Diabetes Flashcards
(9 cards)
Type 1 diabetes mellitus:
- Pathophysiology
- Symptoms (6)
- Signs (4)
- Investigations
- Management
- Management in primary care (6)
T1DM:
- Pathophysiology: autoimmune destruction of pancreatic B cells in islets of langerhans therefore no insulin made so inc glucose in blood. Insulin inc glucose uptake, inhibits lipolysis, reduces protein loss
Muscles store glucose as glycogen via glucose 6 phosphatase. Liver can convert to glucose hence buffers bgc.
- Symptoms: acute onset polyuria/dipsia (osmotic diuresis), fatigue, weight loss, blurry vision
- Signs: hyperkal, dehydrated signs
- Ix: autoab testing GAD/ICA/IAA/IA2/, serum c peptide low, fasting (>7) + random glucose (>11.1) (if assymptomatic both these need to occur on 2 separate occasions). cbg should be (4.4-6.1mmol). Also TFTS, FBC, U+Es, anti TTG, urine dip
- mx: basal bolus - insulin OD long acting then short acting before meals - change sites due to lipodystrophy, weight gain, hypoglycemia. Reduce dose if renal impairment, increase dose if on steroids
Add metformin if bmi >25
Self monitoring 4x day before meals + bed (targets 5-7 when waking, 4-7 during day)
Monitor hba1c every 3-6 months
- mx in primary care:
- same day referral
- ensure access to diabetes team
- provide insulin care when ill
- screen for complications + other autoimmune diseases
Type 2 diabetes mellitus:
- Definition
- Risk factors - modifiable and non modifiable
- Signs
- Symptoms (4)
- Investigations
- Management
Type 2 diabetes mellitus:
- Definition: obesity and repeated insulin leads to progressive resistance as b cells become damaged
- Risk factors - modifiable and non modifiable: fx, asian, age, obesity, dec exercise, high carb diet
- Signs: acanthosis nigricans
- Symptoms (4): fatigue, weight loss, polyuria/dip, slow healing infections
- Investigations: fasting + random glucose - if symptomatic then these are diagnostic, hba1c>48 (if no symptoms must repeat to confirm diagnosis), OGTT (>11 (if above 7.8 but under 11 means not diabetic but does have impaired tolerance)
Can’t use hba1c to diagnose if: hemoglobiopathies, hemolytic anaemia, iron deficiency, gestational diab, hiv, child, ckd
- Management:
1. diet low glycemic, immunisation, if loose 15kg can reverse it
2. metformin + titrate up (target <48)
3. If inc to 58 then add either ddp4 inhib, pioglitazone, sulfonylurea, sglt2 inhib (target <53)
4. If still not met add another or metformin + insulin or switch one of the drugs to glp1 mimetic if bmi >35 under specialist care
Check hba1c every 3-6 months then 6 monthly if stable.
