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finals > Gen Med > Flashcards

Gen Med Flashcards

1
Q

presentation of cushings

A

moon face, buffalo hump, facial plethora
striae, bruising and poor wound healing
increased central fat, muscle wasting of limbs (thin limbs)
diabetes, hypertension, hyperpigmentation

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2
Q

causes of cushings syndrome

A 
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

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3
Q

investogations fot cushings

A 
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)
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4
Q

management of cushings

A

surgical removal of source
(adrenalectomy, pituitary adenomectomy, removal of lung cancer)

medical
metyrapone and ketaconazole

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5
Q

presentation of adrenal insufficency

A

hyperpigmentation (mucosa, palmer creases, sun exposed areas)
hypertension, postural hypotension
wt loss, N&V, abdo pain

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6
Q

causes of adrenal insufficency

A 
primary = addisons, tuberculosis, congenital adrenal hyperplasia, cancer mets (lung, breast, lymphoma)
secondary = pituatary adenoma
tertiary = withdrawal of long term steroids
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7
Q

investigations of adrenal insufficency

A

low NA, high K
high renin, low aldosterone
high morning cortisol
short synACTHen test (high cortisol after rules out addisons)

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8
Q

symptoms of hypercalcaemia

A

confusion, depression, fatigue
constipation
kidney stones, polyuria
muscle weakness, bone pain/osteoporosis

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9
Q

symptoms of hypocalcaemia

A

tetany, cramps, parathesia, convulsion

prolonged QT

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10
Q

causes of hypercalcaemia

A

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)

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11
Q

management of hypercalcaemia

A

IV fluids
furosemide
bisphophanates
calcitonin

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12
Q

MEN

A

type 1 = hyperparathyroidism, pancreatic tumour, pituitary tumour
type 2a = medullary thyroid cancer, pheochromocytoma, hyperparathyroidism
type 2b = medullary thyroid cancer, pheochromocytoma

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13
Q

management of DI

A 
central = desmopressin
nephrogenic = thiazide
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14
Q

AML

A

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)

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15
Q

CML

A 
Phildelphia chromosome (translocation of chromosome 9:22)
Results in fusion gene BCR/ABL – dysregulates haematopoiesis via tyrosine kinase
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16
Q

ALL

A

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

17
Q

CLL

A

malignant clonal disorder of B cells involving the bone marrow and peripheral blood
may infiltrate lymphatic tissue, spleen, liver

18
Q

blood films of leukaemias

A

AML - blast cells > 20% of cells and Auer rods
CML - mature myeloid cells with raised eos and baso
ALL - leukocyte lymphoblasts
CLL - B lymphocytes

19
Q

FBC of leukaemias

A

AML - pancytopenia
CML - raised WCC, anaemia
ALL - raised lymphoblasts
CLL - clonal B lymphocytes > 5x10^9

20
Q

management of TB

A 
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

21
Q

nephritic and nephrotic syndrome

A

nephrotic (membranous, minimal change, FSG)
protienuria, oedema, hypoalbuminaemia

nephritic (IgA, post infection, RPGN)
haematuria, hypertension, oliguria

22
Q

IgA nephropathy

A

nephritic syndrome, may progress to ESRF
24-48hrs after URTI
deposition of IgA in mesangial cells
steroids

23
Q

post infection GN

A

nephritic
strep pyogenes - 4weeks after URTI
IC deposits in mesangium -> complement actvation and destruction of glomerular cells -> RPGN
supportive +/- Abx

24
Q

membranous GN

A 
nephrotic
most common in adults
IC deposits -> complement activation against BM protiens -> GBM thickening
rule of 1/3
steroids
25
Q

minimal change GN

A 
nephrotic
most common in children
T cell mediated, C3 and IgM deposits
electromicroscopy = podocyte foot process fusion
steroids
26
Q

RPGN

A

nephritic -> can rapidly develop into ESRF
crescent on biopsy
causes = post infection, anti GBM, SLE, wegeners
steroids

27
Q

Focal segmental glomerulosclerosis

A

nephritic or nephrotic
caused by reflux, vasculitis, Alports
biopsy = segmental scarring, IgM and complement deposits
steroids

finals (13 decks)

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