Gen Med Flashcards
presentation of cushings
moon face, buffalo hump, facial plethora
striae, bruising and poor wound healing
increased central fat, muscle wasting of limbs (thin limbs)
diabetes, hypertension, hyperpigmentation
causes of cushings syndrome
ACTH dependent pituatary adenoma (cushings disease) ectopic ACTH (small cell lung cancer) ectopic CRH (thyroid carcinoma)
ACTH independent
adrenal adenoma, carcinoma, nodular hyperplasia
exogenous corticosteroid use
investogations fot cushings
late night salivary cortisol dex suppression test (give at night, measure in morning, unsuppressed = cushings) plasma ACTH (low -> adrenal CT, high -> pituitary MRI or CT CAP)
management of cushings
surgical removal of source
(adrenalectomy, pituitary adenomectomy, removal of lung cancer)
medical
metyrapone and ketaconazole
presentation of adrenal insufficency
hyperpigmentation (mucosa, palmer creases, sun exposed areas)
hypertension, postural hypotension
wt loss, N&V, abdo pain
causes of adrenal insufficency
primary = addisons, tuberculosis, congenital adrenal hyperplasia, cancer mets (lung, breast, lymphoma) secondary = pituatary adenoma tertiary = withdrawal of long term steroids
investigations of adrenal insufficency
low NA, high K
high renin, low aldosterone
high morning cortisol
short synACTHen test (high cortisol after rules out addisons)
symptoms of hypercalcaemia
confusion, depression, fatigue
constipation
kidney stones, polyuria
muscle weakness, bone pain/osteoporosis
symptoms of hypocalcaemia
tetany, cramps, parathesia, convulsion
prolonged QT
causes of hypercalcaemia
hyperparathyroidism (adenoma = PTH -> reabsorption from kidneys, osteoclast activity, gut absorption by increaseing 1, 25 DHCC)
malignancy (bone involvement - osteoclast activity, secretion of PTHrP or 1, 25 DHCC)
congenital (uninhibited secrtetion of PTH)
management of hypercalcaemia
IV fluids
furosemide
bisphophanates
calcitonin
MEN
type 1 = hyperparathyroidism, pancreatic tumour, pituitary tumour
type 2a = medullary thyroid cancer, pheochromocytoma, hyperparathyroidism
type 2b = medullary thyroid cancer, pheochromocytoma
management of DI
central = desmopressin nephrogenic = thiazide
AML
Clonal proliferation of myeloid blast cells in the bone marrow
These blast cells are unable to differentiate into RBCs, platelets, neutrophils and accumulate in the bone marrow resulting in bone marrow failure (i.e. neutropenia, thrombocytopenia, anaemia)
CML
Phildelphia chromosome (translocation of chromosome 9:22) Results in fusion gene BCR/ABL – dysregulates haematopoiesis via tyrosine kinase
ALL
Malignant clonal disorder in where lymphocyte progenitor is genetrically altered resulting in uncontrolled proliferation
This leads to infiltration into bone marrow preventing differentiation of other cells resulting in pancytopenia
CLL
malignant clonal disorder of B cells involving the bone marrow and peripheral blood
may infiltrate lymphatic tissue, spleen, liver
blood films of leukaemias
AML - blast cells > 20% of cells and Auer rods
CML - mature myeloid cells with raised eos and baso
ALL - leukocyte lymphoblasts
CLL - B lymphocytes
FBC of leukaemias
AML - pancytopenia
CML - raised WCC, anaemia
ALL - raised lymphoblasts
CLL - clonal B lymphocytes > 5x10^9
management of TB
Initial phase - first 2 months (RIPE) Rifampicin (red urine) Isoniazid (neuropathy, give prophylactic pydrodoxine) Pyrazinamide (gout) Ethambutol (optic neuritis)
Continuation phase - next 4 months
Rifampicin
Isoniazid
nephritic and nephrotic syndrome
nephrotic (membranous, minimal change, FSG)
protienuria, oedema, hypoalbuminaemia
nephritic (IgA, post infection, RPGN)
haematuria, hypertension, oliguria
IgA nephropathy
nephritic syndrome, may progress to ESRF
24-48hrs after URTI
deposition of IgA in mesangial cells
steroids
post infection GN
nephritic
strep pyogenes - 4weeks after URTI
IC deposits in mesangium -> complement actvation and destruction of glomerular cells -> RPGN
supportive +/- Abx
membranous GN
nephrotic most common in adults IC deposits -> complement activation against BM protiens -> GBM thickening rule of 1/3 steroids
minimal change GN
nephrotic most common in children T cell mediated, C3 and IgM deposits electromicroscopy = podocyte foot process fusion steroids
RPGN
nephritic -> can rapidly develop into ESRF
crescent on biopsy
causes = post infection, anti GBM, SLE, wegeners
steroids
Focal segmental glomerulosclerosis
nephritic or nephrotic
caused by reflux, vasculitis, Alports
biopsy = segmental scarring, IgM and complement deposits
steroids
