Causes of non visible haematuria
Transient/spurious
- UTI
- Menstruation
- Vigorous exercise (settles in 3 days)
- Sex
Persistent
- Cancer (bladder, renal, prostate)
- Stones
- BPH
- Prostatits
- Urethritis
- Renal disease
What can cause blood to appear red in absence of blood
Food
- Beetroot, rhubarb
Drugs
- Rifampicin
- Doxorubicin
Investigations for non visible haematuria
+ how do you diagnose persistent
Urine dip for testing
- Persistent diagnosed if blood present in 2/3 samples tested 2-3 weeks apart
Also test renal function, ACR and blood pressure
What does haematuria + ACR suggest
Glomerular disease (increased permeability)
- IgA nephropathy
- Thin basement membrane disease
- Alport syndrome
When should haematuria be referred (Urgent)
Urgent 2 week
Aged 45+ and
- Unexplained visible haematuria without UTI
- Visible haematuria that persists after UTI treatment
Aged 60+ and
- Unexplained non visible haematuria and dysuria or raised WCC
When should haematuria be referred (non urgent)
Aged 60+ with recurrent or persistent UTI
How do you interpret ABG
4 steps
What is an anion gap in metabolic acidosis
(Na+ + K+) - (HCO3- + Cl-) = AG (how many more cations than anions - Normal 8-14 mmol/L) *sometimes K+ is excluded
Serum is normally kept neutral. Many anions aren’t included in calculation (albumin, phosphates, sulphates, lactate, ketones), these are the “gap” (cations - anions - AG = 0)
If AG is high, this suggests a more serious life threatening cause of metabolic acidosis.
Causes of metabolic acidosis with a normal anion gap (AKA Hyperchloraemic)
Causes of metabolic acidosis with a raised anion gap
Lactic acidosis (↑ lactate)
- Shock
- Sepsis
- Hypoxia
Ketotic acidosis (↑ Ketones)
- Diabetic acidosis
- Alcohol
Urate
- Renal failure
Acid poisoning
- Salicylates
- Methanol
What are the 2 types of metabolic acidosis due to high lactate levels
Lactic acidosis:
Type A - Sepsis, shock, hypoxia, burns
Type B - Metformin
What is the mechanism behind metabolic alkalosis
Key principle is: RAAS System activated, and aldosterone causes reabsorption of Na+ in exchange for H+ DST.
Examples
- ECF depletion - Sodium and chloride ion loss. -> activation of RAAS system -> Raised aldosterone level
- Hypokalaemia - K+ shift from cells to ECF, exchanges for H+ (H+/K+ pump), causing loss of hydrogen ions in serum.
Causes of metabolic alkalosis
Vomiting/aspiration
Diuretic use
Hypokalaemia
Primary hyperaldosteronism
Cushing’s
Liquorice, carbenoxolone
Causes of respiratory alkalosis
Hyperventilation (increased CO2 expulsion, less in blood, so blood less acidic)
Causes of respiratory acidosis
Hypoventilation (CO2 not being expelled)
In metabolic alkalosis why should chlorine be given in fluid
Enables kidneys to reabsorb sodium without HCO3- and allows kidney to excrete bicarbonate
What electrolyte should be given with insulin and why
Potassium. Insulin causes inward shift of potassium
Treatment approaches to acid base disorders
MAc - Replace buffer or remove acid (treat cause, fluid, oxygen (Lactate), insulin (DKA))
MAl - Correct volume, potassium and chloride. Stop diuretics.
RAc - Improve ventilation +- oxygen (NIV)
RAl - Reduce hyperventilation stimulus
In what patient groups should urine dip not be used for UTI diagnosis, what should be done instead
Women >65 - Urine culture
Men - MSU culture. Investigate for prostatitis too
Catheterised patients - Urine culture from fresh catheter or via catheter port.
These groups have asymptomatic bacteriuria and sensitivity and specificity are low. Catheters usually harmlessly colonised.
Nephrotic syndrome triad
What antibiotic can be used for acute bronchitis
Doxycycline
- If CRP>100 offer immediately
- If systemically unwell or pre existing comorbidities
What suggests pneumonia instead of bronchitis
Features like
- Sputum, wheeze, breathlessness
- Malaise, myalgia, fever
- Focal chest signs OE
Leads showing change, site of heart and coronary artery affected in ECG
Septal - V1, V2 - Left anterior descending
Anterior - V3, V4 - Left anterior descending
Inferior - II,III, aVF - Right coronary
Lateral- I, aVL, aVR, V5, V6 - Left circumflex
How can you differentiate the ACS conditions?
What are their differences in occlusion, and what are the implications for the heart in each
ECG, Troponins