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
causes of primary hypogonadism
- trauma
- torsion
- Chemo/RDT
- Tumours
- Post orchitis
- chromosome abnormalities e.g. klinefelter 47 xxy
- renal failure, liver failure and alcohol excess are all toxic to leydig cells
secondary hypogonadism causes
- prolactinoma
- hypopituitarism
- kallmans syndro me (also colour blind and anosmia)
- systemic illness
- laurence moon biedl/ prader willi
what is the cause of gynaecomastia if a patients has LOW Testosterone but high LH
- primary hypogonadism e.g. klinfelters
what is the cause of gynaecomastia with low testosterone and normal LH
- Piuitary/hypothalamic disease
what is the cause of gynaecomastia with elevated testosterone with high estradiol
- androgen exposure; testicular tumour
what is the cause of gynaecomastia with elevated estradiol and elevated SBHG
- oestrogen exposure, testicular/ adrenal tumour
when do you treat low testosterone
- if less than 8 on 2 morning or <15 if LH is high. and muscle bulk decrease = testogel
who is CI to testosterone
- nephrosis, high ca, polycythamiea breast, protate or lvier ca
rx for adolescents with gynaecomastia-
resolves in 3yrs alone
- otherwise tamoxiffen 6months but unlciensed
1st line rx for those that cant take sildenafil in Erectile dynfsunction
- vacuum device
what drugs cause ED
- AntiHTN
- diuretics
- antidepressants
- antipsychotics
- anticonvulsants
- hormonal treatment
- fibrates
- h2 blockers
presentation of de quervains/ subacute thyroditis (hyper then hypoth)
- painful goitre and raised ESR
what is reidel thyroiditis
- fibrous tissue replaces normal thyroid parencyma = painless goitre
drugs that cause hypoTH
- Lithium
- amiodarone
what TH do Postpartum women get
- Hypo
what is the most common cause of hypoTH in developing world
- iodine deficiency
what happens to TSH and T4 in sick euthyroid
- both low
what happens to TSH and T4 in poor compliance to thyroxine
- normal t4, high tsh ; lagging tsh as usually only take meds before bloods
what situations is TBG high
- pregnancy
- high oestrogen
- hepatitis
TBG is low in
- nephrotic syndrome and ,malnutrition
- drugs e.g. androgens, steroids, phenytoin
- CLD and acromegaly
Toxic mmultinodular goitre on nuclear scintigtaphy indicates what thyroid problem
- toxic multinodular goitre (secrete thyroid and compressive sx due to enlarged gland e..g sob/ dysphagia
who should we screen for TH problem
- those with af
- those with hyperlipidaemia
- DM annually
- if T1DM during 1st trimester and post delivery
- on amiodarone or lithium; 6month
- down.turners/addisons
rx for thyroid eye disease-
- support e.g. artificial tears
- fresnel prism on one spectacle
- methylpred
- surgical decompression
what happens to neutrophiils in graves
and ca? and esr and lft?
neutropenia
- high
what are graves abs types
= IgG anti-TSHr
what is the result of nuclear scintigraphy identifying hot nodule
- thyroid adenoma
rx subacute thyroiditis
- NSAIDs
rx for HyperTH
- BB and titrate to help with sx
- propylthiouracil, carbmiazole
- use as titration block or block and replace
when do you use propylthiouracil in HyperTH
- 1st trimester or thyroid storm. otherwise not preferred due to liver injury
radioiodine therapy and pregnancy relation
- do not give it in pregnancy
- avoid pregnancy for 6 months in women and 4 months men
when do you refer someone with subclinical hyperTH
- If nodule/goitre
- if despitre rx TSH <0.1 persistently or if >65yrs or post menopausal or at risk of osteoporosis or have CVD or sx
thyroid storm rx
- propanolol
- carbimazole/propylthio
- lugols solution = iodine after 4hrs
- steroids; dexa
- avoid aspirin
what is thyrotoxic periodic paralysis
- most common in asian males
- vigorous exercise/ high carb meal
- flaccid ascending paralysis; proximal > distal
- depressed/ absent DTR
MOA thyrotoxic periodic paralysis
- shift of k+ as overactive na k+ ATPase pump = low serum k+ = paralysis
rx thyrotoxic periodic paralysis
- Propanolol
- replace k+
- treat hyperTH
DO NOT GIVE IV GLUCOSE
how to treat myxoedema coma
ABCDE - must do ABG -Thyroid hormone replacement - correct metabolic issues; \: hypoventilation = intubate and ventilate
