifestyle?

A

basal-bolus

52
Q

Give two pieces of advice to T1D patient during illness?

A
  1. Insulin requirements usually increase, therefore increase insulin dose if glucose rises
  2. Maintain calories (fruit juice, milk)
  3. Check BMs 4hrly and test for ketonuria
53
Q

Two side effects of insulin?

A

hypoglycaemia
lipohypertrophy (injection site)
weight gain in t2D if given with metformin

54
Q

Two macrovascular complications of diabetes?

55
Q

Three microvascular complications of diabetes?

A

Diabetic feet
Nephropathy
Neuropathy
Retinopathy

56
Q

Discuss three aspects of diabetic feet

A

Ischaemia- ulcers (painfu;), critical toes, absent pulses

Neuropathy- loss of protective sensation, deformity, injury/infection, ulcers (painless)

57
Q

How does diabetic eye disease present? Three examples

A 
Retinopathy
maculopathy
cataracts (lens develops cloudy patches)
glaucoma
CN palsies
58
Q

Discuss two features of retinopathy

A 
Background Retinopathy 
  Dots: microaneurysms 
  Blot haemorrhages 
  Hard exudates: yellow lipid patches 
Pre-proliferative Retinopathy 
  Cotton-wool spots (retinal infarcts) 
  Venous beading 
  Haemorrhages 
Proliferative Retinopathy 
  New vessels 
  Pre-retinal or vitreous haemorrhage
59
Q

Describe three clinical aspects of diabetic neuropathy

A
  1. Glove and stocking- length dependent
  2. Absent ankle jerks
  3. Numbness, tingling, pain
  4. Mononeuropathy- CN3/6 palsies
  5. Autonomic neuropathy
60
Q

Two features of autonomic neuropathy in diabetes?

A

postural hypotension
diarrhoea
urinary retention

61
Q

Three diabetic emergencies?

A

DKA
Hypoglycaemia
HHS

62
Q

Why does dehydration arise in DKA?

A

severe hyperglycaemia due to triggered gluconeogenesis results in osmotic diuresis. Increased ketones also causes vomititing

63
Q

Three signs and symptoms of DKA

A 
  Abdo pain + vomiting 
  Gradual drowsiness 
  Sighing “Kussmaul” hyperventilation 
  Dehydration 
  Ketotic breath
64
Q

Three features of DKA diagnosis?

A

Acidosis (↑AG): pH <7.3 (± HCO 3 <15mM)

Hyperglycaemia: ≥11.1mM (or known DM)

Ketonaemia: ≥3mM (≥2+ on dipstix)

65
Q

Three investigations for DKA?

A
  1. Bloods- glucose, U+Es, FBC, cultures
  2. Urine- ketones and glucose
  3. VBG- acidosis and K+
  4. Cap- glucose and ketones
66
Q

Three complications of DKA?

A
  1. Cerebral oedema if excess fluid administration
  2. Aspiration pneumonia
  3. Hypokalaemia
  4. Hypophosphataemia
  5. Thromboembolism
67
Q

What is whipple’s triad?

A

1 Low plasma glucose ≤3mM
2 Symptoms consistent with hypoglycaemia
3 Relief of symptoms by glucose administration

68
Q

Two autonomic symptoms of hypoglycaemia

A 
  Sweating 
  Anxiety 
  Hunger 
  Tremor 
  Palpitations
69
Q

Two neuroglycopenic symptoms of hypoglycaemia?

A 
  Confusion 
  Drowsiness 
  Seizures 
  Personality change 
  Focal neurology (e.g. CN3)  
  Coma (<2.2)
70
Q

Three causes of hypoglycaemia aside from in known diabetic

A 
liver failure
addison's
pituitary insufficiency
islet cell tumours= insulinoma
drugs
71
Q

Patient orientated and alert with hypoglycaemia. What do you give them?

A

oral carb- lucozade/toast

72
Q

Hypoglycaemic patient drowsy/confused but swallow intact. What do you give them?

A

buccal carb- glucogel

73
Q

Hypoglycaemic patient unconscious. What do you give them?

A

IV dextrose

74
Q

Hypoglycaemia patient is unconscious and deteriorating. What do you give them?

A

1mg glucagon IM/SC

75
Q

What is the definition of hypoglycaemia in people WITHOUT diabetes?

A

plasma glucose <2.5 mmol/L PLUS symptoms

76
Q

What is the biochemical definition of hypoglycemia in people with diabetes?

A

glucose <4mmol/L

77
Q

Which investigation should be conducted if hypo patient has symptoms when fasting?

A

72-hour fast test

78
Q

Why is beta hydroxybuyrate measured in diabetic patients?

A

=ketone body

79
Q

If pt is hypo with elevated insulin and c-peptide, what does this suggest?

A

endogenous insulin excess of sulphonylurea ingestion

80
Q

If pt has hypo with high insulin but low c-peptide, what does this suggest?

