Endocrine Flashcards
definition of hypoglycemia
< 3.3
what is Whipple’s triad for hypoglycaemia
symptoms of hypoglycemia, blood glucose level low, resolve of symptoms after blood glucose level back to normal
causes of hypoglycemia in known diabetes
hypoglycaemia (using sulphonylureas eg gliclazide, insulin)
dec glucose delivery (missed meal, fasting)
inc glucose utilisation (exercise)
dec endogenous glucose production (alcohol)
inc insulin sensitivity (weight loss)
dec insulin clearance (renal failure)
pregnancy - tight control
causes of hypoglycemia in non-diabetes
pituitary insufficiency - low ACTH
Addison’s disease - low BP, low NA, high K, low aldosterone and ACTH
exogenous drugs (quinine, chloroquine, B-blocker overdose, valproate, aspirin, insulin)
post-meal hypoglycemia
liver disease
Immune Hypo (anti-insulin Ab, or Hodgkins)
non-pancreatic neoplasm (small cell, fibroma, sacroma)
NIPH syndrome - noninsulinoma pancreatogenous hypoglycaemia (islet cell hyperplasia)
starvation + malnutirition
hypothyroidism (myxoedema coma)
symptoms of hypoglycaemia
lethergy weakness sweating shaking tingling lips and tongues uhnger palpitations headache double visions difficulty concentrating slurred speech confusion change in behavior coma
what scale is used to represent the symptoms of hypoglycaemia
Edinburgh hypo scale - 11 most common hypoglycaemic symptoms
Autonomic nervous system
- sweat
- palpitation
- shaking
- hunger
Neuroglycaemic
- confusion/drowsy
- dec GCS
- slurred speech
- odd behaviour
- incoordination
General
- malaise
- Nausea
what are the investigations for hypoglycaemia
- blood glucose < 3.3
- Bloods: FBC/UE/LFT, blood glucose, HBA1c, serum insulin
- C peptide (elevated if endogenous insulin production – either insulinoma or sulfonylurea use)
- Beta-hydroxybutyrate - < 2.7 mmol/L, low = diagnosis of mesenchymal tumour
- serum sulfonylurea
- TSH – hypothyroidism can cause hypoglycaemia
- serum cortisol – pituitary insufficiency
management of hypoglycemia if GCS is 15
If GCS15:
- Fast acting sugar: 7/8 jelly babies (not chocolate), 10-20g dextrogel. and
- Long acting: 2 toast/ cereal
- Check BG after 15mins- aim for 5- repeat x3 above management until normal
- BM<3 then 1mg IM glucagon.
GCS<15: assume they cant swallow or IV access cannot rapidly established
- 75ml 20% glucose / 150ml 10% glucose IV or 1mg IM glucagon.
- Check after 15mins- aim for 5 x3 until normal.
pathophysiology of DKA
- Ketoacidosis occurs in starvation states and produces acetone.
- In DM a lack of insulin means that glucose cannot be used, pushing the body into the starvation state.
- A lack of insulin stimulates the release of glucagon from the alpha cells which stimulate glycogen breakdown, gluconeogenesis, release of free fatty acid which are converted by the liver to ketones. = HIGH KETONES.
- Excess glucose excreted by kidneys due to osmotic diuresis = HIGH URINE GLUOCSE.
- lipolysis ketogenesis and metabolic acidosis = METBAOLIC ACIDOSIS.
what are the clinical features of the first presentation of DKA in a T1DM?
sudden onset weight loss ployuria polydipsia non-specific abdo pain drowsy confusion Kussmauls' breathing Ketoci breath N+V dehydration inc urination (osmotic diuresis)
usually due to alcohol intake (because alcohol inc insulin in the blood stream and so less insulin to get glucose into cells)
what are some of the causes of DKA
4Is
infection - UTI, RTI, skin
Infarction - MI, stroke, GI tract, peripheral vasculture
INsufficient insulin
intercurrent illness - many underlying conditions precipitate or aggravate DKA
what are the diagnostic criteria for DKA
BLood glucose > 11
Ketone - urine 2+ or blood > 3mmol/L
Metabolic acidiosis - pH < 7.3 +/- HCO < 15mmol/L
what are some investigations for DKA
FBC - WCC U&E - inc urea, creatinine, dehydration LFT CRP amylase blood glucose blood culture HbA1c.
