diabetes Flashcards
1
Q
what is diabetes?
A
a group of metabolic disorders characterised by hyperglycaemia due to lack of insulin, insulin insensitivity or both.
2
Q
what causes type 1 diabetes?
A
type 1 diabetes is an autoimmune disease whereby there is destruction of B cells.
It is associated with the autoantibodies GAD65 and tyrosine phosphate.
associated with HLA DR3/4
genotype + environmental trigger leads to immune activation.
3
Q
what causes type 2 diabetes
A
obesity and genotype leads to insulin insensitivity.
At first the pancreas produces more insulin to keep up. Eventually there is pancreatic exhaustion and insulin production falls.
eventually all insulin ceases and injections are needed.
4
Q
in general how can the causes of diabetes be classified? i.e. one being not enough insulin is made (T1/2)?
A
not enough insulin
insulin receptor problem
insulin molecule problem
insulin signalling problem post receptor
5
Q
what is type 1.5 diabetes
A
an autosomal dominant condition where type 1 diabetes presents later in life. it is due to autoimmunity against B cells.
often misdiagnosed for type 2.
6
Q
what is MODY?
A
mature onset diabetes of the young.
- T2D in the young
- autosomal dominant cause
- defects in B cells to produce enough insulin
7
Q
apparent from type 1 and 2 diabetes, list some other causes of diabetes
A
Type 1.5
MODY
leprechaunism = receptor problem
lipodystrophic diabetes = signalling problem
secondary: drugs, exocrine pancrease damage, endocrinopathies
8
Q
name the condition that causes diabetes due to insulin receptor dysfunction
A
leprechaunism
9
Q
name the condition that causes diabetes due to post insulin receptor dysfunction ?
A
lipodystrophic diabetes
10
Q
A syndrome that leads to diabetes and deafness is caused by what?
A
mutations in mitochondrial DNA
11
Q
what drugs induce secondary diabetes?
A
thiazides, B blockers, steroids, HIV medication.
12
Q
what are the causes of damage to exocrine pancreas that can lead to diabetes
A
pancreatitis, infection, carcinoma, trauma, pancreatectomy
13
Q
what are the endocrinopathies that can lead to diabetes?
A
cushings, hyperthyroidism
high: GH, adrenaline, glucagon
14
Q
state 2 non-diabetic hyperglycaemias.
A
prediabetes (borderline diabetes) - impaired glucose tolerance test and impaired fasting glucose test are both high but not enough for diabetes.
gestational - diabetes through pregnancy (usually 3rd trimester)
15
Q
what has a stronger genetic link, T1D or T2D?
A
T2D
16
Q
how does the presentation of type 1 and 2 diabetes differ? (not including symptoms) i.e. age of onset, gradual/acute
A
type 1:
- before 20/30 yrs
- rapid onset (weeks) and rapidly fatal if not treated
- usually in lean individual
- less common than type 1 - associated with other autoimmunity
type 2:
- > 40yrs
- slow onset and long time before diagnosis
- usually in overweight and Asians
- associated with obesity, lack of exercise, high calories and alcohol
17
Q
how do the symptoms between type 1 and 2 diabetes differ?
A
type 1 and 2: polydipsia and polyuria and lack of energy
type 1: marked weight loss. although in type 2 there is weight loss it is not as obvious because individual is over weight and there isn’t as dramatic lack of insulin
type 1:
- symptoms of ketoacidosis
- muscle wasting
type 2:
- vague symptoms and more variable e.g. persistent infections (thrush), visual problems and slow healing.
18
Q
what are the symptoms of ketoacidosis?
A
acetone breath dehydration and thirst nausea and vomiting abdominal pain blurry vision hyperventilation
19
Q
what are the two most useful ways to differentiate between type 1 and 2 diabetes?
A
weight loss more obvious in type 1
ketoacidosis: either symptoms of it or by blood test
20
Q
in an osce other than the presenting complaint, what other information would be useful in someone presenting with diabetic symptoms?
A
PMH: pancreatitis, other autoimmune, cushings, previosu stroke
FHx = diabetes, CVS disease, stroke
Drug history = thiazides, B blockers, HIV medication, steroids. also check for diuretics and lithium (other causes of polyuria)
21
Q
what are the differentials for polyuria?
