Diabetes Flashcards
Diabetic emergencies T1D T2D Diabetic complications Gestational, secondary, monogenic diabetes (114 cards)
1
Q
How is DKA defined in terms of measurable components in the blood?
A
- Glucose >11 or known diabetes
- Acidosis- pH<7.3 or bicarb <15
- Ketonaemia- >3 mmol/l or ++ on urine dip
DKA- D= diabetes K= ketonaemia A= acidosis
2
Q
What does an increased anion gap indicate?
A
increased acid production or ingestion of acids
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
4
Q
What is the normal range for anion gap?
A
8-12 mEq/L (if without potassium)
5
Q
What are the principles for the treatment of DKA?
A
- Fluid replacement
- Insulin therapy
- IV glucose therapy/IV dextrose
- Electrolyte replacement (K+)
- Treat underlying trigger
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.
7
Q
Which insulin regimen would be commenced in DKA?
A
fixed rate IV insulin at 6 units/hr , independent of BM
8
Q
What happens to potassium levels during DKA?
A
whole body potassium deficiency despite normal serum potassium results
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
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
11
Q
At what point should IV dextrose be halted in treatment of DKA?
A
until the patient is eating and drinking
12
Q
Define anuric
A
failure of kidneys to produce urine
13
Q
What are the four criteria to safely discontinue the DKA pathway?
A
- Eating and drinking (no n/v)
- Bicarbonate normal range/resolution of acidosis
- Ketones <0.3
- Restarted on normal insulin regime
14
Q
What is the criteria for HHS?
A
- glucose >30mmol/L
- VBG H+ <50 mmol/L
- Vbicarb >15 mmol/L
- Ketones <3 mmol/L
- Serum osmolality >320 mosmol/Kg
15
Q
What is the calculation for serum osmolality?
A
2(Na + K) + glu + urea
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
17
Q
Which conditions can precipitate HHS?
A
gastroenteritis, MI, medications, stroke, any infection, GI bleeding, hypo/hyperthermia, AKI etc etc
18
Q
Does DKA or HHS have a higher risk of mortality/morbidity?
A
HHS
19
Q
What a complication of HHS?
A
thromboembolism
20
Q
What are less common types of diabetes?
A
gestational diabetes, MODY, pancreatic damage, steroid-induced
21
Q
Which is the most common auto-antibody in T1D?
A
anti-GAD antibodies
22
Q
How is T1D diagnosed?
A
clinical S&S + hyperglycaemia (random blood glu >11.1 or fasting blood glucose >7 mmol/l)
23
Q
What are the investigations for T1D?
A
HbA1c, C-peptide, autoantibodies
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)
25
What are complications of T1D?
1. CVD
2. Diabetic eye disease
3. Nephropathy
4. Neuropathy
5. Diabetic foot disease
6. Associated endocrine disease: thyroid, coeliac, addison's
26
Does DKA only occur in T1D?
No, it can also occur in other types!!
27
How does ketogenesis result in acidosis?
ketones are weak acids
28
How come DKA doesn't usually result in serious hyperkalaemia?
body has good mechanism for removing K+ from body by excretion by kidneys
29
What are the syx of DKA?
n/v, polydipsia, confusion, reduced GCS, dehydration, tachycardia, hypotension, dry mucus membranes, polyuria, glycosuria,, ketonuria
30
What are the complications of DKA?
mortality, VTE, arrhythmias (due to K), cerebral oedema, AKI
31
Name five differentials for hyperglycaemia
type 1, type 2, MODY, LADA, pre-diabetes, pancreatitis, haemochromatosis
32
Name five symptoms of T1DM
weight loss, lethargy, polyuria, polydipsia, abdo pain
33
What is the diagnostic criteria for DKA?
glu >11, bicarb <15, pH<7.3, ketones +++
34
Name three complications of DKAs
thromboembolism, AKI, arrhythmias
35
Is HHS or DKA more insidious?
HHS, therefore more difficult to treat
36
What are two criteria necessary to diagnose DKA?
BM >14 and Ketones (urinary or blood)
37
In which other conditions can you have ketosis aside from DKA?
vomiting, fasting, malnutrition
38
Which electrolyte disturbance can arise following IV insulin?
hypokalaemia, therefore monitor and treat with K+
39
Name two genetic associations of T1D?
HLA-D3 and HLA-D4
40
Name two abs present in T1D?
anti-islet, anti-GAD
41
Fasting and random glucose values for diabetes diagnosis?