ABG/VBG - metabolic acidosis, dec bicarb
Urine dip +/- MCS - for infection, ketones, protein, glucose
find infection ECG (exclude MI, tall tented in hyperK) CXR - RTI infection MSU Pregnancy test
beware of pseduohyponatreamia - for every 4mmol dec of glucose –> 1 mmol dec in Na+
what are the 9 steps for treating DKA
ABCDE
• SpO2, ECG, BP/HR, 2 large bore cannulas
1) diagnosis – pH, Ketones, BM
2) immediate treatment
a. 1L 0.9% NaCl over 1 hour if BP > 90
b. If BP < 90, 500ml bolus stat, max 2L if BP still low, call criteria outreach
c. start IV insulin – 50 unites quick releasing insulin in 49.5 ml NaCl 0.9% to give 0.1 unit/ml solution via syringe driver at 0.1units/kg/hour
d. call diabetes speciliast team
3) call critical care for review if
a. venous bicarb < 5 or pH < 7.1
b. drowsy (GCS < 12 or abnor AVPU)
c. pregnant
d. heart failure
e. oliguria or anuria
f. sat < 92% on air
g. persistent hypotension < 90 systolic after 2 L
h. K+ < 3.5mmol/L on admission
4) Essential investigations – as mentioned above
5) Insulin – fixed rate insulin (0.1 unites/kg/hour) + continue long acting insulin
6) IV fluids
a. 1L NaCl 0.9% over 1 hour then
b. 1L NaCl 0.9% over 2 hours then
c. 1L NaCl 0.9% over 2 hours then
d. 1L NaCl 0.9% over 4 hours
e. when glucose < 14 mmol/L continue IVI +/- KCL + 10% glucose 125ml/Hour
7) potassium (start after 2nd IV fluids not resus fluid)
a. if <3.5 senior review (>40 mmol/litre maybe necessary)
b. 3.5-5.5 40mmol KCl per litre of NaCl
c. >5.5 – none
8) Monitoring
a. re-assess hourly for first 4-6 hours
b. check vital signs hourly
c. consider catheter if clinical evidence of poor LV or renal function
d. consider NGT if drowsy
e. treat underlying causes for DKA
f. give LMWH to all (thromboprophylaxis)
g. treatment target
i. blood glucose falls of >3mmol / L / hour until < 14
ii. cap ketones fall of at least 0.5mmol / litre / hour until <0.6
iii. venous bicarbonate rises of > 3 mmol/ litre . hour until > 15
iv. if not improving, inc rate of insulin infusion by 1 unit / hour every hour
9) After recovery
a. transfer to SC insulin if pt able to eat and drink well and pH > 7.3 or blood ketones < 0.6 mmol/L
what is the function of insulin
it moves glucose from bloodstream into cells for energy consumption
which cells is destroyed in T1DM
beta cells of islet of Langerhans in the pancreas
symptoms of T1DM
acute onset
25-50% present with DKA
thin (low BMI)
4Ts - thirst, toilet, thinner, tired
genital itchy or frequent episodes of thursh
wounds heal slowly, boils
recurrent/prolonged infections
what is the investigation regimen of suspect T1/2DM with symptoms
singe episode of test of the following:
fasting blood glucose > 7 or
random blood glucose >11.1 or
2 hour fasted glucose > 11.1 (after 75g of glucose) or
HbA1c of 48
also
1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)
what is the investigation regimen of suspect T1/2DM without symptoms
2 sperate episodes of testing (2 wk apart) of the following:
fasting glucose > 7 or
random glucose > 11 or
HbA1c > 48 on 2 occasions
also
1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)
differentials for T1DM
LADA - latent autoimmune diabetes of adulthood
MODY - Maturity Onset Diabetes of the Young
T2DM
dibaetes insipidus
UTI
what are the different treatment regimen of T1DM
basal-bolus
insulin pump
2 injections per day
1 injection per day
when will basal-bolus (multiple daily injections) regimens be beneficial for patients
good physiological management
can be flexible to those with varied meal/exercise
only for those who can do multiple injections per day
when is insulin pump insulin treatment regimen used
when MDI fails
when is 2 injections per day regimen used?
