Diabetes Flashcards
How many people diagnosed with diabetes in UK
3 million
4.9% of population
How much does DM lower life expectancy by
7 years
Insulin effect on liver
Inhibits gluconeogenesis
Promotes glycogen storage
Insulin effect on muscle
Glucose uptake
Promotes glycogen storage
Insulin effect on adipose tissue
Inhibits lipolysis
Increases fat synthesis
Type 1 onset
Usually juvenile onset (before 35)
Type 2 onset
Mainly after 35
More common in males
Which diabetes is prone to ketosis
Type 1
Which diabetes is prone to weight loss
Type 1
Type 1 Insulin
Insulin deficiency
Ketoacidosis
ALWAYS need insulin
Type 2 insulin
Insulin resistance - may have deficiency
Partial insulin deficiency initially and hyperosmolar state
Need insulin when Beta cells fail over time
Type 1 + autoimmune
GAD and ICA antibodies
Attack B cells
Type 2 + autoimmune
Non autoimmune
Associated with metabolic syndrome
Type 1 + HLA
HLA-DR3 and HLA-DR4 in more than 90%
Islet cell antibodies
Type 2 + HLA
No HLA relation
MZ Twins + Diabetes
50% concordance Type 1
100% concordance Type 2
Symptom duration
Type 1- weeks
Type 2- months/years
Ethnicity Type 1
Higher risk Northern European
Ethnicity Type 2
Higher risk Asian, African, poylnesian, native american
C peptide
Disappears in Type 1
Persists in Type 2
LADA
Latent autoimmune diabetes of adults
Type 1B DM
MODY
Maturity onset diabetes of the young
Rare autosomal form of T2DM
Secondary Diabetes- Pancreatic disease (diseases of exocrine pancreas)
Acute + chronic pancreatitis Trauma Pancreatectomy Neoplasia Cystic Fibrosis Haemochromatosis Thalassaemia Fibrocalculous pancreatopathy
Secondary Diabetes- Endocrine disease (diseases of endocrine pancreas)
Acromegaly Cushing's Glucagonoma Phaeochromocytoma Hyperthyroidism Conn's disease Aldosteronoma Somatostatinoma
Drug-induced Diabetes
Immunosuppressive agents- glucocorticoids, cyclosporin, tacrolimus, sirolimus Beta blockers Beta adrenergic agonists Atypical antipsychotics (clozapine, olanzapine) Thiazide diuretics Phenytoin Levothyroxine Interferon alpha HIV treatment Niacin (B3) Pentamidine
Secondary diabetes- Genetic defects of:
Beta cell function Insulin action (receptor mutations) Genetic syndromes- Down's, Friedreich's ataxia, Huntington's chorea Klinefelter syndrome Prader- Willi Turner
Secondary diabetes- Infections
Congenital rubella
CMV
Secondary diabetes- uncommon forms f immune mediated diabetes
Stiff person syndrome
Anti-insulin receptor antibodies
Diabetes Investigations
Fasting plasma glucose (FPG)
Random plasma glucose (RPG)
75g oral glucose tolerance test (OGTT)
HbA1c
75g Oral glucose tolerance test
Fast for 9 hours
Check fasting plasma glucose
Give 75g of glucose
Check 2 hour plasma glucose
HbA1c
Measure for average glucose control over 3 month period
Normal- below 42 mmol/mol
Generally below 53 indicates well controlled diabetes
Investigating with symptoms
1 diagnostic test
Investigating without symptoms
2 diagnostic tests OR 1 abnormal OGTT
Type 1 Aetiology
Polygenic
Autoantibodies against pancreatic islets
Pancreatic beta cell destruction –> absolute insulin deficiency
LADA
diagnosed in adulthood
Usually non-acute –> can be diagnosed as T2DM
ICA or GAD +ve
Require insulin
T1DM environmental influences
Peak age onset 5-7 years
Puberty
Seasonal variation
Predominantly European population
T1DM Genetic susceptibility
HLA genes on chromosome 6q (MHC)-HLA DR3/4
Genes on chromosomes 2q, 15q and 11q
Pathogenic sequence of T1DM
Genetic susceptibility
Environmental insult (virus)
Development of insulitis (infiltration of activated T lymphocytes)
Activation of autoimmunity
Immune attack on Beta vells
Development of DM (when more than 90% of Beta cells are destroyed)
When do you develop T1DM
When more than 90% of Beta cells are destroyed
Glucose toxicity
