Investigations Flashcards
General radiology
Stored in DICOM, Picture Archiving and Communication System
Checks:
- Name
- Date
- Relevant images are there
- Orientation - metal mark on the left
X-ray
Bone (white) -> Air (black), talk about density
Examples: CXR, AXR, extremity radiographs, mammography
Adv: low dose (NB background), quick, cheap
Disadv: Poor for soft tissue, poor sensitivity and specificity
CT
X-ray tubes and detector - 3D and reconstructed in any plane
Talk about attenuation
Examples: Head injury, acute abdomen, abdo trauma, staging cancer.
Adv: Spatial resolution, sensitive and specific, 3D
Disadv: Ionising rad, iodine contrast => nephrotoxicity, cost and high data load
US
2-15MHz - emit and receive
Examples: pregnancy, brain (neonate), soft tissue, PVD, DVT, abdomen and pelvis
Adv: Portable, non-invasive, not ionising
Disadv: Operator dep, limited depth penetration and anatomical access
MRI
Field alligns to protons and produces an RF signal on returning to rest, depending on the proton content and surrounding milieu
Examples: MSK, neuro, liver, gynae, prostate
Adv: no ionising, soft tissue differentiation, Gadolinium instead of iodine contrast
Disadv: Artefacts (movement), patient unsuitability, less spatial resolution than CT, time and cost
Nuclear Medicine
Radiation source inside the patient, combined with a metabolic function
Examples: V/Q scan, bone scintigraphy, PET-CT
Adv: sensitivity, functional, quantifiable
Disadv: ionising radiation, low specificity, time, spatial resolution
Interventions
Vascular - angioplasty, stent inserting, EVAR (Endovascular aneurysm repair) stent
Non-vascular - liver and biliary tract, GI and urinary tract
Ionising rdiation
ALARA
Background - 2.64mSv/year. X-ray (day) to PET-CT (a few years)
Contrast
Provides higher density to highlight its route.
Barium - GI tract investigation
Risk:
peritonitis if it spills into peritoneal cavity
Iodine - for CT intravascular agent
Injection leads to hot flush and feeling a need to urinate
Risks:
Allergic reaction
Nephropathy - NB susceptibility of renal patients
Gadolinium - MRI (alters the magnetic properties between tissues)
Risks:
Nephrogenic systemic fibrosis (NSF) (reminiscent of scleroderma)
Dentate Nucleus and Globus Pallidus accumulation
Bloods
In general: Assist in diagnosis Screening Evaluate prognosis Monitoring
Different levels 1) FBC U&Es LFT BFT CRP ESR
2)
Folate
Iron Stores
Vitamins
3) Auto-antibodies Tumour markers Genetic tests Viral serology
ECG principles
Measure the electrical activity at the surface, used to infer the vectors of conduction in the heart
Dimensions
1mV = 10mm
Whole page is 10s
Affected by
Electrolyte disturbances
IHD
Hypertrohpy
Common indications
Chest pain
SOB
Palpations
How it is performed
10 electrodes -> 12 leads
4 arm
6 chest
Approach
Patient ID, indications, calibration
Rate - 300/small squares, 6x number of complexes on the rhythm strip
Rhythm - Reg, Reg Irreg, Irreg Irreg Sinus - P followed by QRS AF - no P and irreg irreg QRS A Flutter - sawtooth, atrial rate of 300/min Ventricular - QRSs >120ms
Axis - overall direction of the (ventricular) depolarisation
Normal = -30 to +90, then left deviation is 90
1) If I and aVF +ve then normal
2) If I +ve and aVF -ve, check II. If this is +ve then it is normal
3) Look at I and III.
