Data Interp Flashcards
do you always need to stop NSAIDs in asthmatics
NO - only if q suggests pts asthma is NSAID sensitive ie. they have a wheeze then you should stop (it causes bronchoconstriction)
causes of microcytic anaemia TAILS
Thalassaemia ACD IDA Lead poisoning Sideroblastic anaemia (congenital)
causes of normocytic anaemia 3As & 2Hs
ACD
Acute blood loss
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
causes of macrocytic anaemia ‘Alcoholics may have liver failure’ - AMHLF
Alcoholism Myelodysplastic syndrome, Multiple myeloma Hypothyroidism, Haemolytic anaemia Liver failure Folate + B12 deficiency
WCC + differentials - HIGH neutrophils - causes
BACTERIAL, tissue damage, steroids (reactive neutrophilia)
WCC + differentials - LOW neutrophils - causes
VIRAL, chemo/radiotherapy, clozapine, carbimazole
WCC + differentials - HIGH lymphocytes - causes
VIRAL, lymphoma, CLL
HIGH platelets - two types + causes
REACTIVE - Bleeding, tissue damage, post-splenectomy
PRIMARY - Myeloproliferative disorders
LOW PLATELETS - due to increased destruction - causes
HEPARIN (induced thrombocytopaenia) hypersplenism DIC ITP HUS/TTP
LOW PLATELETS - due to reduced production - causes
infection (viral)
DRUGS (PENICALLIMINE) eg in RhA pts
MDS/MF/MYELOMA
hyponatraemia assessment of what determines causes
fluid status
- hypovolaemia: D, V, Diuretics, Salt losing nephropathy
- euvolaemic: endocrine - hypothyroidism, Adrenal insufficiency, SIADH
- hypervolaemic: 3x failures: HF, liver failure, renal F
euvolaemic hyponatraemia due to SIADH causes (pnemonic SIADH) x5
SCLC + surgery Infections Abscess Drugs - CARBAMAZEPINE, ANTIPSYCHOTICS Head Injury
CNS pathology - stroke, haemorr, T
Lung pathology - pneumonia (Legionella), pneumothorax
Drugs - SSRI, TCA, PPI, Carbamazepine, opiates
Tumours
SURGERY
hypernatraemia causes - all begin with d’s (4)
dehydration
drips ie. too much saline
drugs - with too much sodium
diabetes insipidus - opposite of SIADH
hypernatraemia due to primarily - INCR in SODIUM +/OR LOSS OF WATER & secondaryily - LOW WATER INTAKE
INCR in SODIUM: Medical high intake Dietary high intake Conn's Syndrome RAS Cushing's Syndrome (overactivation of MR by cortisol --> aldosterone like effect)
LOSS OF WATER: Renal losses -Osmotic diuresis -DI NON- renal losess -GI loss -Sweat loss
LOW WATER INTAKE
- child/elderly/dementia
- fasting for surgery
Hypokalaemia (DIRE)
<3.5
DRUGS (LOOP + THIAZIDE diuretics)
Inadeq intake or GI loss (D/V)
RTA
Endocrine (Cushings + Conns)
Hyperkalaemia (DREAD)
>5.3
DRUGS (potassium sparing diuretics+ ACEi)
Renal F
Endocrine (Addisons)
Artefact (v.common - due to clotted sample)
DKA tx with insulin drops K+
raised urea with normal creatinine what should you look at next and what will it show
haemoglobin
-likely to be low as urea raised due to UGI bleed
3 cauess of a raised urea
AKI, UGI haemorrhage, eat a big steak
PRE-RENAL causes of AKI
= 70% of AKIs
UREA rise»_space; Creatinine rise
Dehydration / shock
RAS (precipitated by ACEi or NSAIDs)
POST-RENAL causes of AKI
=20% of AKIs
Creatinine rise > Urea rise
OBSTRUCTION -bladder/hydronephrosis may be palpable Luminal: Stones Mural: TCC, renal cell carcinoma Extra-mural: BPH
INTRINSIC RENAL causes of AKI
= 10% of AKIs
Creatinine rise > Urea rise
Ischaemia (pre-renal --> ATN) Nephrotoxic ABx Tablets (ACEi, NSAIDs) Radiological contrast Injury (rhabdo) Negatively birefringent crystals (gout) Syndromes (GN) Inflammation (vasculitis) Cholesterol emboli
-bladder/hydronephrosis NOT palpable
how can you assess liver ftn x 2 broad categories
HEPATOCTYE INJURY or CHOLESTASIS eg
- BR
- ALT + AST
- ALP
SYNTHETIC FTN (ie. the protein it makes)
- ALBUMIN
- VIT K DEP CLOTTING F’S (2,7,9,10) meas via PT/INR
what does solitary raised BR often mean
HAEMOLYSIS - as BR is a break down product of Hb
-this is a cause of Pre-hepatic J NOT due to liver problems
causes of raised ALP (ALKPHOS)
Any fracture Liver damage K (for kancer) Pagets disease of bone, Pregnancy Hyperparathyroidism Osteomalacia Surgery
where can ALP be found
placenta, bone, liver, bowel wall
AST>ALT in what
Alcoholic hepatitis - because Ash Sahota drinks alcohol
ALT>AST
Other hepatitis
which TB drugs cause Drug induced liver injury
Isoniazid, Pyrazinimide
name 5 cholestatic drugs
flucloxacillin CO-AMOXICLAV nitrofurantoin steroids sulphonylureas
what is a PRE-hepatic pattern of LFTs + some causes
Pattern: BR increase
Cause: HAEMOLYSIS, Gilberts, Crigler-Najjar Syndrome
what is an INTRA-hepatic pattern of LFTs + some causes
