Category Archives: LECTURE


to understand the pathophysiology of diseases , first and foremost , we need to study the normal .

vit d metabolism

so simply:
vit d is carried ( by albumin and proteun carriers) to the liver–> inactive form

then to the kidneys where it is transformed into the active form by wn enzyme here.

PTH increase the production of the actve form of vitamin d(calcitriol) by forming the enzyme required for that transformation(25(OH)vitamin D-1α-hydroxylase).

calcitriol will in turn increase absorption of calcium from the small intestine.

other actions of PTH:
increase Ca reabsorption
increase RESORPTION FROM BONES(get out of the bones calcium!!)
increase phosphate excretion


pssst!!! in renal failure there is lack of prodcution of calcitriol!!! alert: HYPOCALCEMIA, which may be corrected by 2ry hyperparathyroidism




you know whats primary(tumours) and secondary( physiological response to hypocalcemia) .
but what about tertiary??

it is the development of autonomous(doesnt respect the feedback mechanism and keeps secreting PTH) parathyroid hyperplasia AFTER LONG STANDING 2RY HYPERPARWTHYROIDISM( most often in renal failure.

clinical manifestation? —– of hypercalcemia
proximal myopathy
band keratopathy

why is there an increase in urinary cAMP in primary hyperparathyroidism?



important points

The posterior pituitary does not produce its own hormones. rather, hornones are stored here(oxytocin and vasopressin) .they are produced by the hypothalamus.

pituitary function is assessed by the target gland function, not by measuring the pituitary hormone as an isolated event. This is in contrast to target gland function being assessed by the pituitary hormone

kallmans syndrome is isolated decrease in GnRH + anosmia

in pregnancy pituitary gland is enlarged. when postpartum hge happens this leads to ischemic pituitary necrosis.SHEEHAN’S SYNDROME


Adrenocorticotropic hormone, as its name implies, stimulates the adrenal cortex. More specifically, it stimulates secretion of glucocorticoids such as cortisol, and has little control over secretion of aldosterone, the other major steroid hormone from the adrenal cortex.

i always forget this!!!!!!


low blood glucose stimulates production of growth hormones!!! hence insulin stimulation test causes increase GH IN NORMAL PPL AND GH IS NOT ELEVATED IN THIS CASE!! in hypopituitarism that iss…


ACTH is produced in a process that also generates several other hormones

The major attributes of the hormones other than ACTH that are produced in this process are summarized as follows:

Lipotropin: Originally described as having weak lipolytic effects, its major importance is as the precursor to beta-endorphin.

Beta-endorphin and Met-enkephalin: Opioid peptides with pain-alleviation and euphoric effects.(SUBHANALLAH.ALLAH CREATED INNER PAIN RELIEVERS FOR US HUMANS! syukurillah)

Melanocyte-stimulating hormone (MSH): Known to control melanin pigmentation in the skin of most vertebrates.(take note!!!!! in absence of acth, this process is diminished thus DEPIGMENTATION OCCURS IN ARESS NORMALLY PIGMENTED eg; areola)

psssst: kontot notes. will be updated in the future. OSCE ALARM: 3 MORE DAYS IM RUNNING OUT OF TIME STOP PROCRASTINATING.

lillahitaala! itqan fil ‘amal

for the pleasure of my eyes:

normal mri of pituitary gland. oh my cute lil pituitary looking like an edible M&m.



empty sella synd.


and here

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important notes:
there is no definite numbers. it simply means low blood glucose level or relatively low.
in hypolycemia unawareness, its vital to treat them early because they go into coma faster!

what leads to hypoglycemia?
low levels of counterregulatory hormones
low source of glucose
hi insulin

renal impariment leads of hindered degradation of insulin hence decreasing requirements of insulin intake in diabetic patient! ( esp since they may have DM Nephropathy)

females. have overactive parasympathetic flow hence they are more liable to early postprandial hypoglycemia.

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