Diabetes Flashcards
What are the symptoms of diabetes mellitus
polyuria polydipsia weight loss
At what age does diabetes mellitus usually present
5 – 15 but can prison at any stage of life
pathophysiology of diabetes mellitus
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
what symptoms should make you suspect DKA
abdominal pain and nausea and vomiting tachyopnea lethargy
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
start immediate insulin treatment
what are the indications of starting immediate insulin treatment at any age
a short history (weeks of severe symptoms) fame/anorexia moderate/high plasma or urine glucose levels
when taking the history of a diabetic patient what should you include?
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
how would you diagnose diabetes if the patient is symptomatic
random plasma glucose >11.1 or fasting plasma glucose >7.1
how would you diagnose diabetes if patient is asymptomatic
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
how would you monitor Type II diabetes
HbA1c
what is HbA1c a marker of
reflects hypoglycaemic levels over the last three months
what routine lab investigations apart from blood glucose should be performed in diabetes mellitus
HbA1c U+E lipids LFT (T2) urinary albumin (+glucose)
what is HbA1c target in diabetic patients
around 48
what is a normal value for HbA1c
31 – 37
why should you check liver function in type II diabetics
check for non-alcoholic fatty liver disease or non-alcoholic steatohepatitis
What are the aspects of an individual care plan in diabetes care?
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
What should the targets of glycaemic control be?
fasting on waking - 5-7mol plasma BM before meals = 4-7 or after meals 5-9
how often should someone be checking their BMs?
before meals and before bead (total 4xd)
what are the sick day rules?
measure BMs more often / have easily digestive foods or drinks / oral rehydration sachets glucose tablets / gels / additional insulin / blood ketone strips
what are complications of poorly controlled diabetes mellitus?
can be microvascular : retinopathy nephropathy neuropathy inc. autonomic neuropathy
what sare signs nephropathy is occuring in DM?
frothy urine from proteinurea and increased BP
what drug can cause nephropathy esp. in those with DM?
ACEi (used for BP control)
what are the manifestations of autonomic neuropathy?
postural dizzyness, nocturnal diuresis, vomiting, change in taste, sweating
on examination of a foot of a patient with DM you notice 3 signs which makes you suspect Diabetic neuropathy, what are these?
clawed toes, callused heels and metatarsel heads, possible an ulcer if severe
where do ulcers most commonly occur in diabetic neuropathy?
metatarsel heads, between toead and dorsa of toes and heel
what two tests should you do to check sensation in the diabetic foot exam?
- vibration with tuning fork 2. 10g microfilament test
wht signs on fundoscopy would incucate diabetic retinopathy?
cotton wool haemorrages / hard exudats / extra proliferationn of the blood vessels
what is the pathpphysiology of diabetes mellitus type 2?
characterised by insulin resistance there is deficits in insulin action and production leading abnormal glucos metabolism to a hypergkycaemic state - much like DMT1
what HBa1c values are caracterised as pre - diabetes?
39-48
what HBa1c values are characterised as diabetes?
> 48
what BM values are characterised as pre diabetes ?
5.6-6.9
what BM values are characterised as diabetes ?
> 6.9
when would you start pharmacy therapy in the management of DMT2?
HBa1c > 53
What drugs (non diabetes drugs) are used in the management of DMT2?
Hanti-hypertensives / statins / antiplatekets
what are the indications of starting antiplatelets drugs in the management of DMt2?
have existing CVD / 50-70y and at risk of CVD
describe the stepwise diabetes drug management of DMT2?
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
do Bm’s need to be checked in DMT2?
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
what are the additional drugs which can be added to metformin in dual or triple therpay of DMT2?
gliptin / pioglithazone / sulfonyurea / sodium glucose co transporter 2 inhibitors
why is insulin ‘controversial’ In the mamagent on DMT2?
insulin causes weight gain, in T2 diabetes mellitus this can cause a viscious cycle unless you actively counteract CVD RF
what are side effects of metformin?
