diabetes Flashcards
how does alcohol intake increase the risk of hypoglycaemia?
alcohol inhibits gluconeogenesis
may impair hypo awareness and can impact on self care behaviours
auto antibodies associated with type 1 diabetes
GAD
IA-2
Znt8
what is the risk of children getting T1DM if their parents have it?
both - 30%
father - 8%
mother - 5%
what genes represent 50% of familial risk in T1DM?
HLA genes
cause of T!DM
cause unclear - may be genetic, can be triggered by certin viruses (coxsackie B virus, enterovirus)
pancreas stops veing able to produce insulin
T-cell mediated autoimmune disease
is T1DM more common in males or females?
males (post puberty)
can present at any age - peak around 10 to 14yrs
afriian, asian decent more at risk
T1DM presentation
hyperglycaemia, ketones
low insulin, beta cells and ketones
U18 = polyuria, polydipsia, weight loss, excessive tired
adults = rapid weight loss, ketosis, low BMI, fam autoimmune history, blurred vision
pathophysio of T1DM
no insulin being produced means cells can’t take glucose from blood + use it for fuel –> cells think body is being fasted + has no glucose supply
level of glucose keeps rising causing hyperglycaemia
T1DM diagnosis
- symptoms + random glucose >11.1 mmol/l
- asymptomatic + fasting >7 + 2hr post glucose load >11.1
- antibodies - GAD, IA-2, Znt8
how can blood glucose be monitored?
HbA1c - average over RBC lifespan, requires blood sent to lab
capillary glucose
flash glucose monitoring - lag of 5 mins, do cap glucose if hypo suspected
what does chronic exposure to hypergycaemia cause?
damage to endothelial cells of blood vessels - leads to leaky, malfunctioning vessels that are unable to regenerate
high levels of sugar in blood also causes suppression of the immune system + provides optimal environment for infectious organisms to thrive
long term complications of T1DM
macrovascular complications - CAD, peripheral ischaemia, stroke, hypertension
microvascular complications - peripheral neuropathy, retinopathy, nephropathy
infection related - UTIs, pneumonia, fungal infections (oral+vaginal candidiasis), foot infections
T2DM risk factors
older age
ethnicity - black, chinese, south asian
family history
obesity
sendentary lifestyles
high carb diet - esp refind carbs
T2DM presentation
fatigue usually obese no ketone polydispsia, polyuria opportunistic infections signs of complications
HbA1c + glucose levels in diabetes
HbA1c = >48
random glucose = >11
fasting glucose = >7
OGTT 2hr result = >11
What receptors are being over stimulated by the enhanced catecholamine effects in hyperthyroidism to cause her palpitations?
beta-1 receptors
Thyroid hormones increase the bodies sensitivity to catecholamines. The heart contains β1 receptors, which when activated by catecholamines results in an increase in heart rate.
Which test is most likely to be of clinical use in screening for medullary carcinoma recurrence?
serum calcitonin levels
Medullary thyroid cancers often secrete calcitonin and monitoring the serum levels of this hormone is useful in detecting sub clinical recurrence.
what are psammoma bodies?
clusters of calcification
Psammoma bodies consist of clusters of microcalcification. They are most commonly seen in papillary carcinomas.
drug treatment for T2DM
- metformin
- add one of: sulfonylurea, pioglitazone, DPP-4 inhibitor, SGLT-2 inhibitor
- triple therapy with metformin + 2 of above OR metformin + insulin
what drug treatment is preffered in T2DM patients with cardiovascular disease?
SGLT-2 inhibitors
GLP-mimetics
who does hyperosmolar hyperglycaemic state (HHS) commonly affect?
older people with T2DM who experience hyperglycaemia
–> can develop over weeks through a combo of illness + dehydration
high mortality (compared to DKA)
cause of HHS
high refined CHO intake pre-presentation (fizzy drinks)
diuretics and/or steroids
inadequate insulin or oral therapy, stopping medication during illness (swallowing difficulties/nausea)
pathophysio of hyperosmolar hyperglycaemic state (HHS)
hyperglycaemia results in osmotic diuresis with associated loss of sodium + potassium
severe volume depletion results in a significant raised serum osmolarity –> results in hyperviscosity of blood
HHS presentation
severe dehydration + electrolyte disturbances
dry mucous membranes
polyuria + thirst
nausea + vomiting
disorientation, gradual loss of consciousness
diagnosis of HHS (3 things)
hypovolaemia (lack of fluid)
hyperglycaemia (>30) WITHOUT ketonaemia or acidosis
raised serum osmolarity (>320)
complications of HHS
cardiovascular disease - MI, stroke (due to thickened blood)
sepsis - from underlying infection
management of HHS
correct fluid deficit + electrolyte abnormalities
monitor
IV insulin ONLY if ketones or blood glucose falling too slowly
treat underlying cause
prevent thromboembolism - LMWH unless contraindicated
which medication is lactic acidosis a key side effect of?