: hypona+
= water restrict
: hypoglycaemia = IV dextrose
+ hydrocortisone
mortality predictors in myxoedema coma
- age
- temp <34
- HR < 40
- Large amounts of T4 IV
subclinical hypoTH parameters
- TSH >4 with normal t3 and t4 amd mo symptoms
when do we treat subclinical hypoTH
- TSH >10, hyper would be low TSH
- +ve autoantibodies
- past treated graves
- other organ specific autoimmunity (T1DM, myaesthenia, pernicious anaemia etc)
signs of myxoedema coma
- looks hypothyroid
- usually >65yrs - hypothermia
- hyporeflexia
- low BG
- bradycardia
- coma seizures
what type of calcium do we measure on a ABG
= Free ionised
what calcium do you measure on bloods
- total calcium
what happens to ca levels if ph goes down
- gets displaced from albumin so h+ can bind therefore levels increase
what is chvosteks sign
- tap on fcial nerve and pt with hypoca will twitch
what is trousseaus sign
- BP cuff around arm and inflated - tetanic spasm
what other ion is needed for pth release
- mg
which MEN syndrome is hyper PTH associated with
MEN1
MEN1 syndromes
- PTH hyperplasia/adenoma
- pancreatic endocrine tumours
- pituitary prolactinoma
= TSG
Men 2a syndromes
- thyroid - medullary thyroid ca
- adrenal; phaeochromocytoma
- PTH hyperlasia (less often)
men 2b syndromes
- like men 2a = + mucosal neuromas and marfanoid appearance
what syndrome do those with severe hyperPTH get (shown on imaging)
- osteitis fibrosa cystica = subpeiosteal erosions, cysts or brown tumours of phalanges +/- pepper pot skull +/- acroosteolysis
rx for hyperpTH
= definitive = total parathyroidectomy
conservative only if meets criteria; - >50yrs age - no end organ damage - Ca < 0.25 ULMN = increase fluid to prevent stones. avoid thiazides and hifh ca/vit d
calcimimetic if unsuitable for surgery
criteria for total parathyroidectomy due to hyperPTH
- <50yrs
- ca>2.75
- creatinine clearance - reduced by 30%
- 24h urianry ca - >10mmol
- Bone mineral density = t score less than -2.5SD
- bone disease/osteoporosis/renal calculi
signs of hypoca
SPASMODIC
- Spasma
- Perioral paraesthesia
- anxious, irritable, irrational
- seizures
- muscle tone increase
- Orientation impaired
- dermatitis
- impetigo herpetiformis
- chvosteks , cataract, cardiomyopathy
why does addisons disease cause high ca
- Adrenal calcification
which disease cause hyperca
- TB
- Toxopalsmosis
- histopalsmosis
- raynauds
- muscle primaries / leiomyosarcoma
- nephrocalcinosis
- endocrine tumours
- sarcoidosis
how will hyperca show up on ECG
- Reduced QT-i
what are the two cause sof hyperca with albumin raised
urea raised; - dehydration
urea normal; cuffed specifmen
what hyperca investigation results point towards malignancy
- low albumin
- low cl
- alkalosis
- low k
- high PO
- High ALP
how to treat pt with hyperca
- record weight
- stop offendign drugs
- saline to make euvolaemic and U O 200ml/hr
- can need >4l in 24hrs; but careful if CCF
- Furosemide when hypovolaemia corrected - bu tnot if malignant
- if still high >24hrs = bisphosphonates
- then pamidronate
if known mets = IV zolendronic acid
rx hyperphosphotaemia
- oral calcium carbonate but not if high ca
- gut phosphate binders e.g. sevelamer
hypomg ecg changes
- prolonged QT, broad/flat t waves, sometimes short ST
what other metabolic abnormalities are cause dby hypomg
- hypoca
- hypok
rx hypomg
- parenteral mg cl 50mmol in glucose if symptomatic, or with hypoca
what happens to reflexes in hypomg
- hyperreflexia
rx hypermg
- calcium gluconate
- glucose and insulin also lowers
- dialysis in severe CKD
what zona produces mineralocorticoids
- glomerulosa
what muscle isssue do you get in cushings
- proximal myopathy
what result would you expect for dexamethasone suppression test for cushings disease
- normal cortisol in syndrome after low dose
- low cortisol after high dose
what is the next ix if dexa supression test comes back +Ve in both low and high dose
- plasma ACTH . if ACTH undetectable then adrenal tumour
. if detectable = extropic - if detectable need to differentiate between pituitary and high dose and extopic by doing high dose CRH test.
