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PSA > Data Interpretation > Flashcards

Data Interpretation Flashcards

1
Q

What are the causes of microcytic anaemia?

A

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

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2
Q

What are the cause of hypovolaemic hyponatraemia?

A

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

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3
Q

What are the cause of euvolaemic hyponatraemia?

A

SIADH, Psychogenic polydipsia, Hypothyroidism

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4
Q

What are the causes of SIADH?

A

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

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5
Q

What are the causes of normocytic anaemia?

A

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

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6
Q

What are the causes of macrocytic anaemia?

A

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

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7
Q

What are the causes of hypernatraemia?

A

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

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8
Q

What causes hypervolaemic hyponatraemia

A

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

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9
Q

Which drugs can cause neutropenia?

A

Carbimazole (anti-thyroid), Clozapine (antipsychotic)

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10
Q

What causes thrombocytopenia due to reduced destruction?

A

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

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11
Q

What causes thrombocytopenia due to increased destruction?

A

Heparin, hypersplenism, DIC, ITP, HUS

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12
Q

What causes thrombocytosis?

A

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

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13
Q

What causes hypokalaemia?

A

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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14
Q

What causes hyperkalaemia?

A 
DREAD 
Drugs: potassium sparing diuretics and ACE inhibitors
Renal failure 
Endocrine: Addison's disease 
Artefact: clotted sample 
DKA
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15
Q

What can cause increased urea?

A

AKI and GI Bleed

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16
Q

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

A

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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17
Q

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

A

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

18
Q

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

A

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

19
Q

What are the common causes of a raised alk phosphate?

A

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

20
Q

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

A

High bilirubin.

Due to haemolysis or Gilbert’s syndrome

21
Q

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

A

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.

22
Q

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

A

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

23
Q

What are the biochemical changes and causes of primary hypothyroidism?

A

Low T4, High TSH.

Hashimoto’s thyroiditis, drug induced hypothyroidism

24
Q

What are the biochemical changes and causes of secondary hypothyroidism?

A

Low T4, low TSH

Pituitary tumour or damage

25
Q

What are the biochemical changes and causes of primary hyperthyroidism?

A

High T4, Low TSH.

Grave’s disease, toxic nodular goiter, drug-induced hyperthyroidism

26
Q

What are the biochemical changes and causes of secondary hyperthyroidism?

A

High T4, High TSH

Pituitary tumour

27
Q

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

A 
RIPE:
Rotation
Inspiration - 5-6 anterior ribs
Projection - PA or AP?
Exposure - left hemidiaphragm visible to the spine and vertebrae visible behind heart
28
Q

How do you interpret a CXR?

A

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

29
Q

What are the features of pulmonary oedema on CXR?

A 
ABCDE 
Alveolar oedema - bat wings
Kerley B lines - interstitial oedema 
Cardiomegaly 
Diversion of blood to upper lobes - vessels larger in upper zone
pleural Effusions
30
Q

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

A

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

31
Q

How do you interpret an ECG?

A 
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
32
Q

How would you recognise QRS complex deflections?

A

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

33
Q

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

A

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

34
Q

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

A

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

35
Q

What are the features of digoxin toxicity?

A

Confusion, nausea, visual halos, arrhythmias

36
Q

What are the features of lithium toxicity?

A

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

37
Q

What are the features of phenytoin toxicity?

A

Gum hypertrophy, ataxia, nystagmus, peripheral neuropathy, teratogenicity

38
Q

What are the features of gentamicin and vancomicin toxicity?

A

Ototoxicity and nephrotoxicity.

39
Q

How do you manage over anticoagulation from warfarin?

A

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.

40
Q

What are the antiobiotics of choice for neutropenic sepsis?

A

IV PipTaz (PENICILLIN) and IV gentamicin

41
Q

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

A

IV 40-80mg Furosemide

PSA (2 decks)

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