A
diuretics UTI nephrogenic diabetes - pituitary tumour - nephrogenic insensitivity - lithium, hypoK
22
Q
explain the cause of polyuria and polydipsia in diabetes
A
there is excess glucose in the blood and thus more gets filtered and exceeds the Tmax. Therefore glycosuria and water follows by osmosis and thus polyruria.
this leads to dehydration which acts on the thirst centre of the hypothalamus to induce polydipsia
23
Q
explain the cause of weight loss and ketoacidosis in diabetes
A
although more glucose, cells (such as liver) cannot use this because there is no insulin. Therefore the liver instead metabolises proteins (gluconeogenesis) and fats (B oxidation). this leads to muscle wasting and weight loss.
ketones build up from breakdown of fats. some ketones are acidic and thus lead to ketoacidosis
ketoacidosis only usually in T1D when insulin is very low.
24
Q
explain the complications to the microvasculature and microvasculature in diabetes
A
microvasculature: osmotic pressure of the blood damages capillaries and small vessels.
25
how are plasma proteins affected in diabetes
glycosylation of them disrupts their function
26
what happens to non-insulin dependant cells in diabetes. (don't need to include specific organ changes)
glucose enters these cells/
glucose is converted to sorbitol by aldose reductase (NADPH to NADP).
Sorbitol damages the cells by increasing the osmotic pressure
less NADPH means less reducing power - cross linking of proteins.
e.g. eyes, neurons and kidney.
27
what are the 3 types of nerves that can be affected in diabetic neuropathy
sensory
motor
autonomic nervous system
28
explain the problems of sensory neuropathy in diabetes
leads to damage of skin and thus infection and ulcers
| leads to charcot arthropathy (deformity of weight bearing joints due to repeated injury and increased mechanical stress)
29
explain the problem of autonomic neuropathy in diabetes
```
postural hypotension - most common
erectile dysfunction
dry feet
urology - nephrogenic bladder - reduced emptying.
sweating
heart rate doesn't vary with resp rate
```
30
explain the problem of motor neuropathy in diabetes
clawing of toes.
31
how do diabetic foot ulcers occur?
poor sensensation so damage to skin
poor nutrition (poor blood supply) - therefore slow healing
poor immunity - increased risk of infection
32
what are diabetic foot ulcers and what can they lead to?
painless punched out ulcer in area of thick callus
can lead to cellulitis, abscess or osteomyelitis
33
what are the different pathologies in diabetic eye?
retinopathy
-maculopathy
glaucoma
cataracts
34
overall what is causing damage in retinopathy?
increased blood pressure in small vessels leads to microaneurysms and haemorrhages. Proteins leak onto the retina and form plaques. haemorrhages lead to areas of ischaemia
35
what changes are seen in retinopathy?
micro aneurysms: weak small blood vessels dilate and are predisposed to leakage and breaking
hard exudate: lipoproteins and other protein leak out of blood vessles
haemorrhages: rupture of weak vessles
cotton wool spots: areas of axonal debris and ischaemic infarcts
neovascularisation: new blood vessels are made to re-vascularise hypoxic retina. but these are small and prone to rupture.
36
describe the 3 stages of diabetic retinopathy
background retinopathy - microaneurysms, haemorrhage, lipid deposits
pre proliferative retinopathy - same as above + cotton wool spots
proliferative retinopathy - new blood vessel formation. in advanced disease larger vessels also proliferate and retinal detachment
37
what is maculopathy seen in diabetes?
when the retinopathy changes affect the macula specifically. this is more problematic as it will affect vision more greatly.
includes focal/diffuse macular oedema
ischaemic maculopathy: may actually look normal on fundoscope (but acuity will be reduced and can be seen on fluorescin angiography.
clinically significant macular oedema (CSMO): thickened retina and hard exudates - when found near fovea or big enough it is classed as CSMO
38
what is glaucoma and how does diabetes cause it?
glaucoma is caused by increased pressure in the eye and this pressure compresses and damages the optic nerve and can lead to loss of vision
in diabetes there is increased pressure due to sorbitol being produced from glucose and excess water (osmosis). This pressure can lead to glaucoma.
moreover rubeosis iridis (neovascularisation of the iris) can block the angle of the eye (where fluid drains) leading to acute glaucoma
39
what is cataracts and how does diabetes cause it?
cataracts is when the lens of the eye becomes cloudy.
| in diabetes there is excess cross linking of proteins (less NADPH) and thus leads to cataracts
40
what are the risk factors for retinopathy in diabetics?