Beta cells have decreased functionality when exposed to high levels of glucose
–> lowering glucose may increase beta cell function and promote greater insulin secretion
Alpha cells in T2DM
Increased
Leads to increased glucagon/insulin ratio
Classic Osmotic Symptoms
Polyuria Polydipsia Weight loss Nocturia Fatigue Pruritis Blurred Vision Recurrent UTI or GU infections DKA
HHS
Hyperosmolar Hyperglycaemic Syndrome
Diabetes complications
Skin infections Foot problems Retinopathy Erectile dysfunction Arterial disease
Factors in obesity contributing to insulin resistance
Adipokines
Inflammation
Lipids
Insulin resistance
Diminution in the response of the body’s tissues to insulin, so that higher concentrations of serum insulin are required to maintain normal circulating glucose levels; eventually the islet cells can no longer produce adequate amounts of insulin for effective glucose lowering, resulting in hyperglycaemia
Metabolic syndrome
Cluster of conditions that together increase risk of heart disease, stroke + T2DM Central obesity Dyslipidaemia Hypertension Impaired fasting glucose
Metabolic syndrome: Central obesity
BMI > 30 or Waist circumference of: Caucasian men- >94 Caucasian women- >80 South Asian men- >90 South Asian women- >80
Metabolic syndrome: Dyslipidaemia
Increased Triglycerides >150mg/dL
Decreased HDL-cholesterol: <40mg/dL women, <50mg/dL men
Metabolic syndrome: Hypertension
Systolic >130
Diastolic>85
Metabolic syndrome: Impaired fasting glucose
Fasting glucose >6.1mmol/L
Self monitoring blood glucose aims
Pre-prandial: 4-7mmol/L
Post-prandial (2hrs): 5-9mmol/L
Fructosamine
Another glycated protein- lasts around 2 weeks
Can be used if HbA1c invalid e.g. haemoglobinopathy, increased RBC turnover
Useful in glucose control in pregnancy
First line T2DM
Diet
Physical activity- 3x30mins
3-5% weight reduction
Smoking cessation
Smoking in diabetes
1 cigarette is equal to 5 cigarettes for non-diabetic
Diabetic BP control
Aim 140/80
If CVD or renal disease too, 130/80
Diabetic cholesterol control
Diabetic>40 or Diabetic<40 + 1 risk factor= statin
Aim total cholesterol <4, LDL <2
Biguanides
Metformin
Biguanides function
1st line T2DM
Decreases hepatic glucose production (gluconeogenesis and glycogenolysis)
Improve insulin sensitivity in liver + muscle
Doesn’t affect insulin secretion, doesn’t induce hypoglycaemia and doesn’t predispose to weight gain
Biguanides SEs
Nausea Diarrhoea Abdominal pain Anorexia Hypoglycaemia
Biguanides STOP IF
Tissue hypoxia e.g. sepsis or MI
General anaesthesia
Before contrast medium containing iodine –> renal failure + subsequent lactic acidosis
Restart no earlier than 48hr after test of renal function shows no deterioration
Insulin Secretagogues
Sulfonylureas
Meglitinides
Biguanides Contraindictions
Severe hepatic disease
Severe renal disease (CKD stage 4 or eGFR<36ml/min)
–> can cause lactic acidosis
Sulfonylureas examples
Gliclazide Tolbutamide Glibenclamide Glipizide Glimepiride Chlorpropamide
Sulfonylureas function
Oral hypoglycaemic
Increases insulin release from pancreas
Opens K+ channels in beta cells
Sulfonylureas side effects
Hypoglycaemia
Weight gain
Meglitinides examples
Repaglinide
Nateglinide
Meglitinide function
Opens K+ channels in Beta cells to increase insulin release
Short acting agents that promote postprandial release of insulin- Prandial Glucose Regulators (PGRs)
Thiazolidinediones (TZDs)/Glitazones example
Pioglitazone
TZDs MOA
PPAR-gamma agonist
Modulates gene transcription of regions controlling lipid metabolism in the muscle, adipose tissue and liver –> decreases insulin resistance peripherally + increases insulin sensitivity
TZDs SEs
Hypoglycaemia Weight gain Fluid retention Heart failure Liver impairment Bladder cancer Mild anaemia Osteoporosis/fractures
TZDs contraindications
Past/present HF
Osteoporosis
Glucagon like peptide - 1 (GLP-1)
