all begin with ‘d’: - dehydration - drips (i.e. too much IV saline) - drugs (e.g. effervescent tablet preparations or IV preparations with a high Na+ content) - diabetes insipidus (effectively opposite to SIADH)

DIRE - Drugs (loop + thiazide diuretics) - Inadequate intake/intestinal loss (D+V) - Renal tubular acidosis - Endocrine (Cushing’s + Conn’s syndromes)

DREAD - Drugs (K+ sparing diuretics and ACEi) - Renal failure - Endocrine (Addison’s) - Artefact (very common, due to clotted sample) - DKA (NB when insulin is given the K+ drops requiring regular (hourly) monitoring +/− replacement)

Data Interpretation Flashcards by Ailsa Bell

causes ↓ Na+?

↓ VOL
Fluid loss (D+V)
Addison’s disease
Diuretics (any)

✓ VOL
SIADH
Psychogenic polydipsia
Hypothyroidism

↑ VOL
HF
RF
LF (causing hypoalbuminaemia)
Nutritional failure (causing hypo-A-)
Thyroid failure (↓thyroidism; can be ✓volaemic too)

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causes SIADH

SIADH:

Small cell lung tumours
Infection
Abscess
Drugs (carbamazepine and antipsychotics) Head injury

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causes ↑ Na+?

all begin with ‘d’:

dehydration
drips (i.e. too much IV saline)
drugs (e.g. effervescent tablet preparations or IV preparations with a high Na+ content)
diabetes insipidus (effectively opposite to SIADH)

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causes anaemia with low MCV?

Iron deficiency anaemia
Thalassaemia
Sideroblastic anaemia

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causes anaemia with normal MCV?

Anaemia of chronic disease
Acute blood loss
Haemolytic anaemia
Renal failure (chronic)

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causes anaemia with high MCV?

B12/folate deficiency (‘megaloblastic anaemia’) (incl. pernicious anaemia B12)
Excess alcohol
Liver disease (including nonalcoholic causes)
Hypothyroidism
Haematological diseases beginning with ‘M’: 1) myeloproliferative
2) myelodysplastic
3) multiple myeloma

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causes ↓ K+?

DIRE

Drugs (loop + thiazide diuretics)
Inadequate intake/intestinal loss (D+V)
Renal tubular acidosis
Endocrine (Cushing’s + Conn’s syndromes)

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↑ K+?

DREAD

Drugs (K+ sparing diuretics and ACEi)
Renal failure
Endocrine (Addison’s)
Artefact (very common, due to clotted sample)
DKA (NB when insulin is given the K+ drops requiring regular (hourly) monitoring +/− replacement)

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causes ↑ neutrophils?

neutrophilia

Bacterial infection
Tissue damage (inflammation/infarct/ malignancy)
Steroids

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causes ↓ neutrophils?

neutropenia

Viral infection
Chemotherapy or radiotherapy*
Clozapine (antipsychotic)
Carbimazole (antithyroid)

*Patients undergoing chemo or radiotherapy may become neutropenic (or even pancytopenic) in response to infection (‘neutropenic sepsis’). This carries a much higher mortality rate so they must be given urgent IV broad-spectrum Abx (the choice is hospital specific).

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causes ↑ lymphocytes?

lymphocytosis

Viral infection
Lymphoma
CLL (chronic lymphocytic leukaemia)

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causes ↓ platelets?

thrombocytopenia

↓ production:

infection (viral)
drugs (PENICILLAMINE in RA)
the 3 myelo- s

↑ destruction:

HEPARIN
↑ splenism
DIC
ITP
HUS/TTP

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causes ↑ platelets?

thrombocytosis

reactive:

bleeding
tissue damage
post-splenectomy

primary:
- myelo- disorders

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causes prerenal AKI?

70%

Urea rise > creatinine rise

e.g.: Urea 19  (3–7.5 mmol/L)
Creatinine 110 (35–125 μmol/L)

Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss
Renal artery stenosis (AKI in RAS often triggered by ACEI or NSAIDs) and effectively causes ↓ perfusion of the kidneys and prerenal picture

Nb: the creatinine can rise with severe prerenal AKI; to differentiate this from intrinsic and obstructive AKI, multiply the urea by 10; if it exceeds the creatinine (showing a relatively greater increase in urea compared to creatinine) then this suggests a prerenal aetiology

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causes postrenal AKI?
(20%)
(obstructive)

Urea rise < creatinine rise

(Ex - bladder or hydronephrosis PALPABLE depending on level of obstruction)

e.g.: Urea 9 (3–7.5 mmol/L)
Creatinine 342 (35–125 μmol/L)

in lumen: stone or sloughed papilla
in wall: tumour (renal cell, transitional cell), fibrosis
external pressure: BPH, prostate CA, lymphadenopathy, aneurysm

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causes intrinsic renal AKI?

10%

Urea rise < creatinine rise

(Ex: bladder or hydronephrosis NOT palpable)

e.g.: Urea 9 (3–7.5 mmol/L)
Creatinine 342 (35–125 μmol/L)

“INTRINSIC”:

Ischaemia (due to prenal 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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What are the especially nephrotoxic Abx?

can cause intrinsic AKI

gentamicin
vancomycin
tetracyclines

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what can cause ↑ urea?

kidney injury
upper GI haemorrhage

usually indicates RF, however, because it is a breakdown product of amino acids, it can also reflect an upper GI bleed

where haemoglobin has been broken down by gastric acid into urea, which is subsequently absorbed into the blood

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Ix to do if ↑ urea with normal creatinine?

patient who is not dehydrated/have prerenal failure

look at Hb
if ↓
probably upper GI bleed

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liver markers of: hepatocyte injury or cholestasis?

bilirubin
ALT (+AST)
ALP

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markers of liver’s synthetic function?

albumin

- vitamin K-dependent clotting factors (II, VII, IX and X) measured via PT/INR

what does a solitary ↑ bilirubin indicate?

