Endo Flashcards
MODY has what inheritence pattern
- AD
which thyroid disease causes DM
- Hyperthyroid
diagnostic criteria for ix of DM
- Fasting glucose >7
- random glucose > 11.1
above 2x if asymptomatic
- HBA1C > 48 (6.5%)
which patients cann you not use HBA1C to diagnose DM
- IDA untreated
- Haemoglobinopathies
- haemolytic anaemia
- suspected gestational DM
- Kids
- CKD
- Those on drugs that alter BG
define impaired fasting glucose
fasting BM b/ween 6.1-7
define impaired glucose tolerance
- fasting BM <7, 2hr after OGTT 7.8-11.1
clinical significance of IFG and IGT
- If IFG offer OGTT for IGT
- If <11.1 > 7.8 = Impaired glucose tolerance. if above = DM
types of T1DM autoantibodies
- islet cell cytopalsmic
- Glutamic acid decarboxylase
- insulin autoantibodies
- insulinoma associated 2 autoantibofdies
- zinc transporter 8 autoantibodies
what is the course for insulin regime for T1DM called
- DAFNE
- Dose adjustment for normal eating
during infection how much should you increase insulin dose by
25%
when do you start sliding scale preop in T2DM patients that manage with lifestyle/metformin
BM>12 X 2
T2DM rx first step if >48 hba1c
metformin and lifestyle
if > 58 hba1c T2DM rx
Metformin + DPP4I (gliptin) +
or
Metformin + Pioglitazone
or
Metformin + sulphonylurea
or metformin + SGL2I
what should you aim a patients HAB1C to be if original HBA1C = 58
- 53
rx treatment options if triple therapy needed in T1DM
- Metformin + gliptin + Sulphonylurea
or
- metformin + pioglitazone + SU
or metformin + pio/SU + SGLT2i
if triple therapy not tolerated, effective or CI in TDM what is next rx
- if BMI >35
- Metformin + GLP1 + SU
can be used if BMI <35 and cant have insulin
when can you give insulin in T2DM
- HBA1C > 58 and triple therapy hasnt worked and they dotn qualify for GLP1
treatment pathway for T2DM in those that metformin is CI
- Gliptin/ pioglitazone/SU
2ND LEVEL
- Gliptin + pio
- Gliptin + SU
- Pioglit + SU
3RD
- insulin
MOA Metformin-
a biguanide
- increases insulin sensitivity and helps weight
DPP4i MOA
- Block dpp4 which is an enzyme that destroys hormone incretin
glitazone MOA
- Increaes insulin sensitivity
SU MOA-
Increases insulin secretion
how do GLP1 mimetics work
- increase insulin secretion and inhibit glucagon secertion
what hba1c is needed for GLP1 mimetic prescription
- 11mol/l reduction in HBA1C and 3% weight loss after 6 months to justify ongoign subscription
which nerve palsies are common in DM
CN 3 AND 6
isolated mononeuropathy in DM - what is the cause
- occlusion of vasa nevorum
diffuse neuropathy cause in DM
- peripheral nerves with fructose build up
types of DM neuropathy
- symmetrical mainly sensory
- diabetic amyotrophy - wasting of quads asymmetry
- acute painful - crawling up you
- mononeuritis - CN3 AND 6
- autonomic
severe DKA criteria
- tachy/brady
- hypotensive
- GCS 6MMOL/L
- bicarb <12
DKA Dx criteria-
BM > 11
Ketones >3mmol/l
Acidaemia - ph <7.3 or HCO3 <15
rx DKA-
- Slaline -.9% + 20mmol K /L. if BM <14 = 10% dexrrose
- insulin 0.1uints/kg/hr
- restore acid base over 24hrs
if no urine by 2hrs -chatheter
NG if drowsy or protracted vomiting
- CVP monitor if shock
HONK/ HSS diagnosis criteria
BM>33.3
No ketoacidosis
Hyperosmolality > 320
rx HSS
- Fluids 0/9% saline
- LMWH thromboprophylaxis
- oral hypoglycaemia or severe = insulin
What GCS do you need to be in DKA/HONK for intubation
<12
why do you still need to replace k+ in DKA despite high K on bloods
- as it is in the wrong place so once insulin given will shift and they get hypokalaemic
- give extra k if >5.5
what is the 1,2,2,4,6 rule in DKA
- 1L of fluid in 1h
- 2nd bag over 2hrs
- 3rd bag over 2 hrs
- 4rth bag over 4hrs
- 5th bag over 6hrs
what is HDL mainyl made of