Incretin
Gut peptide that augments insulin release when glucose is detected + decreases glucagon secretion
Slows gastric emptying + induces satiety
Stimulate + preserve Beta cells
GLP 1 receptor analogues examples
Exenatide
Liraglutide
Lixisenatide
GLP1 receptor analogues
Injected not oral
Only used in overweight patients (BMI > 35) with poor glucose control
GLP1 receptor analogues SEs
Nausea
Diarrhoea
Pancreatitis
Pancreatic cancer
DDP4 inhibitors/gliptins examples
Sitagliptin Vildagliptin Alogliptin Linagliptin Saxagliptin
DDP inhibitors/gliptins
Oral 1x day
Inhibit GLP1 breakdown
Well tolerated, SEs uncommon
Alpha-glucosidase inhibitors examples
Acarbose
Alpha-glucosidase inhibitors
Decrease breakdown of starch into glucose
Alpha-glucosidase inhibitors SEs
Flatulence
Diarrhoea
Abdo pain/distension
Diabetes medication Prescribing Pathway
Step 1: Lifestyle, try and keep <48
Step 2: Metformin if gone above 48
Step 3: Metformin + Sulfonylurea if gone above 58, try and keep at around 53
Step 4: Triple therapy- metformin, SU + DDP4 inhibitor/insulin/pioglitazone
Step 5: if not better, intensify insulin or add pioglitazone
Metformin dose CIs
Careful with dose if eGFR <45, if below 30 then stop
Not tolerated if patient not overweight
–> SUs instead
Sulfonylurea CIs
If hypoglycaemia a problem
–> DPP4 inhibitor/pioglitazone instead
If metformin is CI or not tolerated
- SU/DPP4 inhibitor/pioglitazone
- Combination of 2 of SU/DPP-4 inhibitor/Pioglitazone
- Consider insulin regime
T2DM indications for insulin therapy
Inadequate glycaemic control on tablets or CI to tablets
Symptomatic hyperglycaemia
Pregnancy
Infection/foot ulcers
Types of Insulin
Human
Analogue
Human Insulin types
Short acting
Intermediate acting
Biphasic
Humulin S
Short acting human insulin
Humulin I
Intermediate acting human insulin
Humulin M3
Biphasic human insulin (mixture of short and intermediate)
Analogue Insulin types
Rapid acting
Long acting (basal insulin)
Biphasic
Novorapid, Lispro
Rapid acting analogue insulin
Lantus, Levmir
Long acting analogue insulin (basal insulin)
Novomix 30
Biphasic analogue insulin
Insulin Injection Sites
Subcutaneous
Abdomen
Thighs
Buttocks
Insulin Regimes
Once daily basal insulin
Premixed insulin twice daily/biphasic
Basal bolus/QDS regimen
Once Daily basal insulin
Once daily intermediate or long-acting insulin
Given with tablets in T2DM
Usually given before bed or 1st thing in morning
Premixed insulin twice daily/biphasic
30% short acting and 70% long acting
Breakfast and lunch
If once daily fails in T2DM
Basal bolus/QDS regimen
1 long acting injection + 3 short acting injections with each meal
Mimics normal physiology
Used primarily in T1DM
Sick Days
Illness causes stress and usually requires more insulin Drink lots of fluids (3L) Sugary fluids if unable to eat Regular glucose monitoring Never stop tablets or insulin
Diabetic Ketoacidosis
State of absolute or relative insulin deficiency resulting in hyperglycaemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
Hyperosmolar hyperglycaemic state (HHS)
Hyperglycaemia resulting in high osmolarity without significant ketoacidosis
Hypoglycaemia
Below 3.6mmol/L
Hypoglycaemia causes
Imbalance between carb intake and insulin/oral hypoglycaemics
Exercise with too much insulin/not enough carbs
Alcohol
Vomiting
Breast feeding
Hypoglycaemia medical causes
Liver disease Progressive renal impairment Hypoadrenalism (T1DM) Hypothyroidism Hypopituitarism Insulinoma
Hypoglycaemia Autonomic Symptoms
Glucose around 3.6mmol/L Sweating Shaking Anxiety Palpitations Hunger Nausea
Hypoglycaemia Neuroglycopenic symptoms
Glucose around 2.7mmol/L Confusion Slurred speech Visual disturbance Drowsiness Aggression
Mild hypoglycaemia management
Conscious, lucid, able to self-treat
Sugary drink
5-7 glucose tablets or 3-4 heaped tsp sugar