A

exogenous insulin excess- insulin injection

81
Q

If pt has hypo and both low insulin and c-peptide, what does this suggest?

A

hypo is not due to insulin excess

82
Q

What is the name for hypoglycaemia that is due to excessive endogenous insulin not associated with insulin injection?

A

endogenous hyperinsulinemic hypoglcaemia

83
Q

What measurement of HbA1c is indicative of DM?

A

6.5% or 48 mmol/mol

84
Q

Aside from the history and glucose levels, what are diagnostic/supportive aids for diabetes?

A
  1. Ketone testing +- bicarbonate 2. Pancreatic auto-atnibodies 3. C peptide
85
Q

Four differentials for diabetes

A 
MODY
T1D
T2D
Pancreatic diabetes
LADA
Secondary diabetes-
86
Q

Two causes of secondary diabetes?

A

acromegaly, thyrotoxicosis, cushing’s syndrome

87
Q

How would you assess for microvascular changes in T1D?

A

feet assessment, creatinine ratio, U&Es, retinal photograph

88
Q

What are the biomedical targets that are reviewed annually in diabetes?

A

BP, cholesterol, HbA1C, body weight

89
Q

What is the first line treatment for T2D?

A

always lifestyle +metformin (somtimes sulfonylureas)

90
Q

What is the second line treatment for T2D?

A

two agents: add SU, flozin, gliptin, glitazone

91
Q

Third line?

A

three agents: add any of second line OR start injectable therapy with GLP-1 agonist or insulin

92
Q

What is the MOA of metformin?

A

suppresses gluconeogensis, reducing glucose output from liver and increases peripheral insulin sensitivity. Also increases AMPL activity

93
Q

Two benefits of metformin?

A

weight reduction, low hypo risk, CV benefit, extensive experience, moderate efficacy

94
Q

What is the MOA of sulfonylurea?

A

increases closure of ATP-K+ channels on membrane of pancreatic beta cells, allowing influx of calcium, causing excocytosis of stored insulin. Causes increased cellular uptake and glycognesis, reduces gluconeogenesis

95
Q

Two benefits of sulfonylureas?

A

high efficacy, extensive experience

96
Q

Two disadvantages of SU?

A

No CV benefit, weight gain, high hypo risk, caution in CKD

97
Q

MOA of gliptins?

A

Inhibit DDP4 which rapdily inactivates GLP1 and GIP which stimulate insulin release and inhibit glucagon. Therefore, increases glucose mediated insulin secretion and suppresses glucagon secretion by enhancing the effects of endogenous incretins

98
Q

Two benefits of gliptins?

A

low/moderate efficacy, low hypo risk, few adverse events

99
Q

What is the MOA of SGLT2 inhibitors?

A

By inhibiting SGLT2, gliflozins prevent the kidneys’ reuptake of glucose from the glomerular filtrate and subsequently lower the glucose level in the blood and promote the excretion of glucose in the urine

100
Q

Two pros of flozins?

A

moderate efficacy, CV benefits, renal benefit, weight loss, low hypo risk

101
Q

Two SE of flozins?

A

risk of GU infections, small risk of DKA

102
Q

What is the MOA of thiazilidinediones?

A

PPAR gamma receptor agonist, resulting in transcriptional activity. increases sensitivity of fat, muscles, and liver to endogenous and exogenous insulin. Reduces hepatic glucose production, decreases lipolysis, increases glucose uptake in muscle

103
Q

SE of glitazones?

A

weight gain, fluid retention, fractures

104
Q

61y man with BMI32, smoker, hypertension, symptomatic. Already on metformin What would be the next treatment intervention?

A

Flozin- promotes weight loss (SU and glitazone would increase weight)

105
Q

Explain the MOA of GLP-1 agonists

A

increases insulin secretion (beta cells), decreases glucagon (alpha cells), increases satiety and suppresses appetite

106
Q

Two SE/disadvntages of GLP-1 agonists?

A

GI side effects, uncertain safety as quite novel, injection…

107
Q

List four points of education to discuss with patients with T1D?

A

glucose/ketone monitoring, sick day rules, driving regulations, exercise and alcohol, pregnancy, targets, complications, admin of insulin

108
Q

Give an example of a SU

A

gliclazide

109
Q

Two contradindications for metformin?

A

chronic heart failure, severe renal disease, DKA, MI, stroke

110
Q

Is T1D or T2D more strongly inheritable?

111
Q

Which form of diabetes is MODY?

A

T2D. Presents in young people with FH of T2D

112
Q

Two key features of diagnosing MODY?

A

under 25

Parent with diabetes, with diabetes in two or more generations

113
Q

Which are the two main forms of monogenic diabetes?

A

MODY and neonatal diabetes mellitus- NDM

114
Q

Patient with hypoglycaemia, as a rule of thumb, what treatment do you give them?

A

10% glucose IV (NOT dextrose!!)

Endocrinology (9 decks)

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