data interpretation Flashcards

1
Q

Causes of microcytic (low MCV) anaemia

A
  • Iron deficiency anaemia
  • Thalaseamia
  • Sideroblastic anaemia
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2
Q

Causes of normocytic (normal MCV) anaemia

A
  • **Anaemia of chronic disease
  • acute blood loss**
  • haemolytic haemia
  • renal failure (chronic)
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3
Q

Causes of macrocytic (high MCV) anaemia

A
  • **B12/folate deficiency
  • Excess alcohol
  • liver disease**
  • hypothyroidism
  • haematological diseases beginning with ‘M”: myeloproliferative, myelodyspastic and multiple myeloma
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4
Q

causes of hypokalaemia

A

DIRE:
* drugs (loop and thiazide diuretics)
* Inadequate intake or intestinal loss (diarrhoea or vomiting)
* renal tubular acidosis
* Endocrine (Cushings and Conns syndromes)

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5
Q

Causes of hyperkalaemia

A

DREAD:
* Drugs (potassium sparing diuretics and ACEi)
* Renal failure
* Endocrine (addisons)
* Artefact (due to clotted sample)
* DKA

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6
Q

causes of hypernatraemia

A

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).

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7
Q

High neutrophils causes

A
  • Bacterial infection
  • tissue damage (inflammation/infarct/malignancy)
  • steroids
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8
Q

low neutrophils causes

A
  • viral infection
  • chemotherapy or radiotherapy
  • Clozapine (antipsychotic)
  • Carbimazole (antithyroid)
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9
Q

high lymphocytes

A
  • viral infection
  • lymphoma
  • chronic lymphocytic leukaemia
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10
Q

causes of low platelets (thrombocytopenia)

A

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

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11
Q

causes of high platelets (thrombocytosis)

A

Reactive:
* bleeding
* tissue damage (infection/inflammation/malignancy)
* postsplenectomy

Primary:
* myeloproliferative disorders

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12
Q

Causes of hyponatraemia

A

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

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13
Q

raised urea indicated

A

AKI or upper GI haemorrhage (normal creatinine in the latter)

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14
Q

Biocehmical disturbance in prerenal AKI (70%)

A

Urea rise&raquo_space;creatinine rise,
e.g.: Urea 19 (3–7.5 mmol/L), Creatinine 110 (35–125 μmol/L)

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15
Q

Causes of pre-renal AKI

A

Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
Renal artery stenosis (RAS)

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16
Q

biocehmical abnormalities in intrinsic renal AKI

A

Urea rise «creatinine rise, bladder or hydronephrosis not palpable,
e.g.: Urea 9 (3–7.5 mmol/L) Creatinine 342 (35–125 μmol/L)

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17
Q

causes of intrinsic AKI (10%)

A

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

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18
Q

nephrotoxic antibiotics

A

gentamicin, vancomycin and tetracyclines

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19
Q

biochemical abnormalities in postrenal AKI (20%)

A

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)

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20
Q

causes of postrenal AKI

A

In lumen: stone or sloughed papilla

In wall: tumour (renal cell, transitional cell), fibrosis

External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm

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21
Q

Causes of raised ALP

A

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.

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22
Q

pattern of LFT derangement in prehepatic

A

increased bilirubin, normal AST/ALT

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23
Q

prehepatic causes

A
  • Haemolysis
  • Gilberts and Crigler-Najjar syndromes
24
Q

pattern of LFT derangement in intrahepatic

A
  • increased bilirubin
  • increased AST/ALT
25
Q

Causes of intrahepatic

A
  • Fatty liver
  • Hepatitis ∗
  • Cirrhosis ∗
  • Malignancy (primary or secondary)
  • Metabolic: Wilson’s disease/haemochromatosis
  • Heart failure (causing hepatic congestion)
26
Q

LFT derangement in posthepatic

A
  • increased bilirubin
  • increased ALP
  • normal AST/ALT
27
Q

Causes of posthepatic

A

In lumen: stone (gallstone),drugs causing cholestasis ∗∗

In wall: tumour (cholangiocarcinoma), primary biliary cirrhosis, sclerosing cholangitis

Extrinsic pressure: pancreatic or gastric cancer, lymph node

28
Q

primary hypothyroidism TFTs

A
  • T4 decreased
  • TSH increased
29
Q

causes of primary hypothyroidism

A
  • hashimotos
  • drug induced
30
Q

TFTs in secondary hypothyroisism

A
  • decreased t4
  • decreased TSH
31
Q

causes

causes of secondary hypothyroidism

A

pituitary tumour or damage

32
Q

primary hyperthyroidism TFTs

A
  • high t4
  • low tsh
33
Q

causes of primary hyperthyroisism

A
  • graves disease
  • toxic nodular goiter
  • drug induced
34
Q

secondary hyperthyroidism TFTs

A
  • high 4
  • high tsh
35
Q

causes secondary hyperthyroidism

A

pituitary tumour

36
Q

change in levothyroxine dose following TFT results

A
37
Q

Quality of Xray film

A

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).

38
Q

when interpreting a CXR what are the main structures to be considered

A
  • 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.
39
Q

signs of heart failure on CXR

A

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.

40
Q

causes of respiratory alkalosis

A

rapid breathing

41
Q

causes of respiratoey acidosis

A

t2rf

42
Q

causes of metabolic alkalosis

A

vomiting, diuretics, conns syndrome

43
Q

causes of metabolic acoidosis

A

lactic acidosis
DKA
renal failure
diarrhoea
ethanol intoxication

44
Q

Left or Right BBB?

A

WiLLiaM MaRRoW

45
Q

Elevated ST segment ECG causes

A
  • infarction (ST segment flat and only raised in some leads), or
  • pericarditis (ST segment convex and raised in all leads).
46
Q

ST segment depression causes ECG

A
  • 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).
47
Q

tall tented T wave

A

Height: if more than two-thirds of the QRS height throughout the ECG then hyperkalaemia is likely present.

48
Q

T wave inversion

A

normal in aVR and I (top middle two) leads; in other leads suggests old infarction/LVH.

49
Q

drugs with narrow therapeutic index

A
  • digoxin
  • theophyline
  • lithium
  • phenytoin
  • gentamicin
  • vancomycin
50
Q

Signs of digoxin toxicity

A

Confusion, nausea, visual halos, and arrhythmias

51
Q

signs of lithium toxicity

A

Early: tremor
Intermediate: tiredness
Late: arrhythmias, seizures, coma, renal failure and diabetes insipidus

52
Q

Signs of phenytoin toxicity

A

gum hypertrophy
ataxia
nystagmus
peripheral neuropathy
teratogenicity

53
Q

gentamicin toxicity

A

ototoxicity
nephrotoxicity

54
Q

vancomycin toxicity

A

ototoxicity and nephrotoxicity

55
Q

Target INR on warfarin

A

2.5 unless recurrent thromboembolism then 3.5

56
Q

management of warfaring INR 5-8 or >8

A
57
Q

management of hyperkalaemia

A

“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 “