Moderate hypoglycaemia management
Conscious but can’t self-administer and needs help
Glucogel (1-2 tubes) or jam, honey, treacle
IM Glucagon
Severe hypoglycaemia treatment
Unconscious- don’t put anything in mouth + recovery position
0.5-1mg IM Glucagon
In hospital, IV Glucose
Severe hypo treatment IV glucose
75ml of 20% glucose or 150ml of 10% glucose over 15 mins
50ml of 50% glucose may be given with care as may cause extravasation leading to chemical burns
Post-hypo treatment
When glucose above 4mmol/L
Longer acting carbs needed- biscuits, bread, milk
Hypo + driving
Inform DVLA
Licence revoked following 1 or more severe hypos during driving
Nocturnal Hypo diagnosis
Rebound hyperglycaemia
Headaches/hangover sensation
3am BM or CGMS (continuous glucose monitoring sensor) over 5 days
Nocturnal Hypo management
Analogue insulins
Pre-bed snack
Change of timing of insulin
Insulin pump therapy
DKA MOA
Ketosis is pathway use in starvation states
Acetone produced as by-product
Cells can’t take up glucose for metabolism
Cells end up in starvation-like state –> ketoacidosis only form of energy production –> FFAs metabolised via Krebs cycle producing ketone bodies
DKA stands for
Severe acidosis
Hyperglycaemia
Ketones present
DKA triggers
Infection e.g. UTI Surgery MI Pancreatitis --> all 4 have glucocorticoid response, increasing levels of cortisol + blood glucose Chemo Antipsychotics Wrong insulin dose High exogenous steroids
DKA presentation
Abdominal pain Kussmaul respiration Drowsiness + confusion Polyuria Polydipsia Vomiting Ketones on breath Dehydration + tachycardia Severe- Na, Cl, K, Ca, Mg + phosphate losses due to osmotic diuresis
DKA Diagnosis
Acidosis- pH<7.30
Hyperglycaemia (usually >14mmol/L)
Ketosis (serum + urine)
DKA investigations
Pregnancy test
ECG, CXR
Urine dip + MSU culture
Bloods- CBG/biochem profile, plasma ketones, ABG/VBG, amylase, osmolality, FBC, blood culture, HbA1c
Plasma osmolality
2(Na) + urea + glucose
Assessing DKA severity
If one or more on admission, ITU: Blood ketones >6 Venous bicarb < 5 pH <7.1 K+<3.5 GCS<12 O2 sats<92% on air SBP<90 Pulse>100 or <60 Anion gap >16
DKA monitoring
Consciousness BP Pulse Temp Glucose Urine output K+ Acidosis
DKA Fluid therapy
2 large bore cannulas
NaCl 0.9%
5% or 10% glucose
DKA NaCl 0.9%
1L start until SBP>90 1L in 1hr 1L in 2hrs (+20mmol KCl) 1L in 4hrs (+KCl) 1L in 4hrs (+KCl)
DKA 5/10% glucose
Start when CBG <12mmol/L and continue at 125ml/hour
If using 10% glucose increase insulin infusion as needed
Increase insulin infusion rate if glucose <6mmol/L
DKA K+
Do not give in first 2 bags because delivery ratio is too rapid
On each subsequent bag of NaCl or glucose, add KCl dependent on serum levels
<3.5- may need additional K+ and delay insulin
3.5-5.5- 20-40mmol/L
>5.5- none
Normal DKA deficits
Typical fluid deficit= 100ml/kg
Typical K+ deficit= 3-5mmol/kg
Insulin during DKA
If known diabetic, continue
Insulin infusion by IV syringe pump
–> 50 units Actrapid made up to 50ml with 0.9% NaCl
DKA insulin infusion
50 units Actrapid made up to 50ml with 0.9% NaCl
Fixed rate IV infusion
–> 0.1units/kg/hr (around 6-8 units/hr)
Aim for bicarb rise of 3mmol/hr and glucose fall 3mmol/L
If not achieved, increase rate by 1 unit/hr
DKA treatment outcomes
Ketones <0.3mmol/L- use blood as urinary ketones persist after resolution
Venous pH>7.3
Venous bicarb>18mmol/L
DKA complications
Aspiration pneumonia Hypo K+ Hypo Mg+ Hypo PO4- VTE Cerebral oedema
Most common cause of DKA death in children
Cerebral oedema
Indicated by sudden CNS decline
Treatment- dexamethasone or mannitol
DKA features
Increased plasma glucose Increased WBC Infection often apyrexial Increased creatinine HypoNa+- common due to osmolar compensation of hyperglycaemia, if increased or normal suspect severe Ketonuria Recurrent ketoacidosis Acidosis Serum amylase increased Non-specific abdo pain