Leaving = LAD
Returning = RAD
P wave - atrial origin
Normally:
Up - II, III, aVF
Inverted - aVR
If absent: AF or hidden due to junctional or ventricular rhythm
If bifid (mitrale): suggestive of Left Atrial Hypertrophy
If peaked (pulmonale): suggestive of Right Atrial Hypertension or elevated K
PR - start of P to start of QRS
Normal - 0.12-0.2
Prolongation suggests AV delay (first degree heart block)
Shortening suggests bypassing pathways e.g. WPW
QRS
Normal <0.12, indicates it is going through the bundles
Prolongation - BBB, metabolic disturbances, ventricular originating
High amplitude - ventricular hypertrophy
Deep (>2mm) and wide (>0.04) Q - post acute MI
QT - start of QRS to end of T
Can vary with rate therefore take corrected
LQT - can lead to VT and death - various causes
ST
Usually isoelectric
Elevated (>1mm in 2 or more limb or >2mm in 2 or more chest) - infarction
Depression (<0.5mm) - ischaemia
T wave
Inverted in aVR, V1 and V2 (or in III in isolation) is normal
Inversion in I, II, V4-6 is abnormal (e.g. following PE)
Tented in hyperkalaemia
J wave - S finish to ST starts
Seen in hypothermia, SAH (subarachnoid haem) and elevated Ca
`
FBC
Level one bloods
NB Artefacts
RBC
Red blood cell (RBC) count - 4.20-5.80 10*12/L
Haemoglobin (Hb) - 130-170 g/L
Mean cell volume (MCV) - 80.0-100.0 fL
Mean cell haemoglobin (MCH) - 27.0-32.0 pg
Outcome
• Low RBC / Hb - Anaemias
• High RBC / Hb - Polycythaemia
Cues to: • Alcohol use • Kidney disease • Liver disease • Sickle cell disease / thalassaemia
Hb range
Men: Hb 130-170g/l
Women: Hb 115-160g/l - menstruation, muscle mass difference, testerone (effects on erythropoetin)
Low Hb
MCV Microcytis - Iron def Cause: Dietary Malabsorptive Chronic blood loss Further investigation: Ferritin and Total Iron Binding capacity
Normal but with Low Hb Anaemia of chronic disease Haemolysis Renal failure Myeloma
Macrocytis
Folate/B12 def
Liver disease
Myelodysplasia
High Hb - Polycythaemia Induced by hypoxia: Smoking (carbon monoxide bound to Hb) Altitude COPD Renal path: Polycystic kidney disease Renal tumours
WBC
Leucocytosis = rise Causes: Infeciton Autoimmune Traumatic injury Leukaemia
Leucopaenia = fall Drugs Early leukaemia Blood dyscrasias B12 def
Cell subtypes
Neutrophils Bacterial infection Acute phase response Auto-immune damage Inflammation
Lymphocytes
Viral infections
Eosinophils
Asthma
Allergic reactions
White blood cell (WBC) count - 4.0-11.0 109/L
Neutrophil count - 2.00-8.00 109/L
Lymphocyte count - 1.00-4.50 109/L
Eosinophil count - 0.00-0.40 109/L
Clotting indices
Use - assess risk of bleeding and pre-procedures
Basis - Vascular, platelet and coagulation phases
Problems:
Inherited
Acquired
Drug therapy
Measures: Platelet Count - 150-400 10*9/L Prothrombin time (PT) International Normalized ratio (INR) Partial thromboplastin time (PTT)
PT - time for citrated plasma to clot on addition of TF and Ca
Extrinsic and common pathways
Measures: def in Factors V / VII / prothrombin / fibrinogen
Prolonged in: Warfarin use, Cirrhosis and decomp LF
aPTT - time for citriated plasma to clot on addition of kaolin and Ca
Intrinsic and common pathways
Measures: def in V / VIII to XII / prothrombin and fibrinogen
Prolonged in: Haemophilia
Low count - thrombocytopenia Decreased production: Marrow suppression Leukaemia Viral infection Drugs Increased destruction: Idiopathic thrombocytopenia purpura (ITP) Hypersplenism
Inflammation markers
Level one bloods
ESR - 2-10mm
CRP - 2-10mm
ESR - Erythrocyte sedimentation rate
How far RBC in a column of blood fall in one hour
NB NOT SPECIFIC - instead it is a surrogate marker
It changes in inflammation or anaemia due to increased fibrinogen / upregulation of CAMs etc.