```
poor glycaemic control
HTN
duration of diabetes
smoking
high lipids
pregnancy
renal disease
```
41
how do diabetic patients with retinopathy present usually?
usually asymptomatic (normal eyesight) until advanced disease
gradual decline of central vision.
haemorrhage: black painless floaters which resolve over several days
severe haemorrhage: may obscure vision completely. again painless
acute glaucoma: sudden painful reduction in vision. urgent referral needed.
42
what is the pathyophysiology behind diabetic nephropathy?
glomerular damage and proteinuria due to:
- increased pressure in glomerulus (due to sugars and osmotic pressure)
- glycosylation of the basement membrane leading to increased collagen IV and mesangial expansion. leads to nodular scleorosis (kimmelsteil Wilson lesion) and BM thickening.
- can present as nephrotic or nephritic syndrome
- progressive proteinuria so eventually classed as nephrotic syndrome
ischaemia due to atherosclerosis of renal artery
Damage from ascending UTI
43
describe the progressive changes in glomerular function seen in diabetes.
1. at first increased filtration simply due to increased osmotic pressure due to sugars (reversible)
2. changes to BM lead to permanent increased GFR
3. GFR now normal (due to beginning of nephropathy) but still microproteinuria (meaning more leaky)
4. eGFR is low (nephropathy) and still proteinuria (leaky)
44
what are the signs and symptoms of diabetic nephropathy?
uncommon to have symptoms in early stage
| oedema and weight gain (loss of proteins)
45
how can we prevent diabetic nephropathy?`
good blood pressure and sugar control
| stop smoking
46
why does diabetes lead to infection
hyperglycaemia and acidaemia lead to impaired immunity
| reduced healing due to poor vasculature
47
what are the 2 ENT infections diabetics get?
malignant necrotising otitis externa
| rhinocerebral mucormyocosis
48
what is malignant necrotising otitis externa?
infection caused by pseudomonas aeruginosa
starts in auditory canal and spreads to soft tissue, cartilage and bone
severe ear pain and ottorhoea
49
what is rhinocerebral mucormycosis ?
infection caused by mould fungus in the sinuses.
occurs in patients with poorly controlled diabetes or ketoacidosis.
spreads to soft tissue and bone necrosis
50
what organisms cause:
- cellulitis
- necrotising fasciitis and diabetic foot
in diabetes
cellulitis:
- staphylococcus aureus and group A B haemolytic streptococcus
necrotising fasciitis and diabetic foot are caused by many organisms at once including the two above and enterobacter and anaerobes
51
why do diabetics get UTIs?
| what organisms are responsible?
neurogenic bladder - incomplete emptying
glycosuria - aids bacterial growth
E.coli and pseudomonas aeruginosa
52
what is the normal plasma glucose level?
3.8-6.5mM
53
what are the different venous glucose blood tests available and how are they used to diagnose diabetes?
random venous plasma glucose >11.1mM
fasting glucose tolerance test >7mM
oral glucose tolerance test (measure after 2 hr) >11.1
need 1 positive if symptomatic
OR 2 positive results if asymptomatic
54
how is prediabetes defined using plasma glucose tests?
fasting 6.1-7mM
| oral: 7.8-11 mM
55
what is HbA1c and how can it be used in diabetes
glycosylated Hb should be 4%-6%
diagnosis if >6.5%
can monitor HbA1c because it is a good predictor of glycaemic control over last 2-3 months. also linked to complications so by monitoring you can know if complications are being minimised.
56
when can HbA1c not be used? what can be used instead?
haemoglobinopathies
| use fructosamine test instead
57
other than blood tests and HbA1c what other tests can be used to diagnosis/assess diabetics?
For type 1:
- Assay for AutoAb (GAD65 and islet cell Ab)
- check for HLA DR3/4
urine dipstick:
- look for glucose
- look for ketones (distinguish between T1D and T2D)
ketoacidosis: plasma ketones >3mM
58
what is plasma C peptide?
tells you how much endogenous insulin is being made
cleaved off endogenous insulin during production of active insulin
59
how do we monitor CVS complications in diabetes
monitor cholesterol and lipid blood levels.
monitor blood pressure (aim <135/80; even lower if renal disease) - check every 6 months
check BMI
60
what treatment is used in diabetes to reduce CVS risk?
statins (40mg simvastatin to all diabetics regardless of IHD)
antihypertensives if >140/90; ACEi if microalbuminuria (despite BP)
aspirin 75mg to reduce CVS events
61
what advice is given to reduce CVS complications of diabetes?
stop smoking (offer cessation service)
reduce lipids
loose weight
62
how can we monitor nephropathy in diabetics?