metformin
diabetic ketoacidosis (DKA)
T1DM (usually young) who is no producing/injecting adequate insulin
increase in counter-regulatory hormones - glucagon, cortisol, growth hormone
life threatening medi emergency
precipitants of DKA
insulin deficiency
increase insulin demand (infections, intoxication, infarction, surgery, steroids)
starvation
pathophysio of DKA
cellls have no fuel + think they are starving so iniate ketogenesis
–> overtime glucose + ketone levels both increase
initially kidneys produce bicarbonate to counteract the ketone acids in the blood + maintain normal pH
–> overtime bicarbonate is used up + blood starts to become acidic = ketoacidosis
DKA presentation
abdo pain + tenderness acetone breath nausea + vomiting polyuria + polydipsia/dehydration altered consciousness
diagnosis of DKA
hyperglycaemia = blood glucose >11
ketosis = blood ketone >3 or >2 on urine dipstick
acidosis = pH < 7.3
priorities in management of DKA
dehydration, potassium imbalance, acidosis = what will kill patient
priority = fluid resuscitation
then insulin infusion
treatment of DKA
FIG-PICK
Fluids - IV saline
Insulin
Glucose - monitor, add dextrose infusion if below certain level
Potassium - monitor
Infection - treat, possible trigger
Chart fluid balance
Ketones - monitor
-> slow infusions
how are patients restarted on an insulin regime post DKA?
patients must be established on a normal insulin regime prior to stopping the insuline + fluid infusion (part of DKA treatment)
complications of DKA
cardiac arrest/arrhmyias secondary to hypokalaemia
adult respiratory distress syndrome
cerebral oedema - esp in kids
gastric dilatation/stasis - risk of aspiration pneumonia
key complication of DKA in kids
cerebral oedema
- rapid correction with fluids + insulin causes rapid shift in water from extracellular space to intracellular space in brain cells
- causes brain to swell + oedematous - brain cell destruction + death
*monitor for headaches, altered behaviour, SLOWLY give fluids
conditions associated with hypoglycaemia
coeliac disease addisons/hypopituitarism hypothyroidism renal failure gastroparesis
risk factors for hypoglycaemia
previous severe hypo
longer duration diabetes
high risk indivdual - old, young, unaware of hypos
T1DM who have been on treatment a while
common causes of hypoglycaemia
missed/delayed meal not enough carbs at last meal increased physical activity too much insulin alcohol - esp. on empty stomach tight control - little reserves for unexpected events
hypoglycaemia presentation
tremor, irritability, anxious
hunger, weakness, fatigue
sweating
pallor, dizziness
hypoglycaemia glucose level
glucose <4 mmol/L
severe hypo can lead to reduced consciousness, coma + death unless treated
ways to reduce hypos
carry emergency supply of carb dense foods + diabetic ID
check blood glucose frequently - esp before bed
never consume alcohol on an empty stomach
be aware stress, illness, exercise effects blood glucose levels
management of hypoglycaemia
rapid acting glucose (lucozade) + slow acting carbs (biscuit + toast) for when rapid is used up
–> 15-20g rapidly absorbed carbohydrate
severe = IV dextrose + intramuscular glucagon
what is monogenic diabetes?
diabetes caused by a mutation in a single gene (mendelian disease)
->results in defects in insulin secretion or insulin action
commonest = MODY
types of monogenic diabetes
defects in insulin secretion
> MODY
> neonatal diabetes
defects in insulin action
>insulin signalling - AKT, INSR
> fat storage - CIDEC
Maturity Onset Diabetes of the Young (MODY)
autosomal dominant
non-insulin dependent diabetes
rare 1-2% of people with diabetes
90% misdiagnosed
what is the typical age of onset of MODY?