rarely used nowadays
good for those unable to give multiple injections
what is the SICK day rule for Diabetes?
management of blood glucose during sickness
1) Sugar - sugar measurement inc, frequency every 2-3 hrs
2) I - Insulin = keep taking it
3) C - keep taking carbohydrate and fluids
4) K = measure ketones (4 hours)
drink at least 3 L of fluid
what is the essential mechanism for T2DM
peripheral resistance to insulin –> blood unable to break down glucose into energy properly
clinical features of T2DM
- Gradual Onset
- Polydipsia (thirst)
- Polyuria, esp nocturia
- Often obese (high BMI)
- Lethargy, blurred vision
- Genital itching (pruritius vulvae), frequent episodes of thrush, UTI
- unintentional weight loss
- DKA rare
- Wounds that heal slowly, boils
- Recurrent/prolonged infections
Treatment for T2DM
• 1st step lifestyle + aim for HbA1c of < 48
• 2nd step metformin if HbA1c > 48 + aim for < 48
• 3rd step/1st intensification if HbA1c > 58 dual therapy & aim for HbA1c < 53
o metformin + DPP-4i
o metformin + pioglitazone
o metformin + SU
o metformin + SGLT-2i
• 4th step/2nd intensification if HbA1c > 58 triple therapy & aim for HbA1c < 53
o metformin + SU + DDP-4i or pioglitazone or SGLT-2i
o metformin + SU + GLP-1
if not tolerate the above combination and have BMI > 35 and specific psychological and other medical problems associated with obesity
BMI >35 and insulin would not be suitable
BMI < 30 and South Asian
• 5th step/3rd intensification Insulin (refer for this)
complications of T2DM
HHS microvascular disease Macrovascular disease inc BP cataracts fatty liver disease
When is the management for ACR > 2.5 in men or 3.5 in women?
ACEi or ARB and maintain BP <130/80
pathophysiology of diabetic foot disease
diabetes causes nerve damage - causes infection and charcoat’s
diabetes causes PVD - ulcers and gangrene
what are the 3 main types of diabetic foot disease?
1) Charcoat’s Arthropathy - refers to progressive degeneration of the weight-bearing joint, a process marked by bony destruction, bone resorption and eventually deformity due to loss of sensation
2) diabetic foot infection - caused by repetitive foot trauma which becomes infected
3) diabetic foot ulcer - caused by repetitive foot trauma due to lack of sensation
clinical features of charcoat’s arhtorpahty
pain redness swelling deformity (skin intact) maybe associated with foot ulcer
clinical features of diabetic foot infections
fever pain red swollen hot to touch purulence
maybe able to see some break in the skin
clinical features of diabetic foot ulcers
eroded ulcer
commonly found on pressure points
can results in dry or wet gangrene
when will you refer a patient with diabetic foot disease
for all diabetic foot pathology refer within 1 day
life-threatening limb injury (refer immediately)
- ulceration with fever
- ulceration with limb ischaemia
- concern of osteomylitis
- gangrene
investigation for charcot’s foot
weight bearing X-ray of foot and ankle
consider MRI
investigation for diabetic foot infection
FBC + blood glucose
soft tissue or bone sample from base of the debrided wound
if this cannot be obtained take a deep swab
consider X-ray
