Renal, Vasc surg, Breast surg, ENT Flashcards
What are the criteria for AKI?
Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours
Give pre-renal causes of AKI
Pre-renal pathology is the most common cause of acute kidney injury. It is due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:
Dehydration
Hypotension (shock)
Heart failure
Give renal causes of AKI
This is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Give post-renal causes of AKI
Post renal acute kidney injury is caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer
How do we determine proteinuria? Where is it found?
CKD
Can be checked using a urine albumin:creatinine ratio (ACR). A result of ≥ 3mg/mmol is significant.
What is the first line treatment for HTN in patients with CKD?
ACE inhibitors are the first line in patients with chronic kidney disease. These are offered to all patients with:
Diabetes plus ACR > 3mg/mmol
Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol
What needs to be monitored in HTN with CKD?
Serum potassium needs to be monitored as chronic kidney disease and ACE inhibitors both cause hyperkalaemia.
Explain the pathophysiology behind anaemia of CKD.
Healthy kidney cells produced erythropoietin. Erythropoietin is the hormone that stimulates production of red blood cells. Damaged kidney cells in CKD cause a drop in erythropoietin. Therefore there is a drop in red blood cells and a subsequent anaemia.
How do we treat anaemia of CKD?
Treat iron deficiency
Anaemia can be treated with erythropoiesis stimulating agents such as exogenous erythropoeitin. Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.
What is osteosclerosis?
Hardening of bones
What is seen on spine XR in renal bone diseasE?
Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as “rugger jersey” spine after the stripes found on a rugby shirt.
Describe the pathophysiology behind renal bone disease.
High serum phosphate occurs due to reduced phosphate excretion. Low active vitamin D because the kidney is essential in metabolising vitamin D to its active form. Active vitamin D is essential in calcium absorption from the intestines and kidneys. Vitamin D also regulates bone turnover.
Secondary hyperparathyroidism occurs because the parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone. This leads to increased osteoclast activity. Osteoclast activity lead to the absorption of calcium from bone.
Give five indications for acute dialysis
A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness
What murmur is heard over an AV fistula?
Stereotypical “machinery murmur” on auscultation
What is STEAL syndrome?
STEAL syndrome is where there is inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. The blood is diverted away from where is was supposed to supply and flows straight into the venous system. This causes distal ischaemia.
What are the criteria for nephritic syndrome?
Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).
Oliguria means there is a significantly reduced urine output.
Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention
What are the criteria for nephrotic syndrome?
Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia
Give three types of glomerulonephritis
Minimal change disease
IgA nephropathy
Goodpasture Syndrome
How do we treat glomerulonephritis?
Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
What is the most common cause of nephrotic syndrome in children, and how is it treated?
The most common cause of nephrotic syndrome in children is minimal change disease. This is usually:
Idiopathic (no identified cause)
Treated successfully with steroids
A pt presents with acute renal failure and haemoptysis. What are the differentials? How do we distinguish between the two?
Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis). Goodpasture syndrome is associated with anti-GBM antibodies, whereas Wegener’s granulomatosis is a type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA). Patients with Wegener’s granulomatosis may also have a wheeze, sinusitis and a saddle-shaped nose.
What is interstitial nephritis?
Interstitial nephritis is term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney. This is different to glomerulonephritis, where there is inflammation around the glomerulus.
How does acute interstitial nephritis present?
Acute interstitial nephritis presents with acute kidney injury and hypertension. There is acute inflammation of the tubules and interstitium. This is usually caused by a hypersensitivity reaction to:
Drugs (e.g. NSAIDS or antibiotics)
Infection
How does chronic tubulointerstitial nephritis present?
Chronic tubulointerstitial nephritis involves chronic inflammation of the tubules and interstitium. It presents with chronic kidney disease.
What is acute tubular necrosis?
Acute tubular necrosis is damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common cause of acute kidney injury. Damage to the kidney cells occurs due to ischaemia or toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible.
How long does it usually take to recover from acute tubular necrosis?
It usually takes 7-21 days to recover.
What is pathognomonic for acute tubular necrosis?
“Muddy brown casts” found on urinalysis is a pathognomonic finding specific to acute tubular necrosis. There can also be renal tubular epithelial cells in the urine.
How do we treat ATN?
Treatment is the same as with other causes of an acute kidney injury:
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
What is renal tubular acidosis?
Renal tubular acidosis is where there is a metabolic acidosis due to pathology in the tubules of the kidney.
What is the function of the renal tubules?
The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH.
What is type 1 renal tubular acidosis?
Type 1 renal tubular acidosis is due to pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions.