usually before 25yrs
types of MODY
transcription factor mutations
> HNF1-alpha (commonest)
> HNF1-beta
> HNF4-alpha
glucokinase
MODY (HNF1-alpha)
commonest transcription factor mutation
lowers amount of insulin made by pancreas
autosomal dominant
adolescence onset
treatment = low dose sulphonylureas
risk of long term complications
MODY (glucokinase)
helps recognise high glucose level in body
onset at birth
usually only slightly higher glucose than normal
no treatment - dietary only
no follow up, complications rare
treatment of neonatal diabetes mellitus
high dose sulphonylureas
treatment for diabetes related nephropathy
ACEi / ARB
pathophysio of diabetes complications
excessive glucose, mitochondria can’t keep up so alternative pathways used
these preciptate -
> polyol pathway - osmotic damage
increased ROS
inflammation
fibrosis
nephropathy in diabetes patients
caused by damage to capillaries in kidneys glomeruli, microvascular changes - angiopathy of capillaries
characterised by proteinuria + diffuse scarring of glomeruli
microalbuminuria is a marker of high risk
types of neuropathy
peripheral - charcot foot, numb
proximal - bum leading to weakness in legs
autonomic - changes in bowel, heart/vessels (fainting)
focal - sudden weakness in one or a group - carpal tunnel, bells palsy
management of diabetes during pregnancy?
Pre-pregnancy counselling
o Good sugar control preconception, limit risk of congenital malformation
Folic acid 5mg – more than in normal pregnancy
Consider change from tablets to insulin (T2DM)
Monitoring everything – HbA1c, BP, blood sugar
preferred blood pressure medication in pregnancy?
labetalol
nifedipine
methydopa
ACEi = tetragenic
types of weight loss surgery?
restrictive
- gastric balloon
- gastric band
- sleeve gastrectomy
malapsorptive
- gastric bypass (roux en y) = gold standard
- bilio-pancreatic diversion
when is orlistat recommended?
BMI >= 30 or >=28 with comorbidities
guidelines for continuation of orlistat
lost >=5% of body weight in first 3 months
lost >=10% of bodyweight in first 6 months
what is orlistat? when is it used?
non-systemic lipase inhibitor - used for weight loss
blocks 30% dietary fat
diet when on orlistat
hypocaloric / low fat diet is essential
150/250 kcal deficit/day
side effects of orlistat
stearrhoea
abdo pain
weird stools
management of pre-existing diabetes in pregnancy
folic acid 5mg (pre-conception-12weeks)
regular eye checks - accelerated retinopathy
consider change from tablets to insulin in T2DM
monitor - HbA1c, BP
high risk - start aspirin at 12 weeks
avoid ACEi + statins - tetratogenic
management of diabetes during labour
maintain good blood glucose
may require IV insulin + IV dextrose
postnatal care of pregnant diabetics
lower insulin dose + be wary of hypoglycaemia, insulin sensitivity will increase after birth + with breast feeding
monitor baby for hypoglycaemia - feed frquently + maintain glood glucose above 2
what are babies of mothers with diabetes at risk of?
neonatal hypoglycaemia
macrosomia (big babies)
polycythaemia (raised haemoglobin)
jaundice (raised bilirubin)
cangenital heart disease
cardiomyopathy
gestational diabetes
diabetes triggered by pregnancy - resolves after birth
caused by reduced insulin sensitivity during pregnancy
gestational diabetes risk factors
previos gestational diabetes
previous macrosomia baby (>= 4.5kg)
BMI >30
black caribbean, middle eastern, south Asian
family history of diabetes - first degree relative
(if RF = OGTT at 24-28weeks)
clinical features of gestational diabetes
large for dates foetus
polyhydramnios (increased amniotic fluid)
glucose on urine dipstick
gestational diabetes management
educate - monitoring, diet+exercise
4 weekly US scans to monitor foetal growth + amniotic fluid - from 28-36weeks
metformin then insulin - glibenclamide if cant tolerate
prevention of DM post preg
6 week postnatal OGTT to ensure resolution
gestational DM management post pregnancy
prevention of DM post preg
6 week postnatal OGTT to ensure resolution
which type of lactic acidosis is diabetes associated to?
Type B
- can also occur in liver disease / leukaemia
Type A is associated with tissue hypoxaemia, infarcted tissue, hypovolaemic shock
when is lactate lowest?
fasted state - rises in exercise
lactic acidosis presentation
hyperventilation
confusion
reduced bicarbonate
raised anion gap (acidosis)
absence of ketone
how is an oral glucose tolerance test carried out?
performed in the morning after a fast
patient drinks a 75g glucose drink at the start of the test
blood sugar is measured before and then 2hrs fter taking drink