GI upset which can be intolerable / renal impairment (do not use if renal function is poor)
what are gliptins and how to they work in DMT2 management?
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
what are pioglithiazones and how to they work in DMT2 management?
increases senstivity to insulin
what are sulfynureas and how to they work in DMT2 management?
ey cholorpomide. Cause increased secretion of insulin by binding to ATP-sensitive potassium channels
what are sodium glucose co transporter 2 inhibitors and how to they work in DMT2 management?
eg dopaglioflozin reduces the ampunt of glucose being absorbed in the kidneys
what are side effects of sodium glucose co transporter 2 inhibitors
GU infections as renal function changed from the medicine
how does metformin work?
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
what is meant by basal insulin?
either long or intermediate acting insulin types
descibe the basal bolus phenomenon found in on diabetic patients?
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
why do DMT2 patients eventually require insulin therapy?
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
what is the onset time + peak of rapid insulins?
10-20mins peaking at 30-90
what is the onset time + peak time + duration of human basal insulin ?
aka nph, onset of 90min, peak at 4h lasting 18-20 h
describe the action of basal analogue isulins
don’t peak at all - this is very similar to normal insulin but takes a few days to reach a steady onset
who tensds to use mixed insulin?
those who struggle with control and may get recurrent infections
what are the pros and cons of mixed insulin
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
why does subcut insulin take longer to get into the system than normal insulin roduced by the body
normal human insulin is just secreted into the digestive tract
does the DVLA need to be informed about diabetes
if on insulin the yes
what two things should be on person in someone with diabetes?
medi-bracelet / card and insulin passport
What is DKA
a biochemical triad of hyperglycaemia ketonaemia Metabolic acidosis with a rapid symptom onset
what causes DKA
acute hyperglycaemia
while the symptoms of DKA
increased thirst polyuria weight loss excess tiredness nausea vomiting dehydration abdominal pain hyperventilation and decreased consciousness
if you suspect a patient has DKA what are the first tests you should perform
capillary blood glucose capillary blood ketones venous PH plus baseline assessment of: U+E especially sodium and potassium eGFR HCO3 lactate
what factors can precipitate DKA
infections/stress non-compliance pregnancy steroid use alcohol use idiopathic
what tests would you perform to find the underlying cause of DKA
MSU cultures ECG chest x-ray beta HCG stool sample CT head blood gases
what level of capillary blood ketones is diagnostic for DKA
> 3
what would DKA cause acidosis or alkalosis
acidosis it’s in the name
what is the first step of the management of DKA if severe
500 mil 0.9 NaCl over 15 minutes and repeat once if necessary (is SBP <100) and call ICU
what classes as severe DKA
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
what is a first step of the management of DKA if non-severe
1 L 0.9 NaCl over one hour
what is the remaining Mx in the management of DKA after fluid has been given?
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
why does potassium need to be so closely monitored in the management of DKA
life-threatening hypokalaemia can occur with incident infusions
what is a contraindication to KCl infusion
anuria
when would you need to replace potassium in the management of DKA
is < 5.5 (is <3.5 call for senior help!!)
what additional management steps may you need to do in the management of DKA and why?