U&E, eGFR, ACR in urine , proteinuria by urinalysis
63
what is the difference between macro and microproteinuria
macro- a lot of proteins - picked up by urine dipstick. indicates renal failure.
microalbuminuria - not picked up by dipstick but can be found by analysis of urine albumin: creatinine ratio. if ACR >3 indicates early renal disease and increased vascular risk
64
how do we treat microalbuminuria and why?
ACEi regardless of BP
| ACEi will reduce glomerular pressure and thus reduce proteinuria
65
is microalbuminuria reversible
yes with good glycaemic control, good blood pressure control, stop smoking and reduce fats
66
what are gliptins?
DPP4 inhibitors (DPP4 normally inhibits GLP1 by breaking it down; GLP1 acts normally to increase insulin release etc)
more GLP1, more insulin, increased satiety and reduced gastric emptying and reduced glucagon release.
67
what are the ADRs of gliptins?
what are the advantages
GI symptoms (reflux, diarrhoea)
pancreatitis
low risk of hypoglycaemia
weight neutral. actually very good drugs and used second line to metformin and sulphonylureas but expensive.
68
how can you monitor someone with diabetic neuropathy ?
peripheral nerve exam
- test sensation: diabetics loose sensation over stocking distribution
- absent ankle reflexes
- claw toe and pes cavus
69
how can we treat diabetic neuropathy?
give vitamin B12 to improve function
depends on the problem:
- symmetric sensory polyneuropathy: amitriptyline, gabapentin and paracetamol
- mononeuritis multiplex: if sudden corticosteroids
- postural hypotension: sometimes fludrocortisone
- amyotrophy: IV immunoglobulins
charcots joints:
- reduce weight bearing by using crutches and bed rest.
- bony repair
70
other than diabetes, what other conditions lead to charcots joints?
```
spina bifida
hereditary sensory motor neuropathy
leprosy
tabes dorsalis
syringomyelia
```
71
name 4 specific diabetic neuropathies and explain what they are
symmetric sensory polyneuropathy: glove and stocking numbness and tingling (worse at night)
amyotrophy: painful wasting of quadriceps due to radiculopathy
mononeuritis multiplex: cranial nerves III and IV
autonomic neuropathy.
72
what are GLP1 receptor agonists? what are the ADRs and advantages?
mimic GLP 1 and thus increase insulin release and satiety, reduce glucagon and gastric emptying.
ADRs: reflux, GI problems (diarrhoea, nausea), low risk of hypoglycaemia
advantage - weight loss.
73
what are sulphonylureas's? what are the ADRs?
antagonise K+ ATP sensitive channels. therefore block them so B cell depolarises and insulin is released.
ADR: weight gain, hypoglycaemia, GI disturbance
74
what is metformin? what are the ADRs? what are the benefits
first line agent for T2D
increases insulin sensitivity - reduces gluconeogenesis and increases glucogenesis.
```
ADRs:
GI symptoms (dyspepsia, flatulence, diarrhoea)
rare - lactic acidosis by reducing renal bicarbonate secretion (more likely if renal problems)
B12 deficiency - rare
```
benefits: no risk of hypo and weight neutral. cardio protective. (usually once started kept on it)
75
how do we check the eyes of a diabetic?
eye examination:
- visual acuity (Snellen chart, fine print reading and ishihara plates)
- visual fields, eye movement and pupil reflexes
fundoscopy:
- best viewed when eyes dilated (but cant drive for 6hours after)
- check red flex first and then retina.
digital retinal photography with mydriasis (dilation of pupil) is gold standard for retinopathy.
76
what do spots on the red reflex during fundoscopy suggest?
vitreous haemorrhage
77
what are the diabetic guidelines for retinal screening
T1D/T2D aged above 12 must be offered annual retinal screening
pregnant diabetics more often.
