data interpretation Flashcards
Causes of microcytic (low MCV) anaemia
- Iron deficiency anaemia
- Thalaseamia
- Sideroblastic anaemia
Causes of normocytic (normal MCV) anaemia
- **Anaemia of chronic disease
- acute blood loss**
- haemolytic haemia
- renal failure (chronic)
Causes of macrocytic (high MCV) anaemia
- **B12/folate deficiency
- Excess alcohol
- liver disease**
- hypothyroidism
- haematological diseases beginning with ‘M”: myeloproliferative, myelodyspastic and multiple myeloma
causes of hypokalaemia
DIRE:
* drugs (loop and thiazide diuretics)
* Inadequate intake or intestinal loss (diarrhoea or vomiting)
* renal tubular acidosis
* Endocrine (Cushings and Conns syndromes)
Causes of hyperkalaemia
DREAD:
* Drugs (potassium sparing diuretics and ACEi)
* Renal failure
* Endocrine (addisons)
* Artefact (due to clotted sample)
* DKA
causes of hypernatraemia
causes all begin with ‘d’:
* dehydration
* drips (i.e. too much IV saline)
* drugs (e.g. effervescent tablet preparations or intravenous preparations with a high sodium content)
* diabetes insipidus (which is effectively the opposite of syndrome of inappropriate antidiuretic hormone (SIADH).
High neutrophils causes
- Bacterial infection
- tissue damage (inflammation/infarct/malignancy)
- steroids
low neutrophils causes
- viral infection
- chemotherapy or radiotherapy
- Clozapine (antipsychotic)
- Carbimazole (antithyroid)
high lymphocytes
- viral infection
- lymphoma
- chronic lymphocytic leukaemia
causes of low platelets (thrombocytopenia)
Reduced production:
* infection (usually viral)
* drugs (esp. penicillamine (e.g. in rheumatoid arthritis treatment))
* myelodysplasia, myelofibrosis, myeloma
Increased destruction:
* heparin
* hypersplenism
* disseminated intravascular coagulation (DIC)
* idiopathic thrombocytopenic purpura (ITP)
* haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura
causes of high platelets (thrombocytosis)
Reactive:
* bleeding
* tissue damage (infection/inflammation/malignancy)
* postsplenectomy
Primary:
* myeloproliferative disorders
Causes of hyponatraemia
Fluid status:
Hypovolaemic
* Fluid loss (especially diarrhoea/vomiting)
* Addisons disease
* Diuretics
Euvolaemia
* SIADH
* Psychogenic polydipsia
* hypothyroidism
Hypovolaemic
* Heart failure
* Renal failure
* Liver failure
* Nutritional failure
* thryoid failure
raised urea indicated
AKI or upper GI haemorrhage (normal creatinine in the latter)
Biocehmical disturbance in prerenal AKI (70%)
Urea rise»_space;creatinine rise,
e.g.: Urea 19 (3–7.5 mmol/L), Creatinine 110 (35–125 μmol/L)
Causes of pre-renal AKI
Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
Renal artery stenosis (RAS)
biocehmical abnormalities in intrinsic renal AKI
Urea rise «creatinine rise, bladder or hydronephrosis not palpable,
e.g.: Urea 9 (3–7.5 mmol/L) Creatinine 342 (35–125 μmol/L)
causes of intrinsic AKI (10%)
INTRINSIC:
* Ischaemia (due to prerenal AKI, causing acute tubular necrosis)
* Nephrotoxic antibiotics ∗∗
* Tablets (ACEI, NSAIDs)
* Radiological contrast
* Injury (rhabdomyolysis)
* Negatively birefringent crystals (gout)
* Syndromes (glomerulonephridites)
* Inflammation (vasculitis)
* Cholesterol emboli
nephrotoxic antibiotics
gentamicin, vancomycin and tetracyclines
biochemical abnormalities in postrenal AKI (20%)
Urea rise «creatinine rise, bladder or hydronephrosis may be palpable depending on level of obstruction,
e.g.: Urea 9 (3–7.5 mmol/L) Creatinine 342 (35–125 μmol/L)
causes of postrenal AKI
In lumen: stone or sloughed papilla
In wall: tumour (renal cell, transitional cell), fibrosis
External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm
Causes of raised ALP
A raised alk phos does not necessarily indicate posthepatic jaundice; common causes may be remembered using the mnemonic ALKPHOS:
* Any fracture
* Liver damage (posthepatic)
* K (for kancer)
* Paget’s disease of bone and Pregnancy
* Hyperparathyroidism
* Osteomalacia
* Surgery.
