Data Interpretation Flashcards
Causes of Hypernatreamia
Dehydration
Drips (too much IV saline)
Drugs (effervescent tablet preparations or IV preparations with a high sodium content, diabetes insipidus
Causes of Microcytic anaemia (low MCV)
Iron deficiency anaemia
(Thalassaemia and Sideroblastic anaemia)
Causes of Normocytic anaemia
anaemia of chronic disease
acute blood loss
(haemolytic anaemia and chronic Renal failure)
causes of macrocytic anaemia
B12/folate deficiency (megaloblastic anaemia)
Excess alcohol
Liver disease (including nonalcoholic causes)
(hypothyroidism, haematological diseases: myeloproliferative, mylodysplastic, multiple myeloma)
Causes of high neutrophils (neutrophilia)
Bacterial infection
(tissue damage (inflammation/infarct/malignancy), steroids)
Causes of low neutrophils (neutropenia)
Viral infection
Chemotherapy or radiotherapy
Clozapine - antipsychotic
Carbimazole - antithyroid
causes of high lymphocytes (lymphocytosis)
Viral infection
Lymphoma
Chronic Lymphocytic Leukemia
Causes of Low platelets (thrombocytopenia)
Reduced production:
Drugs - esp penicillamine (e.g. in rheumatoid arthritis treatment)
(infection, usually viral
Myelodysplasia, myelofibrosis, myeloma)
Increased destruction
Heparin
(hypersplenism
Disseminated intravascular coagulation (DIC)
Idiopathic thrombocytopenia purport (ITP)
Haemolytic Uraemic syndrome/thrombotic thrombocytopenia purpura)
Causes of High platelets
Reactive:
(bleeding
tissue damage (infection/inflammation/malignancy/post-splenectomy) )
Primary:
(Myeloproliferative disorders)
Causes of hyponatraemia
Hypovolaemic:
Diuretics (any type)
(Fluid Loss (esp diarrhoea and vomiting)
Addisons disease )
Euvolemic:
(SIADH, Psychogenic polydipsia, hypothyroidism)
Hypervolaemic
(heart failure, renal failure
Liver failure, nutritional failure, thyroid failure)
Causes of SIADH
‘SIADH’
S- small cell lung tumours
I - infection
A - Abscess
D - Drugs (esp carbamazepine and antipsychotics
H - head injury
Causes of hypokalaemia
‘DIRE’
Drugs - loop and thiazide
(Inadequate intake or intestinal loss (diarrhoea and vomiting), Renal tubular acidosis, Andocrine (bushings and conns)
Causes of Hyperkalaemia
‘DREAD’
Drugs - k-sparing diuretics and ACE-inhibitors
(Renal failure, endocrine (addison’s disease), Artefact, DKA (note: when insulin given in DKA the K drops, requiring hrly monitoring)
what does a raised urea indicate
kidney injury
upper GI Heamorrhage (where haemoglobin has been broken down by gastric acid into urea)
what biochemical disturbance will you see in a pre-renal AKI, and what are the causes
Urea rise»_space; Creatine rise
e.g. urea 19 (normal 3-7.5), Creatinine 110 (normal 35-125)
Caused by dehydration (or if severe, shock) or any cause (sepsis, blood loss). also renal artery stenosis
what biochemical disturbance will you see in a intrinsic-renal AKI, and what are the causes
Urea rise «_space;Creatine rise. Bladder or hydronephrosis not palpable (e.g. urea 9 (3-75.), creatinine 342 (35-125))
‘Intrinsic’ causes:
Ischaemia, NEPHROTIC ANTIBIOTICS (gentamicin, vancomycin and tetracyclines), TABLETS (NSAIDs and ACE-I), Radiological contrast, Injury (rhabdomyolysis), Negatively birefringent crystals (gout), Syndromes (glomerulonephridites), Inflammation (vasculitis), Cholesterol emboli
what biochemical disturbance will you see in a post-renal AKI, and what are the causes
Urea rise «_space;Creatine rise. Bladder or hydronephrosis may be palpable depending on level of obstruction (e.g. urea 9 (3-75.), creatinine 342 (35-125))
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
‘ALKPHOS’
Any fracture, Liver damage (POST hepatic), Kancer, Pagets disease of bone and pregnancy, Hyperparathyroidism, Osteomalacia, Surgery
How can you use the TSH result to indicate how to change the levothyroxine dose (target of TSH is 0.5-5mlU/L)
If TSH <0.5 then decrease the levothyroxine dose
if TSH 0.5-5 then do not change the levothyroxine dose
is TSH >5 then increase the levothyroxine dose
NOTE: always change by smallest increment available
Indication of levothyroxine
Used to treat hypothyroidism
It is taken to replace thyroxine, which would normally be released by the thyroid.
Causes of a pre-hepatic liver injury, and what LFT derangement are you likely to see?
Haemolysis
(Gilberts and crippler najjar syndrome)
Raised Bilirubin
Causes of an intrahepatic liver injury, and what LFT derangement are you likely to see?