(PREhepatic jaundice)

haemolysis
Gilbert’s and Crigler-Najjar syndromes

↑ ALP causes?

“ALKPPHOS”

A ny fracture
L iver damage (posthepatic)
K (Kancer)
P aget's disease
P regnancy
H ↑parathyroid
O steomalacia
S urgery

↑ bilirubin and ↑ AST/ALT?

INTRAhepatic issue

fatty liver
hepatitis + cirrhosis (alcohol, hep A-E, CMV, EBV, AI/PBC/ASC)
(lalso DRUGS - paracetamol, statins, rifampicin)
malignancy
Wilsons, haemo
HF (congestion)

↑ bilirubin and ↑ ALP?

POSThepatic issue - gallstone - DRUGS: (5) - cholangioCA - PBC, PSC - pressure (pancreatic/gastric CA or lymph node)

drugs that can cause obstructive (POSThepatic) jaundice? ↑ bili and ↑ ALP

1) flucloxacillin 2) co-amoxiclav 3) nitrofurantoin 4) steroids 5) sulphonylureas

what is ↓ T4 and ↑ TSH? describe thyroid feedback loop?

1' hypothyroidism (↓ T4 from thyroid causes compensatory TSH) - Hashimoto's - drug-induced hypo releases TRH pituitary releases TSH thyroid releases T3 + T4 these -ve feedback on hypo and pituitary

what is ↓ T4 and TSH?

2' hypothyroidism (↓ TSH from pituitary causing ↓ T4) - pituitary tumour or damage

what is ↑ T4 and ↓ TSH?

``` 1' hyperthyroidism (T4 from thyroid causes ↓ TSH via negative feedback) - Grave's - toxic nodular goitre - drug-induced ```

what is ↑ T4 and ↑ TSH?

2' hyperthyroidism (↑ TSH from pituitary causing ↑T4) - pituitary tumour

if asked to change levothyroxine dose according to TFT results, which to look at? 1) when to ↓ dose? 2) when to keep dose? 3) when to ↑ dose?

TSH - < 0.5 - 0.5-5 - >5 (bc ↑ TSH levels indicate ↓ T4 levels)

usual projection of CXR so that heart is normal sized?

reading a CXR?

A ● trachea should be central (if not collapse -i.e. towards affected side, or pneumothorax - i.e. away from affected side) ● mediastinum - widened (R upper lobe collapse w/ tracheal deviation) or aortic dissection (w/t tracheal deviation) B ● white area= effusion (seen as unilateral and solid) ● pneumonia (seen as unilateral and fluffy) ● oedema (seen as bilateral and fluffy) ● fibrosis (seen as bilateral and honeycomb) ● apices (TB / an apical tumour) C ● heart should be < 50% width of lungs (PA) (>50 = cardiomegaly) ● triangle behind the heart (i.e. sail sign) - left lower lobe collapse D ● costophrenic angles (pleural effusion) ● air under R hemidiaphragm (bowel perforation / recent surgery ● (under the L side is gastric air bubble - normal) E ● bones (rib fractures/lytic lesions usually suggesting mets)

signs of pulmonary oedema on CXR?

"ABCDE" ``` ● 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) ● Effusions (pleural) ```

how to approach ABGs?

``` ● look at O2 (Nb: pt on 60% O2 you would expect PaO2 to be 10 less, i.e > 50kPa) ● look if RF (<8 kPa) type II if ↑ CO2 (COPD) ● check pH (abnormal CO2 = respiratory) (abnormal HCO3- = metabolic) (abnormal both = mixed picture) ```

causes of resp alkalosis?

rapid breathing | SOB or anxiety

causes of resp acidosis?

COPD NM failure restrictive chest wall (same as type II )RF

causes of metabolic alkalosis?

V diuretics Conn's syndrome (↑ aldosterone therefore ↑ Na+ and ↓ K+)

causes of metabolic acidosis?

lactic acidosis DKA renal failure ethanol/methanol/ethylene glycol intox

what is the PR interval?

beginning of P wave to beginning of QRS

what is ST interval?

end of QRS to end of T wave

what is QT interval?

beginning of QRS to end of T wave

what causes the 1st deflection of QRS to look like: "W" in V1 "M" in V6 ?

"W" i LL ia "M" LL left BBB

whats causes 1st deflection of QRS to look like: "M" in V1 "W" in V6 ?

M o RR o W RR right BBB

how to approach ECGs?

● rate (300/ large squares between each QRS) ● rhythm (P waves = sinus) (PR interval and QRS indicate heart block or AF) ● QRS complex (>3 small sq = BBB) (if V1 height + V6 height = >3.5 large sq = LVH) ● ST segment (elevated = infarction) (convex = pericarditis) (depressed = ischaemia) (downsloping in all = DIGOXIN) ● T waves (if >2/3 QRS height throughout, ↑ K+) (inversion = old infarction/LVH - unless in aVR and I)

PR interval >1 large square but constant =?

1st degree heart block

PR interval increasing, then missed = ?

2nd degree heart block | type 1

two or three P-waves for every QRS?

2nd degree heart block | type 2

random (no relationship between P wave and QRS complex?

3rd degree heart block | complete heart block

if no P-waves (and irregular QRS complexes) then it is?

if T waves are "tented" (> 2/3 of the QRS height) throughout the ECG?

↑ K+