Exam topics from feedback Flashcards
Malignant hyperpyrexia
complication of general anesthesia
characterised by hyperpyrexia and muscle rigidity
susceptibility to malignant hyperthermia is inherited in an autosomal dominant fashion
Cause agents of Malignant hyperpyrexia
halothane
suxamethonium
other drugs: antipsychotics (neuroleptic malignant syndrome)
Investigations and management Malignant hyperpyrexia
nvestigations
CK raised
contracture tests with halothane and caffeine
Management
dantrolene - prevents Ca2+ release from the sarcoplasmic reticulum
Pericarditis
Features
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia
Pericarditis causes
Causes viral infections (Coxsackie) tuberculosis uraemia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease hypothyroidism malignancy
Pericarditis ECG
nvestigations
ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
all patients with suspected acute pericarditis should have transthoracic echocardiography
Pericarditis management
treat the underlying cause
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
complications of MI
Acute mitral regurgitation - cute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard.
Ventricular septal defect - Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.
Left ventricular free wall rupture - 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
Upper gastrointestinal bleeding presentation
Patients may present with the following:
Haematemesis and/ or malaena
Epigastric discomfort
Sudden collapse
Duodenum ulcer- Upper GI bleed
major haemorrhage is a posteriorly sited duodenal ulcer - erode the gastroduodenal artery
Pain occurs several hours after eating.
Management of upper GI bleed
Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a minimum)
Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood pending cross matched blood
Early control of airway is vital (e.g. Drowsy patient with liver failure)
Patients with suspected varices should receive terlipressin prior to endoscopy
upper gastrointestinal haemorrhage should undergo Upper GI endoscopy within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist present.
Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis. Portal pressure should be lowered by combination of medical therapy +/- TIPSS.
Surgery
Duodenal ulcer
Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is almost always posteriorly sited and will have invaded the gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the ulcer base to occlude the vessel. The duodenotomy should be longitudinal but closed transversely to avoid stenosis.
For gastric ulcer
Under-running of the bleeding site
Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists
Oesophagitis presentation
Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.
Upper GI Cancer presentation
Usually small volume of blood, except as pre terminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy managed.
Mallory Weiss Tear presentation
Typically brisk small to moderate volume of bright red blood following bout of repeated vomiting. Malaena rare. Usually ceases spontaneously.
Varices presentation
Usually large volume of fresh blood. Swallowed blood may cause malaena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.
Gastric cancer presentation
May be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.
Dieulafoy Lesion presentation
Often no prodromal features prior to haematemesis and malaena, but this arteriovenous malformation may produce quite considerable haemorrhage and may be difficult to detect endoscopically
Gastric ulcer presentation
Small low volume bleeds more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.
Hyperosmolar hyperglycaemia clinical features
high blood sugar results in high osmolarity without significant ketoacidosis
HHS = medical emergency
Clinical features
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
Hyperosmolar hyperglycaemia diagnosis
Diagnosis
1. Hypovolaemia
2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
3. Significantly raised serum osmolarity (> 320 mosmol/kg)
Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
HHS management
The goals of management of HHS can be summarised as follows:
- Normalise the osmolality (gradually)
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
Fluid replacement
Fluid losses in HHS are estimated to be between 100 - 220 ml/kg (e.g. 10-22 litres in an individual weighing 100 kg).
Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid.
If the serum osmolarity is not declining despite positive balance with 0.9% sodium chloride, then the fluid should be switched to 0.45% sodium chloride solution which is more hypotonic relative to the HHS patients serum osmolarity
Fluid replacement alone (without insulin) will gradually lower blood glucose which will reduce osmolality
Rapid changes must be avoided. A safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended. The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.
A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.
Complete normalisation of electrolytes and osmolality may take up to 72 hours.
If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture). The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.
If significant ketonaemia is not present (3β-hydroxy butyrate is less than 1 mmol/L) then do NOT start insulin.
- ovarian teratoma
teratomas comprise dermal, mesodermal and endodermal elements
well-differentiated derivations from at least two of the three germ cell layers (i.e. ectoderm, mesoderm, and endoderm).
USS
chogenic mass with posterior sound attenuation
chogenic, shadowing calcific or dental (tooth) components
luid-fluid levels
multiple thin, echogenic bands caused by the hair in the cyst cavity: the dot-dash pattern (dermoid mesh)
ie Unilocular cyst with a solid intracavitary mass containing hair, skin with subcutis, bone and cartilage
dermoid
dermoid is composed only of dermal and epidermal elements (which are both ectodermal in origin),
Follicular cyst
Rarely greater than 8 cm Glistening membrane Thin walled Unilocular or multilocular Clear or serous fluid contents No solid component
Serous cystadenoma
most common ovarian neoplasm,
unilocular (or at times multilocular) cysts filled with clear watery fluid. The cysts measure 10 cm in average diameter but may be extremely large.
Mucinous cystadenoma
benign cystic tumor lined by a mucinous epithelium.
multilocular cyst with smooth outer and inner surfaces. It tends to be huge in size.
simple cyst management
A pelvic ultrasound is the single most effective way of evaluating an ovarian mass with transvaginal ultrasonography being preferable due to its increased sensitivity over transabdominal ultrasound.