Hyperosmolar Hyperglycaemic Syndrome (HHS)
Severe hyperglycaemia without significant acidosis Typically seen in T2DM Subacute history (1 week) with marked dehydration and hyperglycaemia
HHS and age
Old people experience thirst less acutely + become more dehydrated more readily
Mild renal impairment associated with age
–> increased urinary losses of fluid + electrolytes
HHS Features
Hyperglycaemia >40mmol/L Osmolality >420 Patient often hypernatraemic May or may not be ketonuria No ketoacidosis Severe dehydration
Normal osmolality
275-295
Calculating Osmolality
2(Na+K) + Ur + Glu
HHS clinical features
Dehydration –> stupor –> coma
HHS precipitating factors
Consumption of glucose-rich fluids
Concurrent medication e.g. thiazide diuretics or steroids
Intercurrent illness
HHS Complications
Occlusive events- stroke, MI, DIC, leg ischaemia/rhabdomyolysis, DVT/PE
Give LMWH as prophylaxis
HHS Management
Rehydrate slowly over 48 hours with 0.9% NaCl IV
No insulin bolus
Replace K+ when urine starts to flow
HHS Rehydration
Typical deficit 110-220ml/kg
Avoid 0.45% NaCl
HHS Insulin
Only use insulin if blood glucose not falling by 5mmol/L/hr with rehydration or ketonuria
Slow infusion of 0.05units/kg/hr (max 1unit/hr)
Avoid in first 12 hours
Rapid shifts in glucose should be avoided due to risk of rapid fluid/Na+ shifts and central pontine myelinosis
HHS K+
Replaces when urine starts to flow
May need CVP monitoring
K+ reduces rapidly
Keep plasma glucose at 10-15mmol/L for 1st 24hrs to avoid cerebral oedema
Look for cause, e.g. bowel infarct, drugs etc.
When choosing, giving + monitoring medication- BRAIN + AIMS
Benefits Risks Adverse effects Interactions Necessary prophylaxis Susceptible groups Administering Informing Monitoring Stopping
Diabetic mortality rate
Increased (x2-2.5) due to cardiovascular complications
80% die of CVD
Long term hyperglycaemia leads to
Vessel closure- decreased supply of O2 and nutrients
Vessel permeability- damaged vessels dilate and leak unwanted substances
Diabetes chronic complications- Macrovascular (atherosclerosis)
Coronary Heart disease–> MI, CCF
Cerebrovascular disease –> stroke
Peripheral vascular disease –> ulceration, gangrene, amputation
Diabetes chronic complications- Microvascular
Nephropathy
Retinopathy
Neuropathy (peripheral sensorimotor, autonomic)
Diabetes chronic complications- Other
Skin
Rheumatological
Hepatic
Complications of Diabetes Risk Factors
Smoking- most potent
Hypertension
Dyslipidaemia
Hyperglycaemia- least potent
Diabetic retinopathy
Common
Around 50% of people with diabetes for more than 10 years have it
Non-proliferative Retinopathy
Microaneurysms
Dot and blot haemorrhages
Hard exudates (lipid deposits) and soft exudates (cotton wool spots=retinal ischaemia- only in pre-proliferative- REFER)
Macular oedema (leakage of macular blood vessel- main cause vision loss in this case)
Mild, moderate, severe
Proliferative Retinopathy
Ischaemia of retina –> production of growth factors (GF) –> neovascularisation producing fragile vessels
New vessels on disc and other places
Vitreous haemorrhage
–> vessels prone to haemorrhage, lead to fibrosis/scarring leading to loss of vision
Diabetic Maculopathy
Suspect if visual acuity decreased
Occurs if retinopathy within 1 disc diameter of the macula
Leads to oedema + vision loss
Refer for laser photocoagulation, intravitreal steroids or anti-angiogenic agents
Focal or exudative maculopathy
Hard exudates around macula which leads to macular oedema and visual loss
Ischaemic maculopathy
Due to retinal vessel closure
Diff types of diabetic maculopathy
Focal or exudative
Diffuse
Ischaemic
Diabetic Maculopathy Pathophysiology
Capillary endothelial damage –> vascular leak –> microaneurysm –>
Diabetic Maculopathy Pathophysiology