pattern of LFT derangement in prehepatic
increased bilirubin, normal AST/ALT
prehepatic causes
- Haemolysis
- Gilberts and Crigler-Najjar syndromes
pattern of LFT derangement in intrahepatic
- increased bilirubin
- increased AST/ALT
Causes of intrahepatic
- Fatty liver
- Hepatitis ∗
- Cirrhosis ∗
- Malignancy (primary or secondary)
- Metabolic: Wilson’s disease/haemochromatosis
- Heart failure (causing hepatic congestion)
LFT derangement in posthepatic
- increased bilirubin
- increased ALP
- normal AST/ALT
Causes of posthepatic
In lumen: stone (gallstone),drugs causing cholestasis ∗∗
In wall: tumour (cholangiocarcinoma), primary biliary cirrhosis, sclerosing cholangitis
Extrinsic pressure: pancreatic or gastric cancer, lymph node
primary hypothyroidism TFTs
- T4 decreased
- TSH increased
causes of primary hypothyroidism
- hashimotos
- drug induced
TFTs in secondary hypothyroisism
- decreased t4
- decreased TSH
causes
causes of secondary hypothyroidism
pituitary tumour or damage
primary hyperthyroidism TFTs
- high t4
- low tsh
causes of primary hyperthyroisism
- graves disease
- toxic nodular goiter
- drug induced
secondary hyperthyroidism TFTs
- high 4
- high tsh
causes secondary hyperthyroidism
pituitary tumour
change in levothyroxine dose following TFT results
Quality of Xray film
It is important to check that the film is PRIM:
* Projection (e.g. posterioanterior (PA) (normally) or anterioposterior (AP). If AP, the heart will appear larger. If no label, then it is PA).
* Rotation (e.g. if distance between spinous process and clavicles is equal, then no rotation).
* Inspiration (e.g. if the seventh anterior (down-sloping) rib transects the diaphragm, then adequate).
* Markings (if additional markings, e.g. ‘red mark’, then the radiographer has spotted an abnormality).
when interpreting a CXR what are the main structures to be considered
- Heart, which should be less than 50% of the width of the lungs (in PA film); if more, then cardiomegaly should be considered.∗
- Lungs, where, if a white area is present, then effusion (seen as unilateral and solid), pneumonia (seen as unilateral and fluffy), oedema (seen as bilateral and fluffy∗), or fibrosis (seen as bilateral and honeycomb) should be considered.
- Trachea, which should be central and if not, consider collapse (i.e. towards affected side) or pneumothorax (i.e. away from affected side).
- Mediastinum, which if widened, consider right upper lobe collapse (with tracheal deviation) or aortic dissection (without tracheal deviation).
- Bones, where it is important to look for rib fractures or lytic lesions (i.e. usually suggesting metastases).
- Are the costophrenic angles sharp? If not then this suggests pleural effusion(s).∗
- Is there air under the right hemidiaphragm? This suggests bowel perforation or recent surgery. Under the left side is the gastric air bubble (which is normal).
- Is there a triangle behind the heart (i.e. sail sign)? This suggests left lower lobe collapse.
- Are the apices clear? If not, consider tuberculosis or an apical tumour.
signs of heart failure on CXR
ABCDE signs of pulmonary oedema:
* Alveolar oedema (bat wings)
* Kerley B lines (interstitial oedema)
* Cardiomegaly
* Diversion of blood to upper lobes (where vessels in upper zone are larger than in lower zone),
* pleural Effusions.
causes of respiratory alkalosis
rapid breathing
causes of respiratoey acidosis
t2rf
causes of metabolic alkalosis
vomiting, diuretics, conns syndrome
causes of metabolic acoidosis
lactic acidosis
DKA
renal failure
diarrhoea
ethanol intoxication
Left or Right BBB?
WiLLiaM MaRRoW
Elevated ST segment ECG causes
- infarction (ST segment flat and only raised in some leads), or
- pericarditis (ST segment convex and raised in all leads).
ST segment depression causes ECG
- ischaemia or infarction check troponin to distinguish (ST segment flat and only depressed in some leads);
- digoxin treatment (ST segment down-sloping in all leads).
tall tented T wave
Height: if more than two-thirds of the QRS height throughout the ECG then hyperkalaemia is likely present.
T wave inversion
normal in aVR and I (top middle two) leads; in other leads suggests old infarction/LVH.
drugs with narrow therapeutic index
- digoxin
- theophyline
- lithium
- phenytoin
- gentamicin
- vancomycin
Signs of digoxin toxicity
Confusion, nausea, visual halos, and arrhythmias
signs of lithium toxicity
Early: tremor
Intermediate: tiredness
Late: arrhythmias, seizures, coma, renal failure and diabetes insipidus
Signs of phenytoin toxicity
gum hypertrophy
ataxia
nystagmus
peripheral neuropathy
teratogenicity
gentamicin toxicity
ototoxicity
nephrotoxicity
vancomycin toxicity
ototoxicity and nephrotoxicity
Target INR on warfarin
2.5 unless recurrent thromboembolism then 3.5
management of warfaring INR 5-8 or >8
management of hyperkalaemia
“Dependent on K level, symptoms and ECG (see diagram):
* insulin and dextrose infusion (in moderate-severe hyperkalaemia) - drives carbohydrates into cells and takes K with it
* IV calcium gluconate (in severe kyperkalaemia or with ECG changes) - stabilises cardiac muscle cells
Other options:
* nebulised salbutamol - temporarily drives K into cells
* IV fluids - increases fluid output, which encourages K loss
* oral calcium resonium - draws K out of the gut and into stools (works slow)
* sodium bicarbonate - drives K into cells
* loop diuretics
* dialysis
Further management:
* stop exacerbating drugs e.g. ACEi
* treat underlying cause “
