T1dm Flashcards
definition opf T1dm
metabolic hyperglycaemic condition
caused by absolute insufficiency of pancreatic insulin production
aetiology of T1dm
destruction of insulin producing B cells = insulin deficiency
autoimmune in 90%
genetically susceptable patinets and triggered by env (low concordance in identical twins)
polymorphisms of genes influence the risk - gene encoding preproinsulin and HLA-DQB and HLA-DR, PTPN22 and CTLA-4
gene 6q determines islet sensitivity to damage eg from viruses or cross-reactivity from cow’s milk induced Ab
pancreatic B cell autoantigens involved in initiation or progression of autoimmune islet injury - include: glutamic acid decarboxylase, insulin, insulinoma-associated protein 2 (IA-2) and cation efflux zinc transporter (ZnT8)
secondary dm
- steroids
- anti-HIV drugs
- newer antipsychotics
- protease inhibitors
- pancreatic - pancreatitis, surgery, trauma, pancreatic destruction (eg haemochromatosis, CF), pancreatic ca
- cushing’s disease
- acromegaly
- phaeo
- hyperthyroidism
- glucagonoma
- pregnancy
- congenital lipodystrophy, glycogen storage diseases
- glycogen storage diseases
epidemiology of T1dm
one of the most common chronic diseases in childhood with a prevalence of 0.25% in the UK
usually adolescent, can effect any age
geographic variation
US and northern europe incidence - 8-17/100000 per yr
signs and sx of T1dm
juvenille onset < 30yrs
polyuria/nocturia - osmotic diuresis caused by glycosuria
polydipsia (thirst)
tiredness
weight loss
sx and signs of complications
signs of associated autoimmune conditions
sx and signs of diabetic ketoacidosis
- nausea
- vomiting
- abdo pain
- polyuria
- polydipsia
- drowsiness
- confusion
- coma
- kussmaul breathing - deep and rapid
- ketotic breath
- signs of dehydration - dry mucous membranes, reduced tissue turgor
signs of T1dm complications
fundoscopy - dm retinopathy
examination of feet - neuropathy - 10g monofilament testing and vibration sensation, pulses - dorsalis pedis and posterior tibial pulses
BP
signs of associated autoimmune conditions
vitiligo
Addison’s disease
autoimmune thyroid disease
Ix for T1dm
blood glucose - fasting >7mmol/L or random >11mmol/L - 2 +ve results needed
HbA1c - overall glucose for 2-3mo
FBC - MCV, reticulocytes (increased erythrocyte turnover causes misleading HBa1c)
UE - nephropathy and hyperkalaemia from ACEi
lipid profile
urine albumin creatinine ratio - detect microalbuminuria
urine - glycosuria, high ketones, MSU (microscopy and culture)
CXR - exclude infection
ECG - acute ischemic changes
Ix for pts presenting with suspected DKA
- FBC - high WCC even w/o infection
- UE - high urea and creatinine from dehydration
- LFT
- CRP
- glucose
- amylase may be high
- blood cultures
- ABG - metabolic acidosis with high anion gap
- blood/urinary ketones
Mx of diabetic ketoacidosis
consider HDU/ICU input
central line, arterial line and urinary catheter if server acidosis, hypotensive or oliguric
insulin
fluids
K replacement
monitor blood glucose capillary ketones and UO hourly, UEs 4 hourly VBG at 0. 2.4. 8. 12h and before stopping fixed rate insulin. Monitor phos and mg daily
broad spectrum AB if infection suspected
thromboprophylaxis
NBM for at least 6hr - gastroparesis is common
NG tube if GCS is reduced to prevent vomiting and aspiration
insulin mx in DKA
50U of soluble insulin in 50mL 0.9% saline
start at 0.1U/Kg/h until capillary ketones <0.3, venous pH >7.3 and venous bicarb >18mmol/L
if pt able to drink change to SC insulin
if not - insulin sliding scale
dont stop infusion until 1-2hr after regular SC insulin is restarted
fluid Mx in DKA