Capillary endothelial damage –> vascular leak –> microaneurysm –> capillary occlusion –> local hypoxia and ischaemia –> neovascularisation
Occurs due to increased blood flow in hyperglycaemia
New vessels form on disc or ischaemic areas, proliferate, bleed, fibrose + can detach retina
Microvascular occlusion
Cotton wool spots
Maculopathy screening
Annual digital retinal screen
BP, cholesterol, glycaemic control
Laser photocoagulation
Diabetic Nephropathy
Most common cause of end-stage renal failure in UK
25-30% of T2DM have some degree of nephropathy
Associated with atherosclerosis
Kidneys damaged in 3 main ways
Glomerular damage
Ischaemia- resulting from hypertrophy of afferent and efferent arterioles
Ascending infection
Diabetic Nephropathy RFs
Duration of diabetes Hypertension FH of hypertension Poor glycaemic control Smoking Gender-male Ethnicity- South Asians, Afro-Caribbeans
Diabetic Nephropathy Clinical Triad
Hypertension
Albuminuria (preceded by microalbuminuria)
Declining renal function
–> on renal biopsy: “Kiemmelstein-Wilson” lesion
Microalbuminuria screening
Void urine in morning + measure urine albumin:creatinine ratio (ACR)
Normal men <3.5mg/mmol, normal women <2.5mg/mmol
If elevated, repeat twice- of 2 out of 3 positive, microalbuminuria present
Diabetic Nephropathy management
Maintain BP <130/80 HbA1c<53 Stop metformin eGFR <30 Refer to specialist eGFR<45 Consider renal replacement therapy Consider simultaneous pancreas and kidney transplant for T1DM
Diabetic Neuropathy
Peripheral neuropathy- injury or infection at pressure points (e.g. metatarsal heads)
Ischaemia- critical toes and loss of pulses
Peripheral sensory neuropathy
Glove and stocking distribution
High risk ulceration + amputations if blood supply poor
Numbness, pins and needles, burning and shooting pain
Loss sensation fine touch + proprioception
Loss ankle reflexes, reduced muscle bulk, neuropathic deformity (pes cavus, claw toes, loss transverse arch, rocker bottom sole)
Hands subject to median neuropathy/carpal tunnel
Autonomic Neuropathy- Genitourinary
ED Atonic bladder (difficulty voiding or incontinence) --> self catheterisation
Autonomic Neuropathy- GI
Gastroparesis (recurrent vom + early satiety due to poor gastric flow)- anti emetics, erythromycin, gastric pacing
Chronic constipation/diarrhoea
Gustatory sweating
Autonomic Neuropathy- Cardiovascular
Postural hypotension- fludrocortisone or alpha agonist midodrine
Reduced cerebrovascular autoregulation
Loss of respiratory sinus arrhythmia
Mononeuropathy
CN palsies
Median nerve palsies –> carpal tunnel
–> treat with immunosuppression
Proximal motor neuropathy
Painful atrophy of quads + pelvifermoal muscles
CV complications
Manage CV risks
- smoking cessation
- BP control
- cholesterol control
- glycaemic control
BP management
ACEI
CCB
Thiazide
Alpha blocker or Beta
Cholesterol control
Total cholesterol <4
Treat with statins- all diabetics > 40, all diabetics <40 +1 other RF
Acute MI - complication
4x increased risk
May be silent because autonomic neuropathy
Treatment- aspirin, angioplasty, glucose-insulin infusion, 2ndary prevention
Cerebrovascular disease- complication
If within 3 hours, consider thrombolysis
Aspirin, statins, glucose insulin infusion
Peripheral vascular disease complication
Intermittent claudication, rest pain, buttock pain
Aspirin, vasodilators
Skin complications
Oral/genital candidiasis Skin abscesses Diabetic dermopathy Necrobiosis Lipoidica diabeticorum Granuloma annulare acanthosis nigricans fungal nail infection
Rheumatological complications
Charcot neuropathy
Adhesive capsulitis
Diffuse idiopathic skeletal hyperostosis
Flexor tendinopathy
Hepatic complications
NAFLD
–> non alcoholic steatohepatitis/fibrosis/cirrhosis
Increases ALT and AST more than 2x upper limit needs investigation
Pioglitazone in reducing cirrhosis progression