HTN: remember acei but if black then arb preferred
Pre-diabetes:
- HbA1c
- Fasting glucose
- glucose tolerance
- mx
- when is hba1c not accurate
- pre diabetes levels: hba1c 42-47 (6-6.4), fasting 6.1-6.9, ogtt 7.8-11 -
- mx: lifestyle changes only, yearly follow ups
- hba1c can also be inc if splenectomy, iron anaemia, vitb12/f deficiency
- hba1c dec if: sickle cell, g6-d, spherocytosis, hemodialysis
Acute complications: Hypoglycaemia:
- Definition
- Causes
- Risk factors
- Symptoms (7)
- Signs (3)
- Management
Acute complications: Hypoglycaemia:
- Definition: <2.6
- Causes: inc inulin/meds, not eating/d+v, sepsis, inc ex, addisons, insulinoma, alcoho
- Symptoms (7): sweating, hunger, headache, n+v, confusion, vision changes
- Signs (3): tachycardia
- Management: if conscious rapid drinks 10-20g, or IM 1mg glucagon or iv 10% dextrose 200ml over 15 mins
Acute complications: Diabetic ketoacidosis
- Definition
- Symptoms (4)
- Signs (5)
- Investigations (6) + diagnosis
- Management
- Resolution
- Complications
Acute complications: Diabetic ketoacidosis
- Definition: in t1dm when lack insulin means cells starve so use liver fas and convert to ketones for fuel. This dec ph hence met acidosis and this inc bicarb reab but this then gets used up
- Symptoms (4): n+v, abdo pain, polyuria/dip, lethargic
- Signs (5): acetone breath smell, dehydration (osmotic diuresis), shock, resp distress (deep hypervent), hypokal signs
- Investigations (6) + diagnosis:
bicarb >15mmol
ph <7.3
ketones >3 or ++
bgc >11
hence vbg, blood ketones, cbg, cultures, fbc/u+es, ecg
- Management: high flow oxy, 0.9% nacl 1L over 1 hour, fixed rate insulin 0.1 units/kg/hr (once <14 add 10% dextrose), monitor k, continue long acting insulin but stop short acting . once glucose <14mmol start 10% dextrose alongside saline
- Resolution: ph>7,3, ketones <0.6, bicarb >15, once achieved this + e+d then switch to normal insulin
- Complications: arrhythmias, aki, cerebral oedema, ards
Acute complications: hyperosmolar hyperglycaemic syndrome HHS:
- Definition
- Symptoms (6)
- Signs (5)
- Causes
- Investigations
- Management
- Complications
- DKA vs HHS
Acute complications: hyperosmolar hyperglycaemic syndrome HHS:
- Definition: in t2d, where hyperglyc causes inc serum osm causing osmotic diuresis hence severe volume depletion
- Symptoms (6): few days onset of polyuria/dip, lethargic, n+v, dec consciousness
- Signs (5): dehyd
- Causes: illness, depression, sedatives
- Investigations:
hyperglyc >30
Inc serum osm >320
Ketones <3, bicarb <15, ph>7.3
- Management: iv 0.9% nacl 0.5-1L / hr, monitor k, vte prophylaxis (hyper-viscosity inc), insulin only if bgc isnt decreasing (otherwise central pontine myelinolysis)
- Complications: mi, stroke
- DKA vs HHS
Chronic complications:
- Macrovascular
- Microvascular
macro: cvs disease, peripheral vascular disease, cerebrovascular, infection
micro: neuropathy, retinopathy, nephropathy
Diabetic neuropathy:
- pathophysiology
- symptoms
- mx
- complications
Peripheral neuropathy:
- pathoph: nerve damage results in loss of sensation
- Symptoms: Tends to affect lower legs first bc length sensory neurones longer. acute painful worse at night often when improvement in glycemic control. Or loss of pain/temp/vibtation
- Mx: amitriptyline, duloxetine, gabapentin. If exacerbation of neuropathic pain then tramadol (if localised then just topical capsaicin cream)
Complications: gi autonomic neuropathy (gastroparesis where bloating/vomiting so needs metclopramide, chronic diarrhoea, gord), diabetic foot disease
- foot disease is due to neuropathy loss sensation + peripheral vasc disease causing ischaemia (absent foot pulses/reduced abpi, claudication). Can lead to…
Charcots: slight pain, swollen red joint, progressive joint destruction causing collapse in foot arch ‘rocker bottom foot’, skin ulceration, wound healing poor
Sick day rules:
- t1dm
- t2dm
- DVLA rules
Sick day rules:
- t1dm: check bgc more freq, try maintain normal meal pattern or replace ith carb containing drinks, 3l fluids day
- t2dm: monitor glucose more frequently, stop sulfonylurea, if risk dehyd stop metformin (lact acid) and glp1 ag (aki), for sglt2 inhib check for ketones and stop if v unwell. Restart meds if E+D for 24-48 hours
- DVLA: no severe hypoglyc event in 12 months, driver has full hypog awareness, bgc monitoring at least twice a day, no major diabetes complications - this is if on sulfonylurea, dvla will contact them