78
how do we treat diabetic eye?
primary prevention - educate patient how important glycaemic control is
laser photocoagulopathy - for proliferative retinopathy
intravitreal steroids for maculopathy
anti VEGF for diabetic macular oedema
surgery:
vitrectomy - after a bleed (to remove blood) and to repair any retinal detachments allows for clearer vision.
surgery for cataracts - lens replacement
surgery for glaucoma - reopen drainage system
eye drops for glaucoma
laser treatment for glaucoma.
79
what eye drops are given for glaucoma?
B blockers, prostaglandin analogues
80
what is laser photocoagulopathy?
stops the production of angiogenic factors on ischaemic retina. used to prevent progression of proliferative retinopathy. cannot restore vision.
81
how would you monitor diabetic feet in diabetic patients?
peripheral nerve and peripheral vascular exam (include Doppler)
Xray for bony deformities or osteomyelitis
swab, blood cultures for infections.
82
how can you distinguish between neuropathy and peripheral vascular disease
PVD: absent foot pulses
neuropathy: injury and infection over pressure points
mostly both are present.
83
how do you manage patients with diabetic feet?
educate patient to look at feet regularly, wear comfortable shoes, protect any injuries and visit chiropody to remove callus before necrotic tissue forms
treat infections: flucoxacillin, benzylpenicillin and metronidazole
surgery: endovascular stenting to improve blood supply
84
what are alpha glycosidase inhibitors? what are their ADRs?
e.g. acarbose
blocks enzyme responsible for breakdown of carbohydrates to glucose therefore reduces absorption
ADRs: diarrhoea, bloating, flatulence, abdo pain, weight loss
85
what are SGLT2 inhibtors? what are the ADRs?
inhibit SGLT2 on renal tubules. less glucose is reabsorbed
ADRs: polyuria and polydipsia (due to loss of water by osmosis, UTI, dehydration
86
what are glitazones/TZDs?
what are the ADRs?
what can we say about the half life and when the effects peak?
bind and activate PPARgamma nuclear receptor. increase gene expression for insulin sensitivity e.g. glucogenesis etc. so response to insulin is higher.
weight gain, fluid retention, heart failure, bladder cancer, bone metabolism
long half life - take once a day, and don't offer fine control
effects peak after 1-2 months
no hypoglycaemias.
87
what is the normal regime for treating T2D?
1. diet, exercise
2. metformin (if HbA1c is still high)
3. add sulphonylureas (if HbA1c is still high)
4. start insulin or other oral hypoglycaemics (glitazones, meglitidines, GLP analogs, a-glycosidase inhibitors)
.
88
can T2Ds use combination therapy?
combination therapy: if metformin and insulin together then less insulin is needed (benefit) however more ADRs e.g. higher risk of hypoglycaemia?
Sulphonylureas and TZDs are bound to plasma proteins and thus displace eachother and levels rise
89
list some common ADRs of oral hypoglycaemics?
weight gain - due to increased insulin sensitivity so more glucose for cells to store. (however sometimes weight loss if glucose is excreted by other means i.e. not by increasing storage /insulin sensitivity)
hypoglycaemia
GI symptoms because interfering with glucose absorption
90
why cant oral hypoglycaemics be used forever?
initially T2D is caused by insulin insensitivity and thus drugs like metformin increase this.
sulphonylureas - increases insulin release
but eventually there is prancreatic exhaustion and no more insulin and thus insulin therapy will eventually be needed
91
how is insulin released in normal physiology?
glucose enters B cells of islets of Langerhans.
Glucose enters glycolysis and makes ATP
ATP binds to ATP sensitive K channels to close them
Depolarisation of the cell
VG calcium channels open
Calcium is released into the cell
leads to exocytosis of insulin packaged vesicles.
insulin release is also promoted by amino acids, fatty acids, gastrin, secretin and CCK. insulin is inhibited by noradrenaline and adrenaline.
92
what is the action of insulin?
activates GLUT4 channels in liver, muscle and adipose. therefore glucose is taken up by these cells.
inhibits gluconeogenesis, glucogenolysis and lipolysis
stimulates glucogenesis, fatty acid synthesiss
overall anabolic.
93
how does glucagon work?
released from a cells when glucose is low.
| stimulates glucogenolysis and gluconeogenesis.
