endo conditions Flashcards
primary hyperparathyroidism presentation
-most cases are asymptomatic and diagnosed incidentally on blood test where hypercalcaemia is detected
- symptom mneumonic is: bones, stones, abdominal groans and psychic moans + polydipsia, polyuria
primary hyperparathyroidism bloods findings
hypercalcaemia
low phosphate
normal or high PTH
top causes of primary hyperparathyroidism
solitary adenoma 85%
10% hyperplasia and other stuff less %
pathophysiology of secondary and tertiary hyperparathyroidism vs primary
primary (for the causes listed in other card) PTH goes up first and that leads to ca+ going up and Phosphate to drop
vs
secondary means that the PTH rises DUE TO A ALREADy existing LOW CALCIUM- ex CKD or other kidney problem ect
TERITIARY is basically when secondary has lasted for so long that the parathyroid is so used to overproducing PTH due to the chronically low Ca that it ends up starting to produce PTH even when Ca normalises.
lab finding differences between primary secondary and tertiary hyperparathyroidism
primary and tertiary: high PTH, high Ca difference is CKD usually in tertiary and low vit d potentially
secondary: high pth low calcium and low vit d
associated conditions with primary parathyroidism
MEN
and hypertension
xray findings in primary hyperparahtyroidism
pepperpot skull
osteitis fibrosa cystica
treatment of primary hyperparathyroidism
definitive treatment is with total parathyroidectomy
conservative management if 1) calcium only 0.25 mmol above normal range 2) >50 yo 3) no evidence of end organ damage
non surgical treatment option for patience not suitable for surgery with primary hyperparahtyroidism
cinacalcet, a calcimimetic
‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor
diagnosis of type 2 diabetes
if with glucose:
symptomatic and fasting > 7 and random > 11 and if asymptomatic this needs to be in 2 separate occasions
if with HBA1C > 48 is diagnostic but needs to be done twice if asymptomatic!!!!
what is Impaired fasting glucose and what to do about it
when fasting glucose is 6.2-7 and you do a glucose challenge which needs to be <11 for no diabetes confirmation
first line management of diabetes
metformin ONLY
and you need SGLT-1 as well if CVD OR RISK OF CVD OR HF but start the sglt2 after theyre established on metformin
targets of hba1c with diabetes
48 if on lifestyle or lifestyle+ metformin and 53 if on a drug that may cause hypoglycaemia such as sulfonyluria
what to do if patient is not meeting the target and hba1c <58
you increase metformin from two to 3 times daily and stronger lifestyle factors
when do you need to add a second drug?
if hba1c> 58
what drugs can you add as second line?
DPP-4 inhibitor
pioglitazone
sulfonylurea
if patient doesnt achieve control in 2 drugs?
metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
insulin-based treatment
what if triple therapy not enough?
If triple therapy is not effective or tolerated consider switching one of the drugs for a GLP-1 mimetic:
BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
GLP-1 mimetics should only be added to insulin under specialist care
advice on starting insulin for t2d?
metformin should be continued. In terms of other drugs NICE advice: ‘Review the continued need for other blood glucose-lowering therapies’
NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need
diabetic neuropathy PRESentations
loss of sensation and neuropathic painnn (pins and needles, shock-like pain) in a glove and stocking distribution, not loss of movement
GI autonomic neuropathy: gastroparesis, chronic diarrhoea, GORD
treatment of diabetic neuropathic pain first and second line
same as other neuropathic pain, one of: amitriptyline (TCA), gabapentin, pregabalin (ANTIEPILEPTICS), duloxetine (snri) ,
second line: adding another one from that list
pain management clinic for severe
LOcal neuropathic pain management eg after herpes infection
local capsaicin
acute neuralgia/ exacerbation treatment
tramadol
presentation/ pathophysio of gastroparesis
basically hypomotility of GI tract, leads to
1) erratic control of blood glucose (bc it moves weirdly so absorption can be delayed: big drop glu and then when it suddenly empties: spike in glu)
2) vomiting, bloating
treatment of gastroparesis
prokinetic agents eg. metoclopramide, erythromycin, domperidone
GORD pathophysiology in diabetic autonomic neuropathy
reduced lower oesophageal sphincter pressure
diabetic nephropathy presentation
lke CKD a bit, proteinuria, hypertension, progressive decline in GFR and can lead to ESRF (end stage renal failure)
screening for diabetic nephropathy
annual screening, ACR measured- MORNING (first wee) measurement
pathophysiology of diabetic nephropathy
hyperglycaemia induced damage to renal microvasculature: glomeruloscleritis, tubulointerstitial fibrosis
management of diabetic nephropathy
very good glycemic control, antihypertensives keep bp under 130/80 ACEi or ARB if ACEi >3
low protein intake
dyslipidaemic control: statins