Fasting ≥7mM
| Random ≥11.1mM
42
When is oral glucose tolerance test required?
OGTT (75g) only needed if borderline fasting or random
| glucose measurements.
43
List three secondary causes of diabetes
Drugs
Pancreatic pathologies: CF, chronic panceatitis, pancreatic cancer
Cushings
Phaeo
T4
44
Name two drugs that can induce DM
steroids
thiazides
anti-HIV
45
Aside from hypoglycaemic drugs, what is the management of diabetes?
```
Diet
Exercise
Statins
BP control
Smoking cessation
Yearly/6 months check up
```
46
Define metabolic syndrome
```
Central obesity (↑ waist circumference) and two of:
↑ Triglycerides
↓ HDL
HTN
Hyperglycaemia: DM, IGT, IFG
```
47
Two contraindications to metformin?
GFR<30, tissue hypoxia (sepsis, MI), iodinated contrast media
48
Two side effects of metformin?
nausea, diarrhoea, abdo pain, lactic acidosis
49
Two SE of sulfonylurea?
hypoglycaemia, weight gain
50
Discuss two insulin regimens
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
Which insulin regimen is most appropriate for someone who wants flexibility in their lifestyle?
basal-bolus
52
Give two pieces of advice to T1D patient during illness?
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
Two side effects of insulin?
hypoglycaemia
lipohypertrophy (injection site)
weight gain in t2D if given with metformin
54
Two macrovascular complications of diabetes?
MI
PVD
CVA
55
Three microvascular complications of diabetes?
Diabetic feet
Nephropathy
Neuropathy
Retinopathy
56
Discuss three aspects of diabetic feet
Ischaemia- ulcers (painfu;), critical toes, absent pulses
Neuropathy- loss of protective sensation, deformity, injury/infection, ulcers (painless)
57
How does diabetic eye disease present? Three examples
```
Retinopathy
maculopathy
cataracts (lens develops cloudy patches)
glaucoma
CN palsies
```
58
Discuss two features of retinopathy
```
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
Describe three clinical aspects of diabetic neuropathy
1. Glove and stocking- length dependent
2. Absent ankle jerks
3. Numbness, tingling, pain
4. Mononeuropathy- CN3/6 palsies
5. Autonomic neuropathy
60
Two features of autonomic neuropathy in diabetes?
postural hypotension
diarrhoea
urinary retention
61
Three diabetic emergencies?
DKA
Hypoglycaemia
HHS
62
Why does dehydration arise in DKA?
severe hyperglycaemia due to triggered gluconeogenesis results in osmotic diuresis. Increased ketones also causes vomititing
63
Three signs and symptoms of DKA
```
Abdo pain + vomiting
Gradual drowsiness
Sighing “Kussmaul” hyperventilation
Dehydration
Ketotic breath
```
64
Three features of DKA diagnosis?
Acidosis (↑AG): pH <7.3 (± HCO 3 <15mM)
Hyperglycaemia: ≥11.1mM (or known DM)
Ketonaemia: ≥3mM (≥2+ on dipstix)
65
Three investigations for DKA?
1. Bloods- glucose, U+Es, FBC, cultures
2. Urine- ketones and glucose
3. VBG- acidosis and K+
4. Cap- glucose and ketones
66
Three complications of DKA?
1. Cerebral oedema if excess fluid administration
2. Aspiration pneumonia
3. Hypokalaemia
4. Hypophosphataemia
5. Thromboembolism
67
What is whipple's triad?
1 Low plasma glucose ≤3mM
2 Symptoms consistent with hypoglycaemia
3 Relief of symptoms by glucose administration
68
Two autonomic symptoms of hypoglycaemia
```
Sweating
Anxiety
Hunger
Tremor
Palpitations
```
69
Two neuroglycopenic symptoms of hypoglycaemia?
```
Confusion
Drowsiness
Seizures
Personality change
Focal neurology (e.g. CN3)
Coma (<2.2)
```
70
Three causes of hypoglycaemia aside from in known diabetic
```
liver failure
addison's
pituitary insufficiency
islet cell tumours= insulinoma
drugs
```
71
Patient orientated and alert with hypoglycaemia. What do you give them?
oral carb- lucozade/toast
72
Hypoglycaemic patient drowsy/confused but swallow intact. What do you give them?
buccal carb- glucogel
73
Hypoglycaemic patient unconscious. What do you give them?