94
explain the normal process that occurs when glucose is ingested (relating to the parts that are pharmacologically relevant: alpha glycosidase, ATP K channels, GLP1 and DPP4)
1. complex sugar eaten and digested by amylase
2. alpha glycosidase is an enzyme that breaks down disaccharides to glucose
3. glucose is absorbed into the blood streem
4. glucose goes into B cells and leads to closure of ATP sensitive K channels which leads to insulin release
5. insulin binds muscle, liver and adipose cells to allow glucose to be taken up and anabolic processes to begin.
GLP1 is a hormone released by intensines after eating to increase insulin release and inhibit glucagon and gastric emptying. also promotes fullness,
DPP4 normally breaks down GLP1
95
which T2D drug is best effective at lowering HbA1c?
biguanides e.g. metformin
96
when should metformin be stopped and why?
any serious/unmanageable side effects
if eGFR is less than 30 as this increases risk of lactic acidosis.
97
how often is metformin given?
2-3 times a day due to short half life.
98
what are meglitidines?
rapaglinide
| work by same mechanism as sulphonylureases
99
name 2 sulphonylureas's
gliclazide, tolbutamide
100
when are sulphonylurea's usually taken?
before meals.
101
give 1 example of a glitazones (TZDs)
rosiglitazone
102
name a gliptin
sitagliptin
103
how is borderline diabetes managed?
diet and exercise
| annual reviews
104
what equipment is needed for finger prick glucose monitoring?
lancing devise (pricks finger), needle, alcohol wipes, test strips, cotton balls, plaster and meter reading
105
describe the steps for finger prick glucose monitoring
1. wash hands with warm water to get blood flowing and massage finger
2. put test strip into meter
3. wipe finger with alcohol wipe
4. prick finger and squeeze
5. put strip into blood.
106
how is an insulin syringe used?
using syringe and needle draw up correct amount of insulin (info given by GP)
wipe abdomen/thigh with alcohol wipe
pinch skin/fat and inject at 90 degrees
dispose syringe to avoid infection.
alternate injection site
107
how is an insulin pen used?
usually have two pens, one long acting and one short acting. put cartridges into pen. dial up dose and inject at 90 degrees. change needle daily
easy but expensive
108
how is urinalysis performed?
collect urine.
dip dipstick into it and wait for 30 seconds.
remove and place horizontally and wait for 30sec-1 min
read colours using box as a guide.
109
what are the complications when treating T2D patients
poor compliance due to:
- fear of weight gain
- cant feel long term effects of hyperglycaemia
- don't like injections
- fear of hypoglycaemia.
110
What is classed as hypoglycaemia and what can cause this?
glucose <3mM
| not enough glucose or too much insulin
111
what are the two stages of hypoglycaemia?
stage 1:
- increase in sympathetic NS - sweating, hunger, anxiety, tremor, palpitations, dizzy
- patient should be able to recognise and eat/drink Lucozade
stage 2:
sympathetic NS crashes: confusion, drowsy, seizures, visual problems and coma
112
how is hypoglycaemia treated?
glucose to mouth: glucogel and a long acting sugar (starch) - this is if patient is conscious and can swallow.
if they cant swallow then give IV glucose 75ml
if no IV access give glucagon IM injection
113
what are the different types of insulins?
ultrafast acting/ bolous insulin (novorapid)
- inject just before/after meal for fine control
isophane insulin:
- variable peak 4-12 hours. cheap so favoured by NICE
```
premixed insulin (Novomix)
- both long and short
```
long acting analogue (basal insulin):
- before bed (i.e. when not eating for a while)
114
what are the different insulin regimes?
BD biphasic (premixed insulin used):
- twice daily of novomix
- less injections but control is less fine
QDS regime (a.k.a. basal bolus)
- before meals ultra fast and before bed long acting.
- allows more varied life style (different meal sizes, gym) but more injections required.
Once daily: i.e. long acting before bed. T2D that have recently started on insulin
115
what are the ADRs of insulin?
```
weight gain
risk of hypoglycaemia
lipohypertrophy - fat lump at site of injection if use the same place
painful injection
allergy
```
116
what is DAFNE?
dose adjustment for normal eating
- it is an educational programme for patients to help them better control their diabetes. Also must complete this before they qualify for a pump.
- teaches you how to match dose to carb input
- teaches you how to adjust dose during illness, exercise and menstruation
117
how does the insulin requirement change during a period of infection? what advice is given to patients
despite reduced appeptite and food intake the need for insulin actually increases.