Hepatitis and cirrhosis (may be due to alcohol, virusues (hep A-E, CMV and EBV), drugs (paracetamol overdose, statin, rifampicin), autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hep), Malignancy
Fatty liver, Metabolic (Wilsons disease/haemochromatosis), heart failure (causing hepatic congestion)
Causes of an posthepatic (obstructive) liver injury, and what LFT derangement are you likely to see?
raised bilirubin and ALP
In lumen: Gallstone, drugs causing cholestasis (flucloxacillin, co-amoxiclav, nitrofurantoin, steroids, sulphonylureas)
In wall: tumour, primary billiard cirrhosis, sclerosing cholangitis)
extrinsic pressure: Pancreatic or gastric cancer, lymph node
Causes of primary hypothyroidism, and what deranged thyroid test results are you likely to see?
Hashimoto’s thyroiditis, drug induced hypothyroidism
low T4 from thyroid, causing a compensatory increase in TSH
Causes of secondary hypothyroidism, and what deranged thyroid test results are you likely to see?
Pituitary tumour or damage
low TSH from pituitary causing low T4
Causes of primary hyperthyroidism, and what deranged thyroid test results are you likely to see?
Grave’s disease, toxic nodular goitre, drug-induced hyperthyroidism
high T4 from thyroid causing low TSH (through negative feedback)
Causes of secondary hyperthyroidism, and what deranged thyroid test results are you likely to see?
Pituitary tumour
High TSH from pituitary causing high T4 from thyroid
Explain the cycle/feedback loop of that affects the thyroid
Hypothalamus releases Thyrotropin releasing hormone (TRH), which stimulates the anterior pituitary gland to release Thyroid stimulating hormone (TSH), which stimulates the thyroid to release T3 and T4. High levels of T4 negatively feedback to the hypothalamus and pituitary gland to reduce the amount of TRH and TSH produced, therefore lowering the T4.
Describe the routine used to assess a CXR
Quality: rotation, Inspiration, Projection, exposure
Airway - trachea central, carina, bronchi, hilar visualised
Breathing - Lung fields to the edge, pleura, assess all lobes for consolidation
Circulation - hear size and vessels
Diaphragm - costa-phrenic angles and air?
Everything else: mediastinal contours, bones, soft tissues, tubes, valves, pacemakers and review areas.
signs of pulmonary oedema on a CXR
‘ABCDE’
Alveolar oedema (bat wings), Kelley B lines (interstitial oedema), cardiomegaly, diversion of blood to upper lobes , plural effusions
describe the differences of effusion, pneumonia, oedema and fibrosis on a CXR
all white areas
effusion - unilateral and solid (liquid in the pleura)
Pneumonia - unilateral and fluffy
oedema - bilateral and fluffy (fluid in the lungs, not a definite area like in effusion)
Fibrosis - bilateral and honeycomb
Explain the routine of checking an arterial blood gas
look at inspire O2 conc and compare to paO2 to determine whether patient is hypoxic (can do this by subtracting 10 from the FiO2 and if the PaO2 exceeds this number the patient is not hypoxic)
Check for rest failure - ie PaO2 low or inappropriate normal (as explained above)
Check acid-base status
Describe the different types of resp failure, the way they might breathe, and causes
Type 1 - low (or inappropriately normal) PaO2 with low or normal paCo2
fast/normal breathing
caused by anything that damages the heart or lungs causing SOB
Type 2 - low (or inappropriately normal) PaO2 with high PaCo2
Slow/shallow breathing
caused by some types of COPD and less commonly neuromuscular failure or restrictive chest wall abnormalities
describe how you assess acid-base status
if pH is low - acidotic
if PaCo2 is high - resp cause
is HCO3 is low - metabolic cause
if Ph is high - alkalosis
if PaCO2 is low - resp cause
is HCO3 is high - metabolic cause
If both PaCO2 and HCO3 are raised or low, this indicated compensation
If PaCO2 and HCO3 are abnormal in different directions, then there is co-existant metabolic and resp disease
Causes of resp alkalosis
rapid breathing, this could be due to disease or anxiety
Causes of resp acidosis
same causes as T2 Resp failure - subtype of COPD, neuromuscular failure or restrictive chest wall abnormalities
Causes of metabolic alkalosis
Vomiting, diuretics, conns syndrome
Causes of Metabolic acidosis
lactic acidosis, DKA, renal failure, ethanol/methanol/ethylene glycol intoxication
How to find the rate on an ecg
divide 300 by the number of large squares between QRS complexes
OR
count number of QRS complexes and multiply by 6
Normal rate on an ECG
60-100
How to assess rhythm on an ECG
are there P waves?
