Endo Flashcards
Hyperkalaemia Mx
- 10 u actrapid & 100 ml 20% dextrose (or 200ml 10%)
- 10mL 10%Calcium gluconate
HHS Mx
IV 0.9% saline (1L over 1h)
Which diabetes drug can be used in CKD?
Sitagliptin (DPP4 inhibitor)
Adrenal crisis / adrenal insufficiency crisis
Life-threatening medical emergency where adrenal glands unable to produce enough cortisol and other hormones.
What does cortisol regulate?
- Blood sugar levels
- Blood pressure
- Body’s response to sress
Features of adrenal crisis
- Weakness/fatigue
- Dizziness
- Low BP
- Abdo pain
Causes of adrenal crisis
- Uncontrolled Addison’s (most common)
- Damage to adrenal glands due to infx, trauma/surgery
Adrenal crisis Ix
Plasma cortisol and adrenocorticotrophic hormone
Diabetes 1) level for dx, 2) target level if no trx, 3) target level if trx
1) 48mmol/L
2) 48mmol/L
3) 53mmol/L
Proteinuria + diabetes
1) ddx
2) Mx
1) diabetic nephropathy
2) ACEi
Primary aldosteronism/Conn’s syndrome features
- HTN
^ often early onset - Raised protein aldosterone:renin ratio
- Hypokalaemia (not ALWAYS present)
Mx of prolactinomas
- Cabergoline (dopamine agonist)
PCOS features
- Oligomenorrhoea
- High BMI
- Increased ratio LH:FSH
- +/- mild elevation in prolactin
Postpartum thyroiditis mx
Propanolol
(can occur up 1 year after childbirth)
How to calculate serum osmolality?
2(Na) + glucose + urea
Which diabetes drugs can cause hypos?
Sulfonylureas, e.g., gliclazide
Primary hyperparathyroidism - PTH and Ca levels
PTH: high/normal
Ca: high
Hypothalamic-pituitary-adrenal axis
Hypothalamic-pituitary-gonadal axis
Diabetes insipidus v SIADH
DI - insufficient production of ADH -> so water loss ++ than what we want. Polyuria & polydypsia + hypoNa
SIADH - too much ADH –> decreased UO, hyperNa, fluid overload
Cranial/central DI v nephrogenic and which ix used to distinguish between the two
- Central/cranial: underproduction of ADH by hypothal
- Nephrogenic: kidneys’ ability to react to ADH affected
DDAVP test
Primary polydypsia / psychogenic polydipsia
A condition characterized by excessive thirst and drinking of fluids, leading to an increase in urine output. Thirst is not due to a psychological compulsion, rather than physiological need.
What does water deprivation test distinguish between?
Central DI and primary polydypsia
How does water deprivation test work?
- Abstain from water for 8-12h
- Urine osmolality remains low –> DI
bc even tho ur dehydrated, ur body can’t hold on to water bc of lack of ADH rip so ur urine isn’t really conc bc ur still pissing bestie - Urine osmolality ++ –> PP
bc ur ADH is fine, so ur body is like omg we r dehydrated lets kick in the anti-diuretic plan and ur piss is super concetrated
How does DDAVP test work?
- Admin a synthetic form of ADH (desmopressin)
- Central DI –> urine osmolality increases and UO drops
bc now we are getting in ADH when we prev couldnt really make enough and it be doing its thang - Nephrogenic DI –> urine osmolality remains low and UO stays same really
bc we already had ADH before but our dang kidneys are like ?? what do so that doesnt change
What is tertiary hyperPTH?
Parathyroid glands become autonomously overactive and produce excessive amounts of PTH - a complication of long-standing secondary hyperparathyroidism/ kidney transplant
Ca/PTH/Vit D thang thangs
RAAS system
How does spironolactone work as a diuretic?
It blocks the actions of aldosterone
Paget’s disease
Chronic disorder of bone remodeling, characterised by abnormal bone growth and remodeling.
Paget’s disease features
- Bone pain and deformities
- Fractures
- Elevated ALP
- Sclerotic areas on XR
- Increased uptake on bone scan
What will biochemistry results look like for Heterozygous familial hypercholesterolaemia?
- Raised cholesterol
- Triglyceride normal
- HDL normal
Mx hyperthyroid + breastfeeding
Propylthiouracil
Premature ovarian failure biochem
- high LH and FSH
- low oestrogen
correct statin target 3 months after starting treatment is
total cholesterol <5
Phaeochromocytoma ix
Urinary metanephrines
Addison’s and features
Primary adrenal insufficiency due to autouimmune destruction of adrenal cortex -> no cortisol and aldosterone release
- Fatigue
- Diarrhoea
- Abdo pain
- Anorexia
- Salt craving
- Generalised hyperpigmentation
HypoCa mx
IV calcium gluconate + cardiac monitoring
T2DM levels for dx
- Fasting >= 7.0 mmol/l
- Random >=11.1 mmol/l + symptoms
- Hba1c >= 48 mmol/mol (6.5%)
It is recommended that two separate tests are carried out, on different days, to confirm the diagnosis of diabetes.