IV dextrose
74
Hypoglycaemia patient is unconscious and deteriorating. What do you give them?
1mg glucagon IM/SC
75
What is the definition of hypoglycaemia in people WITHOUT diabetes?
plasma glucose <2.5 mmol/L PLUS symptoms
76
What is the biochemical definition of hypoglycemia in people with diabetes?
glucose <4mmol/L
77
Which investigation should be conducted if hypo patient has symptoms when fasting?
72-hour fast test
78
Why is beta hydroxybuyrate measured in diabetic patients?
=ketone body
79
If pt is hypo with elevated insulin and c-peptide, what does this suggest?
endogenous insulin excess of sulphonylurea ingestion
80
If pt has hypo with high insulin but low c-peptide, what does this suggest?
exogenous insulin excess- insulin injection
81
If pt has hypo and both low insulin and c-peptide, what does this suggest?
hypo is not due to insulin excess
82
What is the name for hypoglycaemia that is due to excessive endogenous insulin not associated with insulin injection?
endogenous hyperinsulinemic hypoglcaemia
83
What measurement of HbA1c is indicative of DM?
6.5% or 48 mmol/mol
84
Aside from the history and glucose levels, what are diagnostic/supportive aids for diabetes?
1. Ketone testing +- bicarbonate 2. Pancreatic auto-atnibodies 3. C peptide
85
Four differentials for diabetes
```
MODY
T1D
T2D
Pancreatic diabetes
LADA
Secondary diabetes-
```
86
Two causes of secondary diabetes?
acromegaly, thyrotoxicosis, cushing's syndrome
87
How would you assess for microvascular changes in T1D?
feet assessment, creatinine ratio, U&Es, retinal photograph
88
What are the biomedical targets that are reviewed annually in diabetes?
BP, cholesterol, HbA1C, body weight
89
What is the first line treatment for T2D?
always lifestyle +metformin (somtimes sulfonylureas)
90
What is the second line treatment for T2D?
two agents: add SU, flozin, gliptin, glitazone
91
Third line?
three agents: add any of second line OR start injectable therapy with GLP-1 agonist or insulin
92
What is the MOA of metformin?
suppresses gluconeogensis, reducing glucose output from liver and increases peripheral insulin sensitivity. Also increases AMPL activity
93
Two benefits of metformin?
weight reduction, low hypo risk, CV benefit, extensive experience, moderate efficacy
94
What is the MOA of sulfonylurea?
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
Two benefits of sulfonylureas?
high efficacy, extensive experience
96
Two disadvantages of SU?
No CV benefit, weight gain, high hypo risk, caution in CKD
97
MOA of gliptins?
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
Two benefits of gliptins?
low/moderate efficacy, low hypo risk, few adverse events
99
What is the MOA of SGLT2 inhibitors?
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
Two pros of flozins?
moderate efficacy, CV benefits, renal benefit, weight loss, low hypo risk
101
Two SE of flozins?
risk of GU infections, small risk of DKA
102
What is the MOA of thiazilidinediones?
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
SE of glitazones?
weight gain, fluid retention, fractures
104
61y man with BMI32, smoker, hypertension, symptomatic. Already on metformin What would be the next treatment intervention?
Flozin- promotes weight loss (SU and glitazone would increase weight)
105
Explain the MOA of GLP-1 agonists
increases insulin secretion (beta cells), decreases glucagon (alpha cells), increases satiety and suppresses appetite
106
Two SE/disadvntages of GLP-1 agonists?
GI side effects, uncertain safety as quite novel, injection...
107
List four points of education to discuss with patients with T1D?
glucose/ketone monitoring, sick day rules, driving regulations, exercise and alcohol, pregnancy, targets, complications, admin of insulin
108
Give an example of a SU
gliclazide
109
Two contradindications for metformin?
chronic heart failure, severe renal disease, DKA, MI, stroke
110
Is T1D or T2D more strongly inheritable?
T2D!
111
Which form of diabetes is MODY?
T2D. Presents in young people with FH of T2D
112
Two key features of diagnosing MODY?
under 25
| Parent with diabetes, with diabetes in two or more generations
113
Which are the two main forms of monogenic diabetes?
MODY and neonatal diabetes mellitus- NDM
114
Patient with hypoglycaemia, as a rule of thumb, what treatment do you give them?
10% glucose IV (NOT dextrose!!)