Patients need to check their blood glucose and ketones in urine >4 times a day
They are advised to seek medical attention if vomiting, diarrhoea, pregnant or signs of DKA.
118
how does insulin requirements change with exercise?
less insulin is required.
119
what general advice is given to both T1D and T2D in helping them manage diabetes
life style advice (stop smoking)
educate about long term complications
tell them about HbA1c and target of 6.5-7.5
how to use equipment
record blood sugars on daily basis so GP can look at day to day control on the chart.
seek help if pregnant
check for foot ulcer and other complications.
120
which diabetic patients are most likely to get
DKA
hyperglycaemic hyperosmolar nonketotic coma??
DKA - type 1
| HONK - also known as hyperglycaemic hyperosmotic state - type 2
121
biochemically how is HONK defined?
high glucose
high osmolality
normal ketones
no acidosis
122
what can HONK lead to?
CNS signs
rhabdomyolysis
DIC and DVTs
leg ischaemia
123
how is HONK managed?
ABCDE + investigations (i.e. bloods etc)
give LMWH
rehydrate slowly with 0.9% saline
may need to give insulin if glucose doesn't drop
look for cause:
- MI, Drugs, bowel infarct, infection (pneumonia, pyelonephritis)
124
other than DKA and HONK what is another acute complication of DM?
lactic acidosis
lactate in blood >5mM
125
what is lactic acidosis in DM patients caused by ? therefore how is it managed?
metformin and sepsis
| stop metformin and treat sepsis
126
what are the different ways of having diabetes in pregnancy?
previous T1/2D
| new onset gestation
127
what are the complications of diabetes in pregnancy?
```
miscarriage
preterm
pre-eclampsia
congenital malformations
macrosomia
```
128
what increases the risk of gestational diabetes?
```
over 25
family history
previous gestational diabetes
Asian
overweight
HIV positive
```
129
when should pregnant women be screen for gestational diabetes
oral glucose tolerance test at 16-18 weeks
6 weeks after birth fasting glucose tolerance test to see if diabetes persist (even if negative, 50% of these women will go on to develop chronic DM)
130
what advice should be given to pregnant women to reduce risk of gestational diabetes?
weight and glycaemic control
131
which diabetic drugs should be stopped in pregnancy
oral hypoglycaemics except metformin
132
why are elderly patients more prone to complications of diabetes
poor/eratic diet
reduced mental state so less able to pick up signs of complications
isolated so less able to get help
often symptoms are mistaken for other co-morbidities e.g. dementia, delirium, UTI
polypharmacy
impaired hepatic/renal metabolism
deteriorate faster
133
how often are elderly patients screened for diabetes?
annually
134
what are the main steps in managing DKA
ABCDE (repeat regularly)
- Airways: if vomiting, recovery position, NG tube
- Breathing: (probably hyperventilation) 100% O2 by face mask
- Circulation: likely to be in shock - fluid resus if <90mmHg. insert 2 large bore cannulas. If unresponsive send to ICU
- Disability : if patient unconscious consider cerebral oedema
- Exposure
Get results: - regularly check
- venous blood gas: HCO3, pH
- glucose, ketones, U&Es (H+ leads to K+)
- ABG
- ECG in case of hyperK
- CXR, blood cultures and midstream urine - in case of infection (no fever in DKA)
- urine dipstick
- FBC (WCC may be raised even if absence of infection)
cover the following:
- correct fluid loss
- correct hyperglycaemia
- correct electrolytes
- correct acidosis
- treat cause e.g. infection - e.g. start broad spec Abx
- manage complications
Monitor
135
why may signs of infection be different for patients with DKA?
fever is masked so need to be aware of this
136
why is creatinine not a good measure of renal function in DKA?
creatinine cross links ketones and so not true value
137
what are the triggers to DKA?
```
infection
wrong insulin dose
antipsychotic meds/chemotherapy
MI
trauma
```
138
how is DKA diagnosed? include criteria for severe DKA
DKA:
- acidaemia <7.3
- hyperglycaemia
- ketonaemia
severe (one or more):
- pH <7.1
- Ketones >6mM
- HCO3 venous <5mM
- anion gap >16
- GCS <12
- O2 sats <92%
- BP <90mmHg
- tachy/bradycardia
139
how can you assess dehydration (useful for DKA)?