- phospholipids
what is LDL mainly made of
- cholesterol
who do you screen for hyperlipidaemia
- fhx of hyperlipidaemia
- cornear arcus <50yrs
- xanthomata or xanthalasma
and those at risk of CVD
types of hyperlipidaemia
- common primary (70%)
- familial primary
- secondary
- mixed
familial hyperlipidaemia types
1 LP, 2 LD. 3 gets V, 4 is E, 5 gets more
T1 = Deficient in LPL and apoc2
T2a and b = Deficient in LDLr and
apob100
T3= APOE
T4= VLDL overproduction
what builds up in the different familial hyperLD
1 = Cholesterol and TG AND Chylomicrons
2a = LDL, cholesterol
2b = LDL, VLDL. Cholesterol
3 = VLDL chylomicrons
4= VLDL AND TG
Inheritance patterns for familial hyperLD
1 = AR
2A and B = AD
3= AR
sx of familial hyperld by type
1 = pancreatitis 2 = xanthomata achilles, corneal arcus 3= palmar xanthoma 4= pancreatitis
which familial hyperlipdaemia type gives highest risk CHD
- Type 3
- has apoe2 mutation but needs second hit such as HypoTH, DM. ETOH, OBESE,
special tests for hyperLD
- Apolipoproteien A
= A1 = HDL
= B100 = VLDL, LDL - LIPOPROTEIN A - >300 = CVD
- HOMOCYSTEINE = risk marker
- apo e genotyping
2nd line drug fo rhigh cholesterol and MOA
- Ezitimibe; stops cholesterol absorption by inhibiting
Primary prevention for high cholesterol is given in which patients
- QRISK >10%
- T1DM MOST
- CKD EGFR <60
Give atorvatstatin 20mg OD
QRISK should not be used in which pt
- T1DM
- CKD <60 egfr
- albuminuria
- familial hyperlipidaemmia
QRISK underestimates risk in which pts
- mental health
- HIV
- On cholesterol altering meds e.g. steroids, antipsych
- autoimmune disorder ps
what total cholesterol level indicates possible familial high cholesterol
- > 7.5 with fhx of premature coronary heart disease
who should you refer for assessment for high cholesterol possibly familial
- > 7.5 Non HDL with or without fhx
- >9 TC
when can you increase dose in CKD for staitin
- if > 40% reduction in non HDL nto achieved and egfr >30. otherwise talk to renal specialist
causes of hypoglycaemia in non diabetics
- EXPLAIN
- EXogenous drugs
- Pituitary insufficiency
- Liver failure
- Addisons disease
- Islet cell tumours
- Non pancreatic neoplasma
in kids also
= nesidioblastosis; beta cell hyperplasia
how does alcohol cause hypoglycaemia
- inhibits gluconeogenesis
- depleted glycogen stores due to starvation
how do BB cause hypoglycaemia
- inhibition of hepatic glucose which is promoted by Symp NS
- increase glycogenolysis in liver
how does aspirin cause hypoglycaemia
- hepatic gluconeogenesis reduced and increase in insulin secretion , increases glucose utilization in peripheral tissues
- also lactate high as enzyme for pyruvate conversion blocked by salicylate
how do Ace- i causes hypoglycaemia
- increased sensitivity of peripheral tissues , block Ang II as one of the counter regulatory hormones with similar effects as adrenaline
= speeds up absoption of subcut insulin
how does pentamidine cause hypoglycaemia
- rx for jirovecii
- surge of pancreatic cells then destruction and IDDM
how does quinine cause hypoglycaemia
- increase insulin release in non DM patients
what is whipples triad of hypoglycaemia
- low BG
- symptoms of low GB
- Resolve after sugars given
how to investigate fasting hypoglycaemia if symptomatic
- Bloods; glucose, c peptide, insulin, ketones
how to investigate post prandial hypoglycaemia
- OGTT ix
how does benign pancreatic cell tumour present
- fasting hypo + whipples triad
how to check for insulinoma
- give IV insulin and measure c peptide
- should go down but if does not then = insulinoma
IN PCOS what is the finding of LH:FSH ration
high LH:FSH
when to stop COCP in PCOS-
After 3-4 months of hirsutism stopped. why? high VTE risk