2021-10-02T06:44:34+03:00[Europe/Moscow] en true <p>pulmonary oedema - Ix</p>, <p>nipple discharge - ddx</p>, <p>duct ectasia</p>, <p>DCIS</p>, <p>intraductal papilloma</p>, <p>paget's disease (of breast)</p>, <p>bell's palsy</p>, <p>acute tubulointerstitial nephritis (ATIN)</p>, <p>acute tubular necrosis (ATN)</p> flashcards
Med

Med

  • pulmonary oedema - Ix

    investigations inc:

    - FBE

    - UECs

    - ABG/VBG

    - ECG (MI, arrhythmia)

    - Chest x-ray

    - Echocardiogram

  • nipple discharge - ddx

    - ductal ectasia

    - intraductal papilloma

    - breast ca (rarely)

    (incr prolactin --> inc breastfeeding, pituitary adenoma, dopamine antagonists)

  • duct ectasia

    caused by multiple ducts releasing green/yellow discharge, generally only on manipulation of the nipple.

  • DCIS

    more commonly incidental finding (routine screening in asymptomatic women)

    occasional presents with lump/blood nipple discharge

    DCIS always needs be excluded (even tho intraductal papilloma more common)

  • intraductal papilloma

    isolated bloody nipple discharge

  • paget's disease (of breast)

    presents as a change to nipple appearance (rather than discharge), such as ulceration, crusting or inversion

  • bell's palsy

    acute idiopathic peripheral facial nerve palsy

    usually self-resolves starting at 3weeks, can take up to 2months (if no signs of recovery by 6weeks = start Ix)

  • acute tubulointerstitial nephritis (ATIN)

    type IV hypersensitivity reaction

    often triggered by medx within days of commencing it (eg NSAIDs/sulpha drugs/penicillins)

    ssx - fever

    - maculopapular rash

    - flank pain

    - arthralgia

    can be asymptomatic

  • acute tubular necrosis (ATN)

    most common cause of AKI in hospital

    involves acute tubular necrosis includes renal tubular cell damage and death precipitated by an acute ischaemia/toxicity/sepsis

    --> intrarenal vasoconstriction or a direct effect of drug toxicity is caused by an ischemic event, nephrotoxic mechanism, or a mixture of both

    4 clinical stages

    - initiation (acute decr GFR + sudden incr creatinine)

    - extension (ongoing hypoxia following ischaemic event + inflammatory response)

    - maintenance (cell repair + blood flow returns to normal

    - recovery (maintenance continues with ongoing cellular differentiation + improving GFR)