Pattern: BR & ALT/AST increase
Causes: Hepatitis, Cirrhosis, Fatty Liver, Malignancy (1’ or 2’), Metabolic: Wilsons disease/haemochromatosis, HF (causing hepatic congestion)
what is a POST-HEPATIC (Obstructive) pattern of LFTs + some causes
Pattern: BR & ALP increased
Causes:
-luminal: stone (GS), drugs causing cholestasis
-mural: tumour (cholangiocarcinoma), PBC, PSC
-extramural: pancreatic or gastric C, LN
Q on changing levothyroxine dose according to TFT result - what should you be guided by
TSH level 0.5-5 = target
-change by the SMALLEST increment offerred
IF <0.5 –> DECR DOSE
IF >5 –> INCR DOSE
on what CXR view can you assess the size of the heart
ONLY on PA (NORMAL)
on AP the heart automatically appears larger
how is rotation on a cxr assessed
distance between spinal processes and clavicles equidistant
what happens to trachea in lung collapse + pneumothorax
COLLAPSE - TOWARDS affected side
PNEUMOTHROAX - away
widened mediastinum on CXR (2)
Aortic dissection
RUL collapse with tracheal deviation
triangle behind heart on CXR
sail sign
-LEFT LOWER LOBE COLLAPSE
A-E of P.Oedema
ALVEOLAR SHADOWING (bat wing) Kerley B-lines (interstitial oedema) Cardiomegaly Diversion of the upper lobe Effusions
LVH criteria
QRS deflection of V1 ADDED to QRRS deflection of V6 (in terms of LARGE SQUARES) >= 3.5 = LVH
ST segment depression due to what (3)
Ischaemia Infarction - check trop to distinguish - will be in some leads DIGOXIN - will be downsloping in ALL leads
in what leads is T WAVE INVERSION NORMAL
Leads I & aVR (top middle two)
-in other leads TWI = OLD INFARCT/LVH
what type of drugs require monitoring
NARROW TI drugs
how to change drug doses of narrow TI drugs
If low serum drug level AND inadequate clinical response – INCREASE drug level
If low serum drug level BUT adequate clinical response – do NOT increase drug
If high serum drug level AND adequate clinical response – DECREASE drug level
-Except GENTAMICIN – the FREQ of administration is decreased, not the amount (by 12h, so instead of drug every 24h give every 36h)
Features of toxicity of drugs with narrow TI: Digoxin Lithium Phenytoin Theophylline Gentamicin Vancomycin
Digoxin - confusion, nausea, visual haloes, arrythmias
Lithium - early: tremor, intermed: tired, late: arrythmias, seizure, coma, ARF, DInsipidus
Phenytoin - gum hypertrophy, ataxia, nystagmus, periph neuropathy, teratogenicity
Theophylline - N/A
Gentamicin - ototoxic, nephrotoxic
Vancomycin - ototoxic, nephrotoxic
Gentamicin dosing - based on what 2 things + what is usual
Dose by patient WEIGHT and RENAL FTN (serum creatinine)
· Usual dose (high-dose regimen) = 5-7mg/kg, OD (24-hourly)
· Renal failure (<20mL/min CrCl) = 1mg/kg, BD (12-hourly)
· IE = 1mg/kg, TDS (8-hourly)
Gentamicin dosing - OD regimen monitoring + divided daily dosing
OD REGIMEN MONITORING:
- Measure levels at particular times (6-14 HRS after last infusion)
- Plot on a NORMOGRAM (see below)
- Use nomogram to determine FREQUENCY of dosing (every 24, 36 or 48 hours)
DIVIDED DAILY DOSING:
-normogram exists but usually, daily peaks + troughs are used to guide tx
Paracetamol OD <1 hr + >1 hr
<1hr –> activated charcoal–> Ix: paracetamol level ≥4hr after ingestion –>? NAC
If below the treatment line at 4 hours post-ingestion, no NAC is required
o If staggered overdose taken or time not known of ingestion, use NAC
> 1hr –> Ix: paracetamol level ≥4 hours after ingestion –>? NAC
o Use NAC graph to decide whether to administer
what happens to LFTs in para OD
o ALT, AST: very high [peak at 72 hours post-ingestion]
o ALP: normal
o PT: if >180 seconds on day 4 will need transplantation
when to stop warfarin before surgery
5 days
warfarin INR targets
AF, DVT, cardioversion, cardiomyopathy, MI –> 2-3
Recurrent VTE on warfarin, mechanical heart valve –>3-4
warfarin OD
Major bleed (–>hypotension OR bleed in a confined space – i.e. skull, eye)
o Stop warfarin
o IV vitamin K (5mg, slow IV) – Phytomenadione
o IV PCC – Beriplex
warfarin + INR>8 + minor bleeding
Stop warfarin, IV VIT K (1-3mg; repeat in 24hrs if still high), restart warfarin when INR <5
warfarin + INR>8 + no bleeding
Stop warfarin, PO VIT K (repeat in 24hrs if still high), restart warfarin when INR <5
warfarin + INR 5-8 + minor bleeding
Stop warfarin, IV vitamin K (1-3mg), restart warfarin when INR <5
warfarin + INR 5-8 + no bleeding
Withhold 1-2 doses of warfarin, consider reducing maintenance dose
neutropenic sepsis mx
IV meds always (30% mortality so need to be aggressive)
- IV Piperacillin with Tazobactam + Gentamicin