```
cap refil
weak pulse
sunken eyes
dry mucus membranes
hypotension
oligiouria
cool peripheries
```
140
how do we correct fluid loss in DKA?
give 500ml 0.9% saline over 15mins. repeat up to 2 litres. if not responding seek ITU advice.
maintainance: 1L every 2 hours.
141
how is hyperglycaemia in DKA corrected?
```
IV fluids should occur 1 to 2 hours before insulin therapy
add actrarapid (short acting insulin) to 0.9% saline and infuse.
continue patient on long acting insulin
```
avoid hypoglycaemia - when glucose <14mM start on 10% glucose infusion too
142
what electrolyte abnormalities could be found in DKA? how are they solved?
hypo or hyperkalaemia
- hypo: K+ replacement started immediately with IV fluids (before any insulin therapy)
- hyper : insulin therapy will correct this
hypophosphataemic:
- KPO4 replacement but may lead to hypocalcaemia
hyponatraemia is common due to osmotic compensation for high glucose.
hypoMg
143
how can the acidosis in DKA be corrected?
NaHCO3 is infused if the acidosis is life threatening
144
what are the complications of DKA?
cerebral oedema
risk of VTE
aspiration pneumonia
145
how is cerebral oedema in DKA managed?
look for signs: headache, irritable, low HR, high BP, cranial nerve palsy
ensure hypoglycaemia, haemorrhage/thrombosis are all excluded
treat with mannitol and hypertonic NaCl
elevate head of the bed
146
how is risk of DVT in DKA reduced
LMWH and TED stockings
147
how is aspiration pneumonia treated in DKA
Abx
148
how do we monitor a patient with DKA?
```
pulse, resp rate , BP - every hour
fluid balance
ECG
Cap glucose - hourly
cap ketones - hourly
U&Es, blood gas, FBC- 2 to 4 hrly
neurological exam for cerebral oedema
```
149
in DKA when does cerebral oedema normally occur?
at initiation of treatment and gets worse throughout.
150
what is the name given to describe the type of ventilation in DKA
kussmaul hyperventilation - deep breathing
151
how is plasma osmolality calculated?
2 [Na] + [urea] + [ glucose]
152
what are the important points to consider when managing young children with T1D?
educate child and family members and inform teachers:
- how to fingerprick etc
- insulin therapy
- diet and exercise
- detecting hypo/HONK/DKA
- what to do during infection
recommend flu vaccine.
153
why is it sometimes difficult to maintain glucose in adolescence?
non adherence due to life stresses and stigma/bullying
154
When can a person come off metformin ?
Not usually stopped because of its benefits
| Lowers sugar, weight loss and cardio protective
155
what are the causes of diarrhoea in diabetes?
pancreatic insufficiency --> poor enzyme production i.e. steatorrhoea
enteric neuropathy
metformin side effect
156
give examples of some sulphonylureas
Tolbutamide
Glibenclamide
glipizide
157
what is DKA?
complication of type 1 diabetes where by there is very low/ absolute insulin deficiency where ketones build up in the blood causing acidosis.
defined by hyperglycaemia (>11mM), ketonaemia (>3mM) and acidosis (<7.3 or HCO3 <15)
158
what complication is usually seen in type 2 diabetes rather than DKA?
hyperglycaemic hyperosmotic state
159
describe the pathophysiology behind DKA?
low insulin
high glucose --> saturates kidneys --> dehydration
B oxidation of fats --> beta hydroxybutyrate (acidic)
160
what are the complications of DKA?
```
cerebral oedema
pulmonary oedema
hypo or hyper K
hypoglycaemia (from insulin therapy)
death
```
161
what factors can precipitate hyperglycaemic hyperosmotic state?
consumption of glucose rich food
thiazides, steroids
illness
162
If a diabetic patient on treatment presents with bruising and an increased INR, which diabetic medication is most likely to be the cause?
GLP 1 analogues
163
what are the rules concerning hypoglycaemia and driving?
if hypoglycaemic <4mM, stop driving in a safe way. have a carbohydrate snack. wait for 45 mins and re-check blood sugars. only drive when glucose is >4mM
driving with diabetes is okay if:
- there has not been any severe hypoglycaemic event in the previous 12 months
- the driver has full hypoglycaemic awareness
- the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
- the driver must demonstrate an understanding of the risks of hypoglycaemia
- there are no other debarring complications of diabetes