How does type 1 renal tubular acidosis present?
FTT in children
CKD
Bone disease
Hypokalaemia
How do we treat type 1 renal tubular acidosis?
Oral bicarbonate
What is type 4 renal tubular acidosis caused by?
Caused by reduced aldosterone. This can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.
How do we manage type 4 renal tubular acidosis?
Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.
What is haemolytic uraemic syndrome?
Haemolytic uraemic syndrome (HUS) occurs when there is thrombosis in small blood vessels throughout the body.
What is the triad in HUS?
Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)
What usually causes HUS?
The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin.
How does HUS present?
E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea.
Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:
How do we manage HUS?
HUS is a medical emergency and has up to 10% mortality. The condition is self limiting and supportive management is the mainstay of treatment:
Antihypertensives
Blood transfusions
Dialysis
70-80% of patients make a full recovery.
What is rhabdomyolysis?
Rhabdomyolysis is a condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.
What is released when myocytes apoptose?
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine kinase
What does myoglobin do to the kidney?
Myoglobin in particular is toxic to the kidney in high concentrations. This results in acute kidney injury. The acute kidney injury causes the breakdown products to further accumulate in the blood.
How does rhabdomyolysis present?
Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine
How do we manage rhabdomyolysis?
Suspect rhabdomyolysis in patients with trauma, crush injury, prolonged immobilisation or excessive exercise.
IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.
Why might we give IV sodium bicarbonate in rhabdomyolysis?
Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.
Why might we give IV mannitol in rhabdomyolysis?
This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.
Which arrhythmia does hyperkalaemia cause?
Ventricular fibrillation
What ECG signs are seen in hyperkalaemia?
Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes
How do we treat hyperkalaemia?
Patients with a potassium ≤ 6 mmol/L with otherwise stable renal function don’t need urgent treatment and may just require a change in diet and medications (i.e. stopping their spironolactone or ACE inhibitor).
Patients with a potassium ≥ 6 mmol/L and ECG changes need urgent treatment.
Patients with a potassium ≥ 6.5 mmol/L regardless of the ECG need urgent treatment.
The mainstay of treatment is with an insulin and dextrose infusion and IV calcium gluconate:
Insulin (e.g. actrapid 10 units) and dextrose (e.g. 50mls of 50%) drives carbohydrates into cells and takes potassium with it, reducing the blood potassium.
Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias.
How do we treat polycystic kidney disease?
Mostly supportive
Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease. It is recommended by NICE in certain situations although it should be initiated and monitored by a specialist.
What one symptom most likely indicates critical limb ischaemia?
The features are pain at rest, non-healing ulcers and gangrene.
Define gangrene
Gangrene refers to the death of the tissue, specifically due to an inadequate blood supply.
What are the features of critical limb ischaemia?
(burning) Pain (worse at night)
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold
What is the triad in Leriche syndrome?
Thigh/buttock claudication
Absent femoral pulses
Male impotence
What is blocked in Leriche syndrome?
Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery.
How do we assess difficult to palpate pulses?
Using a hand-held Doppler
How does PAD present on inspection?
Skin pallor
Cyanosis
Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
Muscle wasting
Hair loss
Ulcers
Poor wound healing
Gangrene (breakdown of skin and a dark red/black change in colouration)
How do we perform the first part of the Buerger’s test?
Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test.
The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.
What will happen to the leg in the second part of the Buerger’s test to a healthy and non-healthy leg?
The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:
Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration
How do arterial ulcers present?
Are smaller than venous ulcers
Are deeper than venous ulcers
Have well defined borders
Have a “punched-out” appearance
Occur peripherally (e.g., on the toes)
Have reduced bleeding
Are painful
How do venous ulcers present?
Occur after a minor injury to the leg
Are larger than arterial ulcers
Are more superficial than arterial ulcers
Have irregular, gently sloping borders
Affect the gaiter area of the leg (from the mid-calf down to the ankle)
Are less painful than arterial ulcers
Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)
How do we analyse ABPI?
0.9 – 1.3 is normal
0.6 – 0.9 indicates mild peripheral arterial disease
0.3 – 0.6 indicates moderate to severe peripheral arterial disease
Less than 0.3 indicates severe disease to critical ischaemic
How do we treat intermittent claudication medically?
Atorvastatin 80mg
Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
How do we treat intermittent cluadication surgically?
Endovascular angioplasty and stenting
Endarterectomy – cutting the vessel open and removing the atheromatous plaque
Bypass surgery – using a graft to bypass the blockage
What is the main contraindication for compression stockings?
Peripheral arterial disease
When do we use ventilation-perfusion scan over CTPA?