result: dose goes s up in pituitary disease but not in ACTH production
what is nelson syndrome
- in cushings disease if oyu have bilateral adreneloctomy, this is a complication
- increased skin pigment due to high acth from enlarging pituitary tumour as adrenelectomy removes -ve feedback
summary; pitutiatary tumour post adrenelectomy
what drugs can you give in ectopic acth production preop or awaiting radiation
- ketoconazole
- metyrapone
- fluconazole
- decrease cortisol secretion
ix for hyperaldosteronism
- plasma aldosterone:renin ratio = screen
results:
= high aldosterone: renin = primary, high aldo and high renin = secondary - fludrocortisone supression test; supressed plasma renin activity = primary
rx for bilateral adrenal hyperplasia-
spironolactone, elperenone
what is conns syndrome
- adenoma of the zona glomerulosa
rx conns
- lap adrenelectomy. spironolactone 4 weeks preop
what is the other name for primary hyperaldosteronism
- conns
what is barters syndrome
- AR
- Congenital salt wasting = sodium and cl leakk in LOH due to mutated transporters
- presents as child FTT, poyuria, polydipsia, BP normal == NA loss so voluem deplete so ADH and raas kicks in
= hyperaldosteronism secondart
rx barters syndrome
- k+ replace
- nsaids
- acei- i
short synacthen test results in addisons / primary adrenal insufficiency
- levels of cortisol fail to rise
ix for addisons disease
- 9am acth level = high level with low cortisol = addisons
addisonian crisis symptoms
- hyperpigment
- low na
- high k
- hypoglycaemia
- shock/low bp
rx adissonian crisis
- rehydrate with 1L 0.9% saline + bolus dexamethasone pre ACTH test
if ACTH comes back
- then hydrocortisone IM 6hrly till stable
- glucos eig hypoglycaemia
what do you do to long term steroid dose if antibiotics or febrile illness
- double it
if someone on steroids vomit what should they do
- emergence hydrocortisone injection and seek advice immediately
what is waterhouse friedrickson syndrome
- sepsis from menigicocaemia with associated adrenal haemorrhage;
what MEN syndrome is phaeochromo and paraganglioma a part of
- MEN2
treatment of phaeochromocytoma-
alpha block (phetolamine) then beta block (propranolol)
- then op and remove.
- then 24hr urine metanephrones 2wks post op
what is pituitary apoplexia
- acute haemorrhage or infarction of pituitary
pituitary apoplexy sx
- headache
- vomiting
- visual disturbances
- ophthalmoplegia = CNIII most common
- meningismus
- fever
- low consciousness
- death
predisposing factors for pituitary apoplexy
- hypertension
- head traum
- cardiac surgery
- ICP raise
- DM
- Acromegaly
- cushings
- oestrogens
- anticoag
- bromocriptine
- gnrh analogies
- RDT
RX Pituitary apoplexy
- monitor fluuids
- replace deficient hormones
- surfery if needed
- ltm monitor
indications for surgery in pituitary apoplexy
- diminished level of consciousness
- hypothalamic disturbance
- visual impairment
CI for insulin tolerance test
- heart disease
- epilepsys
- adrenal failure
microadenoma in putitary vs macro
- < 1cm
- >1cm
3 types of pituitary tumours
- chromophobe; non secretory
- acidophil; GH or PRL
- basophil; ACTH
rx prolactinoma
- <1cm; bromocriptine = dopamine agonists
> 1cm = start with above then possible surgery if pressure symptoms
ix for acromegaly
- IGF1 and basal GH. if either or hight (GH >0.4) then OGTT. if lwoest GH after is >1mcg/l = confirmed
rx acromegaly
- surgery
- somatostatin analogyes
diabetes insipidus rx
- crania; desmopressin
- nephrogenic; treeat cause or bendroflumethiazide
causes of diabetes insipidus (nephrogenic)
- inherited
- low k+. high ca
- lithium, demelocycline
- CKD
- Post obstructive uropathy