Data Interpretation Flashcards by Ade Ned

What are the causes of microcytic anaemia?

(low MCV): iron deficiency anaemia. thalassaemia, sideroblastic aenamia

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What are the cause of hypovolaemic hyponatraemia?

Fluid loss (D&V), Addison’s disease, Diuretics

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What are the cause of euvolaemic hyponatraemia?

SIADH, Psychogenic polydipsia, Hypothyroidism

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What are the causes of SIADH?

Small cell lung carcinoma, Infection, Abscess, Drugs (carbamezapine, antipsychotics) and Head Injury

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What are the causes of normocytic anaemia?

(normal MCV): anaemia of chronic disease, acute blood loss, haemolytic anaemia, chronic renal failure

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What are the causes of macrocytic anaemia?

(high MCV): b12 or folate deficiency, excess alcohol, liver disease, hypothyroidism, haematological disease beginning with ‘M’ myeloproliferative, multiple myeloma, myelodysplastic

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What are the causes of hypernatraemia?

Dehydration, Drips ( too much IV saline), Drugs ( effervescent preparations and IV preps with high sodium), diabetes insipidus

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What causes hypervolaemic hyponatraemia

Heart failure, renal failure, liver failure, nutritional failure, thyroid failure

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Which drugs can cause neutropenia?

Carbimazole (anti-thyroid), Clozapine (antipsychotic)

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What causes thrombocytopenia due to reduced destruction?

Infection, drugs (penicillamine), myelodysplasia, myelofibrosis, myeloma

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What causes thrombocytopenia due to increased destruction?

Heparin, hypersplenism, DIC, ITP, HUS

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What causes thrombocytosis?

Reactive is due to bleeding, tissue damage (infection, inflammation, malignancy), post-splenectomy. Primary occurs due to myeloproliferative disorders.

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What causes hypokalaemia?

DIRE
Drugs: loop diuretics, thiazide diuretics,
Inadequate intake or intestinal loss (diarrhoea/vomiting)
Renal tubular acidosis
Endocrine: Cushing’s and Conn’s syndrome

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What causes hyperkalaemia?

DREAD 
Drugs: potassium sparing diuretics and ACE inhibitors
Renal failure 
Endocrine: Addison's disease 
Artefact: clotted sample 
DKA

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What can cause increased urea?

AKI and GI Bleed

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What is the biochemical disturbance is seen in pre-renal AKI? What percentage of AKIs is pre-renal? What causes it?

Urea rise more than a creatinine rise. 70%. Dehydration of any cause or renal artery stenosis (can be triggered by ACEI and NSAID).

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What is the biochemical disturbance is seen in renal AKI? What percentage of AKIs is renal? What causes it?

Urea rise less than creatinine rise. 10%. INTRINSIC. Ischaemia due to AKI and therefore acute tubular necrosis. Nephrotoxic antibiotics (gentamicin, vancomycin, tetracycline), Radiological contrast, Injury (rhabdomyolysis_, Negatively bifringent crystals (gout), Syndromes (glomerulonephridites), Inflammation (vasculitis), Cholesterol emboli

What is the biochemical disturbance is seen in post-renal AKI? What percentage of AKIs is post-renal? What causes it?

Urea rise less than creatinine rise. 20%.
In lumen: stone, sloughed papilla
In wall: renal cell carcinoma, transitional cell carcinoma, fibrosis
External pressure: BPH, Prostate cancer, lymphadenopathy, aneurysm

What are the common causes of a raised alk phosphate?

ALKPPHOS
Any fracture, Liver damage (posthepatic), K for kancer, Paget’s disease, Pregnancy, Hyperparathyroidism, Osteomalacia, Surgery

What is the pattern of PRE-HEPATIC LFT derangement and what are the causes?

High bilirubin.

Due to haemolysis or Gilbert’s syndrome

What is the pattern of INTRA-HEPATIC LFT derangement and what are the causes?

High bilirubin and AST/ALT (T for tissue therefore hepatic).
Fatty liver
Hepatitis and Cirrhosis due to alcohol, viruses (Hep A-E, CMV, EBV) and drugs (paracetamol, statins, rifampicin)
Malignancy
Metabolic (wilson’s disease, haemochromatosis)
Heart failure, leading to hepatic congestion.