High in: 1. Myeloma 2. SLE 3. Temporal arteritis 4. Polymayalgia rheumatica Rarely: carcinoma/chronic infection
CRP - C-Reactive Protein
Marker of tissue injury
NOT SPECIFIC - bacterial or auto-immune
If over 100, likely to be bacteria
LFTs
To access liver function and toxicity of drugs
Albumin - 35-50 g/L
Total Bilirubin - 0-20 umol/L
Alkaline Phosphatase - 30-130 U/L
Alanine Transaminase - 7-40 U/L
Albumin
Functions:
Provides plasma oncotic pressure
Source of protein for metabolic functions
“Chaperone” for other chemicals - calcium
Hypoalbuminaemia:
Liver disease – impaired synthetic function
Inflammation – liver switched to CRP synthesis
Malnutrition
Nephrotic syndrome – urinary loss of protein
Bilirubin
Product of RBC recycling
Harmful; not very soluble
Modified by liver enzyme UGT1A1 (UDPglucuronosyltransferase1A) which transforms it from a lipophilic molecule into a water-soluble
excretable metabolite - Conjugated or “direct” bilirubin
Elevation (>35) => Jaundice
1. Pre-hepatic - haemolysis, congential
2. Hepatic - alcohol, viral, drugs, autoimmune, heritable, neoplastic
3. Post-hepatic
Benign - gallstones, cholangitis, biliary stricture
Malignant - pancreatic cancer, cholangiocarcinoma
Alkaline phosphatase (ALP)
The point of this is that it is meant to be an intracellular enzyme
Found in biliary tree and bile ducts BUT also found in bone and placenta
Elevated:
• Liver disease (cholestasis / obstructive jaundice)
• Bone disease (osteoblast activity)
• Pregnancy
Alanine Aminotransferase (ALT)
Similar to above - Intracellular liver enzyme
Elevation: Hepatocellular damage: Active hepatitis - viral, alcohol, drugs, toxins Ischaemic injury Liver enzyme induction Drugs - e.g. statins induce it Toxins
U&Es
Level 1 bloods
Marker of kidney function
Serum Sodium - 133-146 mmol/L Serum Potassium - 3.5-5.3 mmol/L Serum Creatinine - 62-115 umol/L Serum Urea - 2.5-7.8 mmol/L Estimated GFR - 90-125ml/min Serum Bicarbonate - 22-29 mmol/L
NB eGFR is a better measure the sCr alone (taking into account sCr, age, sex, gender, race)
Urea Elevated Renal disease Dehydration Upper GI bleed Steroids
Sodium Primary (extracellular) electrolyte Independ of ECF vol Alterations in serum sodium reflect alterations in either sodium OR water. Hyponatraemia = serum sodium <133mmol/l Hypernatraemia = serum sodium >146mmol/l
Low Na
Hypovolaemia - dehydration, extrarenal loss (GI tract, burns), diuretics, Addison’s
Euvolaemia - drugs, malignancy, pulmonary disorder, neurological disorders
Hypervolaemia - Cardiac failure, renal failure, nephrotic syndrome, cirrhosis
Potassium
Primary intracellular electrolyte
Hyperkalaemia = serum potassium >5.3mmol/l
Hypokalaemia = serum potassium <3.5mmol/l
NB Cardiac dysrhythmias - but may be asymptomatic until point of arrest
NB to check potassium after giving ACEi
Hyperkalaemia Causes: Potassium retention 1. Renal failure 2. Decreased mineralocorticoids Addison’s Spironolactone ACEi / ARB 3. Potassium-sparing diuretics Amiloride Potassium release from intracellular space Haemolysis Trauma Cytotoxic therapy for malignancy
6 ECG changes Tented T waves Prolonged PR Reduced amplitude of P wave Widening of QRS Sinusoidal rhythm VF/VT or asystole
Treatment 10ml CaCl 10% IV (5min) 50ml Dextrose 50% with 10 units of soluble insulin IV (NB NaKATPase) Stop drugs ACEi Consider dialysis
Hypokalaemia GI loss Diarrhoea and vomiting Renal loss 1. Diuretics – loop / thiazides 2. Mineralocorticoid excess (Conn’s, Cushing’s Steroid therapy) 3. Poor intake 4. Shift to intracellular compartment (insulin)