Anterior pituitary hormones
- Growth hormone
- Adrenocorticotrophic hormone
- TSH
- FSH
- LH
- Prolactin
Posterior pituitary hormones
- Oxytocin
- ADH
Addison’s ix
- screening test: 9am cortisol level (usually high, but low in Addisons)
- confirmatory dx: short synACTHen test (will see that cortisol still doesn’t rise:()
Addisons biochem features
- Low Na
- High K
- Low glucose
(Aldosterone makes kidneys keep Na and excrete K, but we have lack of aldost +
Cortisol increases glucose, but we have lack of cortisol)
Addisons mx (same for adrenalectomy) - chronic
- Mineralocorticoid, e.g., fludrocortisone (replaces aldost)
- Glucocorticoid, e.g., hydrocortisone (replaces cortisol)
+ sick day rules: double steroids when unwell
Draw adrenals and what each layer produces
Addisonian crisis mx
- IV high dose hydrocortisone
( at high doses, has both MR and GC effects)
± IV fluids
± IV glucose
Hyper Ca classification
2.2-2.6norm
Mild <3
Mod 3-3.5
Severe >3.5
Hyperca mx
- IV saline 4-6L. in 24h
- IV zoledronate 4mg (once hydrated)
DM Mx
- Metformin
- sulfonylurea (e.g., gliclazide), thiazolidinedione (e.g., pioglitazone), gliptin/dpp4i (sitagliptin), or SGLT-2i (empagliflozin)
- triple therapy
Preferred 2nd line for thos with CVD risk/HF is SGLT2i
Ankle swelling + erythema + loss of foot sensation in T2DM
Charcot arthropathy
Bisphosphonate use + jaw pain + swelling
osteonecrosis of jaw
Normal Ca but high ALP
Paget’s disease of bone
Osteoporosis mx
- bisphosphonate
(-PPI) - Ca
- Vit D
Osteomalacia v osteoporosis
Osteomalacia
- normal bone mass
- little sun light exposure -> low Phosphate
- low Ca, high ALP
- mx: vit D
Osteoporosis
- low bone mass
- post menopause/older peeps
- normal bloods
- mx: bisphosp
Metformin use + impaired renal function + acidosis
Metformin induced lactic acidosis
DKA mx
- Fluid bolus + 1L 0.9% NaCl over 1 h
- FRII 0.1unit/kg/hr (& continue long acting insulin if any)
- When glucose <14mmol/L -> 10% glucose 125ml/h & consider reducing insulin to 0.05unit/kg/hr
Features for DKA
- Hyperglycaemia >11mmol/L (usually 4-6)
- Ketones >= 3mmol/L
- Acidaemia pH <7.1
HypoK v Hyper K features
Hypo
- muscle weakness
- hypotonia
-hyporeflexia
- cramps
- fatigue!!
Hyper
- CP / palp
- Tinnitus
- Light headedness
- Tachy
HypoK v hyperK ECG
HypoK
- Small T waves
- U waves
Hyper K
- Tented T waves
- Widened QRS
Sudden decline in GCS after correcting hyponatraemia
Osmotic demyelination syndrome
Acute HypoNa <130mmol + syx mx
3% hypertonic saline under higher level care + 6hourly monitoring
+ stop any Na lowering drugs (e.g., diuretics, ACEi, SSRIs)
Which drugs are Na lowering?
- diuretics
- SSRIs
- ACEis
HypoNa Ix (if asyx/chronic)
Assess fluid status + take urinary Na
SIADH mx
Treat underlying cause + fluid restrict
What can be used in refractory cases SIADH?
tolvaptan
Cushings syndrome and syndrome v disease
Cushings syndrome = excess corticol
Cushings disease = due to pituitary adenoma
Cushings Ix
Cushings syndrome
1. 24h urinary cortisol OR overnight (low dose) 1mg dexamethasone suppression test OR salivary cortisol
2. If +ve, perform 2nd test from above -> positive = confirmed
(dexamethasone is basc acting on same Rs as cortisol, so we should get -ve feedback and thus low cortisol)
Cushings disease
Serum midnight ACTH -> normal/high
^High dose dexamethasone suppression test
- If suppressed -> cushing’s disease -> pituitary MRI
- If not suppressed -> ectopic ACTH -> CT TAP
Serum midnight ACTH -> low
^ACTH independent cause -> CT TAP ?adrenal carcinoma
Definitive mx cushings disease,
otherwise long term complx
transsphenoidal resection pituitary adenoma
complx: DM, osteoporosis
Primary hyper PTH mx
parathyroidectomy
Secondary hyperPTH mx
treat CKD: treat hyper phosphataemia w phosphate binders (e.g., calcium carbonate)
Tertiary hyperPTH mx
Mostly self limiting
Surgery if refractory hyperCa or syx
Secondary hyperPTH cause
PTH hyperplasia due to controling chronic hypoCa, usually due to CKD
chvostek sign
facial twitching after tapping anterior to tragus (hypoCa)
Causes of hypokalaemia
- Insufficient dietary intake
- Vomiting/diarrhoea
- Diuretic meds
- Conn’s syndrome
- CKD
Nelsons syndrome
Complx of adrenalectomy
abnormal hormone secretion, enlargement of the pituitary gland, and the development adenomas. It occurs in an estimated 15 to 25 percent