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
what are the overall ongoing aims of in the management of DKA
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
it during the infusion of insulin you notice that the patient is not responding what should you do
check infusion and line patency and then increase insulin by 1 to 2 units
what is the definition of hypoglycaemia
blood glucose of less than 3.9
how does hypoglycaemia causes symptoms
low plasma glucose causes an impaired brain function
what are the features of hypoglycaemia
autonomic: trembling palpitations sweating anxiety hunger neuroglycopenic: decrease levels of consciousness confusion weakness drowsiness dizziness difficulty speaking non-specific symptoms: nausea headache
what is Whipple’s triad
fasting hyperglycaemia levels less than 50 mg/dL symptoms of hypoglycaemia immediate relief of symptoms with IV glucose
does hypoglycaemia more commonly occurring type I or type II and why
more commonly in type I as on insulin and there are no preservative mechanisms
what are the risk factors for severe hypoglycaemia in type I diabetes
history of severe episodes HbA1c less than 48 long duration of diabetes renal impairment impaired awareness of hypoglycaemia extremities of age
what are the risk factors for severe hypoglycaemia in type II diabetes
advanced age cognitive impairment depression aggressive treatment of glycaemia impaired awareness of hypoglycaemia duration of insulin therapy renal impairment and other comorbidities Solfinurea + insulin
describe what occurs if blood glucose was below 3.8
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
describe what occurs of blood glucose falls below 3.5
adrenaline is produced causing autonomic symptoms of glgenolysis and gluconeogenesis
describe what occurs if blood glucose falls below 3.2/3.3
neuroglycopenic Sx occur
what would get if blood glucose falls below 3
ECG changes
what would occur if blood glucose falls to 3- 2.8
neurophysiological symptoms with decreased EEG waves and cognitive dysfunction
how do you screen for hypoglycaemia
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
in which patients would you want to relax HbA1c target as well as the blood glucose level targets
those with frequent hypoglycaemic episodes want to find a balance
what is the management of hypoglycaemia in a patient who is conscious and able to swallow
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
what is the management of hypoglycaemia in a patient who is unresponsive or unconscious
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
when would glucagon not work
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
it hypo glycaemia has been caused by sulphonyurea or long acting insulin what should you be aware of
hypo may persist up to 24 – 36 hours
what conditions can cause secondary hyper glycaemia or diabetes
cystic fibrosis haemochromatosis chronic pancreatitis PCOS Cushing’s pancreatic cancer glucagonoma pancreatectomy
what drugs can cause secondary hypoglycaemia/diabetes
corticosteroids thiazide diuretics beta blockers and statins
how does cystic fibrosis cause diabetes
the thick mucus blocks ducks in the pancreas causing scarring this leads to destruction of the islet cells and type I diabetes mellitus
how does haemochromatosis cause diabetes
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
how does chronic pancreatitis cause diabetes
information of the pancreas causes scarring and damage –> DMT1
how does PCOS cause diabetes
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
how does cushings is cause diabetes
increase cortisol causes an increase in blood glucose and an increase blood pressure leading to type II diabetes
how does pancreatic cancer lead to diabetes
causes insulin resistance
what is a glucagonoma
tumour producing access glucagon causing an increase in blood sugars
how do most drugs cause diabetes, which are exceptions to this
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
why are beta-blockers potentially dangerous in diabetes
they block insulin secretion (B1 blockers less lilely) also mask Sx of Hypo such as tachycardia
what is mono genic diabetes
a raw form of diabetes caused by a single genetic mutation
what feature in type I diabetes should be a red flag for mono genic diabetes
have very strong family history / onset before six months of life / -related conditions such as cysts in kidneys or gout
what are the two types of mono genic diabetes
maturity onset of the young / neonatal diabetes
what is a presentation of mono genic neonatal diabetes
low birth weight presenting before six months can be transient but then returned later in life
how do you diagnose monogenic diabetes?
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
what is the treatment of monogenic DM
treated like Type II with lifestyle –> but then add sulfynurea or insulin in neonated treat with sulfinuea unless v severe then add insulin
What is charcots disease?
complication of neuropathy in the foot which can be caused by diabetes or other neurogenic conditions
What is the pathophysiology of charcots disease?
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
what is a presentation of charcots disease?
redness and swelling heat and can have pain depending on the extent of the neuropathy often looks similar to cellulitis
what are the risk factors for charcots disease?
long-term duration of diabetes/diabetic neuropathy/injury to the foot/have existing ulceration
how would you prevent charcots disease?
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
what is the management of charcots disease?
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