if yes then sinus rhythm, no then AF
if PR interval is constant and <1large square then Sinus rhythm without heart block
if PR interval not constant or over 1 large block then this is sinus rhythm with heart block:
- constant but >1 large square = 1st degree
- Increasing, then missing a QRS is Second degree heart block type 1 (wenkebach)
- two or three waves for every QRS then second degree heart block type 2
- if no relationship between waves and QRS complexes, third degree heart block
How to assess QRS complexes on an ECG
width:
If <3 small squares, no bundle branch block
if >3 small squares, BBB
- first deflection of QRS in V1 is down, and in V6 is up, then Left BBB (WiLLiaM)
- first deflection of QRS in V1 is up, and in V6 is down, then Right BBB (MaRRoW)
Height:
add the largest deflection in V1 to that of V6 (in terms of large squares), if this is over 3.5 large squares then Left ventricular hypertrophy is present
if small then consider pericardial effusion
How to assess an ST segment on a an ECG
if elevated:
Infarction (ST segment flat and raised in some leads)
Pericarditis (ST segment convex and raised in all leads)
Ischaemia (ST Segment flat and only depressing in some leads)
DIGOXIN (ST segment down-sloping in all leads) (reverse tick)
Which leads/vessels are effected in Superior/anterior/Lateral/inferior
Septal - V1, V2 (Ventricular septum artery, branch of the LAD, effected. therefore often occurs with Anterior MI)
Anterior - V3, V4 (LAD)
Lateral - I, aVL, aVR, V5, V6 (left circumflex coronary artery)
Inferior - II, III, aVF (Right coronary artery)
How to assess T-waves in an ECG
Height:
if >2/3 of QRS height throughout the ECG then hyperkalaemia
inversion: normal in aVR and I, in other leads may suggest an old infarction/Left ventricular hypertrophy (LVH)
narrow therapeutic index
a small difference in blood concentration between therapeutic and toxic effects
most common drugs with a narrow therapeutic index
Digoxin, theophylline, lithium, phenytoin, gentamicin and vancomycin
digoxin drug class, indication, and signs of toxicity
cardiac glycoside - used to control heart problems such as AF/flutter/HF
Confusion, nausea, visual halos, arrhythmia
Theophylline drug class and indication and signs of toxicity
bronchodilator, used to manage lung disease such as asthma, bronchitis, emphysema
lithium indication and signs of toxicity
mania/depression
Early: tremor
Intermediate: tiredness
Late: arrhythmias, seizures, coma, renal failure, diabetes insipidus
phenytoin drug class and indication and signs of toxicity
Anti-convulsant
epilepsy - tonic clonic/focal seizures
Gum hypertrophy, ataxia, nystagmus, peripheral neuropathy and teratogenicity
gentamicin drug class and signs of toxicity
aminoglycoside antibiotic
ototoxicity and nephrotoxicity
Vancomycin drug class
amino glycoside antibiotics
ototoxicity and nephrotoxicity
what to do if INR is in-between 2.5 and 6
reduce warfarin dose
if minor bleeding with INR >5 then give IV vitamin K 1-3mg
what to do if INR is 6-8
omit 2 days then recheck, and give reduced dose
if minor bleeding with INR >5 then give IV vitamin K 1-3mg
What to do if INR is >8
omit warfarin and give 1-5mg oral vitamin K
if minor bleeding with INR >5 then give IV vitamin K 1-3mg
If regularly takes ACEi and then develops AKI due to NSAID use, what should be stopped?
Both NSAID and ACEi
ACEi can exacerbate AKI
Where can you find info on how you should adjust warfarin dose depending on INR in the BNF?
Oral anticoagulants page
Neutropenic sepsis (pneumonia and pain) with raised K, raised Urea, normal Cr. Currently on ACEi and codeine. Wants to go home. what do you do?
Stop ACEi as hyperkalemia probably caused by this
Prescribe Pip Tax and Gent IV
Prescribe Paracetamol - is okay as kidney function is fine
What to prescribe UTI in pregnancy
First Trimester - Co-Amoxiclav, nitrofurantoin, cephalosporin
NOTE: make sure to stop contraception
How do you change to dose of steroids when the person taking them becomes unwell (if they are on them long term, and illness not to do with steroid use)
Double them - called ‘sick day rules’
Side effects of digoxin
Bradycardia, arrhythmia, dizziness, vomiting, diarrhoea, eosinophilia, skin and vision reactions
Which medications can exacerbate asthma
Beta blockers and NSAIDs
Need to be weary of this when discontinuing drugs due to asthmatic exacerbation
Stop drugs that worsen asthma - NSAIDs and Bisolprolol
Withhold any drugs that they are giving in nebulisers (ie salbutamol)
What to give in heart failure to stop oedema, 1st and second line
loop diuretics: furosemide and the bumetanide if resistant
Drugs commonly used to treat AF
Bisoprolol
Diltizem - CCB (non-dihydropyridine, used in angina and hypertension)
Digoxin
Side effects of Diltiazem
Abdominal pain; dizziness; drowsiness; flushing; headache; nausea; palpitations; peripheral oedema; skin reactions; tachycardia; vomiting
How should you approach stopping steroids
Gradual withdrawal if:
- more than 40mg prep daily for more than one week
- received more than 3 weeks treatment
- recently recieved repeated courses
if otherwise, can stop immediately
Diabetes diagnosis/treatment criteria
Healthy:
HbA1C 42mmol/mol
fasting glucose 3.9-5.6mmol/L
Pre-diabetes:
HbA1c 42-48mmol/mol
fasting 5.7-6.9mmol/l
Diabetic:
HbA1c over 48mmol/mol
fasting >7mmol/l
Target HbA1c if diabetic is 48. if at risk of diabetes is 42