What is the pattern of POST-HEPATIC LFT derangement and what are the causes?

High bilirubin and ALP
In lumen: gallstone, drugs causing cholestasis (flucloxacillin, coamoxiclav, nitrifurantoin, steroids, sulphonylureas)
In wall: cholangiocarcinoma, PBC, Sclerosing cholangitis
Extrinsic pressure: pancreatic and gastric cancer, lymph node

What are the biochemical changes and causes of primary hypothyroidism?

Low T4, High TSH.

Hashimoto’s thyroiditis, drug induced hypothyroidism

What are the biochemical changes and causes of secondary hypothyroidism?

Low T4, low TSH

Pituitary tumour or damage

What are the biochemical changes and causes of primary hyperthyroidism?

High T4, Low TSH. | Grave's disease, toxic nodular goiter, drug-induced hyperthyroidism

What are the biochemical changes and causes of secondary hyperthyroidism?

High T4, High TSH | Pituitary tumour

How do you assess the quality of film of an CXR?

``` RIPE: Rotation Inspiration - 5-6 anterior ribs Projection - PA or AP? Exposure - left hemidiaphragm visible to the spine and vertebrae visible behind heart ```

How do you interpret a CXR?

ABCDE Airway - trachea, bronchi, hilar structures Breathing - lungs, pleura Cardiac - heart size, heart borders, Diaphragm - assess the diaphragm, costophrenic angles, Everything else - aortic knuckle, aortic-pulmonary window, bones, soft tissue, tubes, valves, pacemakers

What are the features of pulmonary oedema on CXR?

``` ABCDE Alveolar oedema - bat wings Kerley B lines - interstitial oedema Cardiomegaly Diversion of blood to upper lobes - vessels larger in upper zone pleural Effusions ```

How do you recognise type 1 and type 2 respiratory failure on ABG?

Type 1: low or normal PaCO2, with fast or normal breathing | Type 2: high PaCO2, slow and shallow breathing, this is for blue bloaters of COPD or neuromuscular failure

How do you interpret an ECG?

``` Rate: 300 divided by number of large squares between QRS Rhythm: regular or irregular Right and Left Axis Deviation P waves P-R intervals QRS complex ST Segment T waves ```

How would you recognise QRS complex deflections?

WiLLiaM MaRRoW W in 1st deflection of QRS in V1, LL BBB, M in 1st deflection of QRS in V6 M in 1st deflection of QRS in V1, RR BBB, W in 1st deflection of QRS in V6

What kind of drugs usually need monitoring? Which drugs are most commonly monitored?

Those with a narrow therapeutic index. Digoxin, phenytoin, lithium, theophylline, gentamicin, vancomycin.

What action do you take if gentamicin is above the therapeutic range?

Decrease in frequency by 12hours rather than reducing the dose. I.e. from 24 hours to 36 hours.

What are the features of digoxin toxicity?

Confusion, nausea, visual halos, arrhythmias

What are the features of lithium toxicity?

Early - tremor. Intermediate - tiredness. Late - arrhythmias, seizures, coma, renal failure, diabetes insipidus.

What are the features of phenytoin toxicity?

Gum hypertrophy, ataxia, nystagmus, peripheral neuropathy, teratogenicity

What are the features of gentamicin and vancomicin toxicity?

Ototoxicity and nephrotoxicity.

How do you manage over anticoagulation from warfarin?

INR <6, reduce warfarin dose. INR 6-8, omit warfarin for 2 days and reduce dose, INR >8 omit warfarin and give 1-5 mg oral vitamin K. If minor bleeding with INR >5 then give IV vit K. If major bleed, then stop warfarin, 5-10 mg IV vit K and prothrombin complex Beriplex.

What are the antiobiotics of choice for neutropenic sepsis?

IV PipTaz (PENICILLIN) and IV gentamicin

Whats the dose and route for furosemide in acute heart failure?

IV 40-80mg Furosemide