If the patient has significant kidney impairment or a contrast allergy.
How do we manage DVT/PE?
In most patients, NICE (2020) recommend treatment dose apixaban or rivaroxaban. It should be started immediately in patients where DVT or PE is suspected, and there is a delay in getting the scan.
What is the first-line anticoagulant in pregnancy?
Low molecular weight heparin (LMWH)
What are varicose veins?
Varicose veins are distended superficial veins measuring more than 3mm in diameter, usually affecting the legs.
What are reticular veins?
Reticular veins are dilated blood vessels in the skin measuring less than 1-3mm in diameter.
What are Telangiectasia?
Telangiectasia refers to dilated blood vessels in the skin measuring less than 1mm in diameter. They are also known as spider veins or thread veins.
How do varicose veins form?
The deep and superficial veins are connected by vessels called the perforating veins (or perforators), which allow blood to flow from the superficial veins to the deep veins. When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them. This leads to dilatation and engorgement of the superficial veins, forming varicose veins.
Why do the lower legs become brown in chronic venous insufficiency?
When blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs. This gives a brown discolouration to the lower legs.
Why does venous eczema form in chronic venous insufficiency?
Pooling of blood in the distal tissues results in inflammation. The skin becomes dry and inflamed, referred to as venous eczema.
How do we perform the Tap test?
Tap test – apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.
How do we perform the cough test?
Cough test – apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).
How do we perform Trendenlenburg’s test?
With the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.
How do we perform Perthe’s test?
Perthes test – apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.
How do we manage varicose veins?
Varicose veins in pregnancy often improve after delivery.
Simple treatment measures include:
Weight loss if appropriate
Staying physically active
Keeping the leg elevated when possible to help drainage
Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)
Surgical options:
Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation
Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein
Stripping – the veins are ligated and pulled out of the leg
How do we manage chronic venous insufficiency?
Management involves:
Keeping the skin healthy
Improving venous drainage to the legs
Managing complications
The skin is kept healthy by:
Monitoring skin health and avoiding skin damage
Regular use of emollients (e.g., diprobase, oilatum, cetraben and doublebase)
Topical steroids to treat flares of venous eczema
Very potent topical steroids to treat flares of lipodermatosclerosis
How do we manage arterial ulcers?
The management of arterial ulcers is the same as peripheral arterial disease, with an urgent referral to vascular to consider surgical revascularisation. If the underlying arterial disease is effectively treated, the ulcer should heal rapidly. Debridement and compression are not used in arterial ulcers.
How do we manage venous ulcers?
Good wound care
What is the difference between primary and secondary lymphoedema?
Primary lymphoedema is a rare, genetic condition, which usually presents before aged 30. It is a result of faulty development of the lymphatic system.
Secondary lymphoedema is due to a separate condition that affects the lymphatic system. The most common example is when patients develop lymphoedema after breast cancer surgery, due to the removal of axillary lymph nodes in the armpit.
What is lipoedema?
Lipoedema is an important differential diagnosis, where there is an abnormal build-up of fat tissue in the limbs, often the legs. The feet are spared in lipoedema, unlike lymphoedema. This affects women more often than men.
What is Stemmer’s sign?
Stemmer’s sign can be used to assess for lymphoedema. The skin at the bottom of the second toe or middle finger is gently pinched together using two fingers. If it is possible to lift and “tent” the skin, Stemmer’s sign is negative. If it is not possible to pinch the skin together, lift and “tent” it, Stemmer’s sign is positive, suggesting lymphoedema.
How do we manage lymphoedema?
A specialist lymphoedema service manages patients with lymphoedema.
Non-surgical treatment options include:
Massage techniques to manually drain the lymphatic system (manual lymphatic drainage)
Compression bandages
Specific lymphoedema exercises to improve lymph drainage
Weight loss if overweight
Good skin care
How do we screen for AAA?
All men in England are offered a screening ultrasound scan at age 65 to detect asymptomatic AAA. Early detection of an AAA means preventative measures can stop it from expanding further or rupturing.
What is an AAA?
Abdominal aortic aneurysm (AAA) refers to dilation of the abdominal aorta, with a diameter of more than 3cm.
How do we monitor small-medium AAAs?
The Public Health England (updated 2017) screening and surveillance programme recommends follow up scans:
Yearly for patients with aneurysms 3-4.4cm
3 monthly for patients with aneurysms 4.5-5.4cm
The NICE guidelines (2020) recommend elective repair for patients with any of:
Symptomatic aneurysm
Diameter growing more than 1cm per year
Diameter above 5.5cm