500mL 0.9% saline over 15-30min until systolic BP is >100mmHg
then 1L 2hrly x3 and 1L 3hrly x3
IV dextrose when glucose reaches 15mmol/L:
- 1L 5% dextrose over 8hrs when blood glucose is 7-15mmol/L
- 500mL 10% dextrose over 4h when blood glucose <7mmol/L
K replacement for DKA
start in the second fluid bag if passing urine
adjust amount of K accoriding to the plasma K
- if >5.5mmol/l = none
- iof 2.5-5.5 mmol/L = 40mmol/L
- if <2.5mmol/L = 60-80mmol/L
glycaemic control in T1dm
advice and pt education - nurse specialists and dieticiants
self adjust doses based on exercise, glucose, calorie intake and carb counting
avoid binge drinking - danger of delayed hyperglycaemia
SC insulin - short acting (Lispro, aspart, glulisine) 3x daily before meals and one long acting (isophane, glargine, getemir) once daily. Rotate injection sites
insulin pumps may give better control - but expensive and cumbersome and DKA may occur if pump malfunctions - give if attempts to reach HbA1c = hypoglycaemia or person unable to meet target
DAFNE (dose adjustment for normal eating) - calculate carb intake and adjust dose accordingly
monitor - sx, regular finger prick tests, monitor HbA1c (target <7%) every 3-6mo
screening and Mx of complications and cardiovascular risk
treatment of hypoglycaemia in T1dm
if low consciousness - 50mL of 50% glucose IV or 1mg glucagon IM
if conscious and cooperative - 50g oral glucose eg luczade, milk, sugar, 3 dextrose tablets - then starchy snack
shouldnt drive for 45mins
complications of t1dm
DKA
microvascular - retinopathy, nephropathy, neuropathy
macrovascular - PVD, IHD, stroke, TIA, MI, renovascular disease, limb ischemia
suseptible to infections - especially on feet
complication of insulin:
- weight gain,
- fat hypertrophy at insulin injection sites
- hypoglycaemia caused by missing a meal or insulin OD
DKA presentation
low insuin and high counter-regulatory hormones = hepatic gluconeogenesis and low peripheral glucose utilisation
renal reabsorptive capacity of glucose is exceeded = glycosuria, osmotic diuresis and dehydration
increased lipolysis = ketogenesis and metabolic acidosis
ppte by infection, errors in mx, new dx, other medical disease or no cause identified
hypoglycaemia sx
neuroglycopenic and adrenergic signs:
- personality chnage
- fits
- confusion
- coma
- pallor
- sweating
- tremor
- tachycardia
- palpitations
- dizzyness
- hunger
- focal neurological sx
may be masked by autonomic neuropathy, B blockers and brain adapting to recurrent episodes
prognosis of T1dm
depends on early dx, good glycaemic control and compliance with screening and treatment
vascular disease and renal failure are major causes of increased morbidity and mortality
latent autoimmune diabetes of adults (LADA)
form of t1dm
slower progression to insulin dependance later in life
dx criteria for dm
sx of hyperglycaemia and raised venous glucose detected once
or - raised benous glucose twice ot oral glucose tolerance test 2h value >11.1mmol/L
HbA1c >48mmol/mol - avoid in pregnancy, children, T1dm , haemoglobinopathies
differentiating T1 and T2dm
T1
- before puberty
- HLAD3 and D4
- autoimmune B cell destruction
- polydipsia, polyuria, weight loss, ketosis, persistent hyperglycaemia despite diet and med, islet cell Ab, autoAb, anti-glutamic acid decarboxylase Ab, ketonuria
T2
- older
- no HLA
- insulin resistence/B cell dysfunction
- present with complications
general Mx of dm
education and lifestyle - exercise to increase insulin sensitivity, healthy eating - low sat fats, low sugarm increase starch carbohydrate, moderate protein
bariatric surgery
global vascular risk - statin, control BP
foot care
DVLA