Women with small (less than 50 mm diameter) simple ovarian cysts generally do not require follow-up as these cysts are very likely to be physiological and almost always resolve within 3 menstrual cycles.
Women with simple ovarian cysts of 50–70 mm in diameter should have yearly ultrasound follow-up and those with larger simple cysts should be considered for either further imaging (MRI) or surgical intervention.
Alcohol units calculation
multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000
Pulmonary hypertension
What is this
Pulmonary hypertension is an increase of blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, leg swelling and other symptoms.
Pulmonary hypertension pressure and causes
= mean pulmonary arterial pressure that is greater than 25 mmHg.
causes by heart failure, chronic lung disease
chronic thromboembolic pulmonary hypertension
Pulmonary hypertension presentation
Presentation Symptoms exertional dyspnea, chest pain, and syncope fatigue and lethargy Physical examination loud P2 on auscultation right ventricular heave right-sided 4th heart sound murmurs holosystolic murmur of tricuspid regurgitation systolic ejection murmur diastolic pulmonic regurgitation (in severe cases)
Pulmonary hypertension treatment
Treatment
Conservative
continuous long-term oxygen therapy
indication
to maintain adequate oxygenation
Medical
note that there are a myriad of causes of pulmonary hypertension
treatment should be aimed at treating and optimizing the underlying condition (e.g., anticoagulation in patients with recurrent pulmonary embolisms)
vasoactive agents
indication
pulmonary hypertension targeted therapy
medication options
calcium channel blockers
prostacyclin pathway agonists (e.g., epoprostenol, treprostinil, and iloprost)
endothelin receptor antagonists (e.g., bosentan, macitentan, and ambrisentan)
nitric oxide-cyclic GMP enhancer (e.g., sildenafil and tadalafil)
Myeloma presentation
The median age at presentation is 70-years-old.
Use the mnemonicCRABBI:
Calcium - Hypercalcaemia occurs as a result of increased osteoclast activity within the bones
This leads to constipation, nausea, anorexia and confusion
Renal
Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules
This causes renal damage which presents as dehydration and increasing thirst
Other causes of renal impairment in myeloma include amyloidosis, nephrocalcinosis, nephrolithiasis
Anaemia
Bone marrow crowding suppresses erythropoiesis leading to anaemia
This causes fatigue and pallor
Bleeding
bone marrow crowding also results in thrombocytopenia which puts patients at increased risk of bleeding and bruising
Bones
Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions
This may present as pain (especially in the back) and increases the risk of fragility fractures
Infection
a reduction in the production of normal immunoglobulins results in increased susceptibility to infection
Myeloma investigations
Investigations
Bloods will show anaemia (FBC) and thrombocytopenia (FBC); raised urea and creatinine (U&E) and raised calcium
Peripheral blood film: rouleaux formation
Serum or urine protein electrophoresis: raised concentrations of monoclonal IgA/IgG proteins will be present in the serum. In the urine, they are known as Bence Jones proteins
Bone marrow aspiration and trephine biopsy: confirms the diagnosis if the number of plasma cells is significantly raised
Whole-body MRI (or CT if MRI is not suitable) is used to survey the skeleton for bone lesions
Myeloma diagnosis
Symptomatic multiple myeloma is defined at diagnosis by the presence of the following three factors:
Monoclonal plasma cells in the bone marrow >10%
Monoclonal protein within the serum or the urine (as determined by electrophoresis)
Evidence of end-organ damage e.g. hypercalcaemia, elevated creatinine, anaemia or lytic bone lesions/fractures
myeloma management
For patients who are suitable for autologous stem cell transplantation* induction therapy consists of Bortezomib + Dexamethasone
For patients who are unsuitable for autologous stem cell transplantation*, induction therapy consists of Thalidomide + an Alkylating agent + Dexamethasone
Pain: treat with analgesia (using the WHO analgesic ladder)
Pathological fracture: Zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly.
Infection: patients receive annual influenza vaccinations. They may also receive Immunoglobulin replacement therapy.
VTE prophylaxis
Fatigue: treat all possible underlying causes. If symptoms persist consider an erythropoietin analogue.
NSAIDS in myeloma
abnormal creatinine and urea point towards reduced kidney function most likely due a nephrotoxic drug. NSAIDs (ibuprofen, naproxen) are known to precipitate renal failure in patients with multiple myeloma (MM)
Anastomotic leak
Causes and feature s
leak of luminal contents from a surgical join’
most important complication in GI surgery
Causes
Emergent surgery or prolonged operative time
Decreased perfusion of the anastomosed bowel segments
Increased pressure within the anastomosis
Clinical features
Postoperative fever, tachycardia
(usually 5–7 days following surgery)
Abdominal distention, pain, and peritoneal signs
Tender incision wound, purulent (or feculent) drainage
Anastomotic leak diagnosis and treatment
Diagnostics
Elevated inflammatory parameters
X-ray
/CT scan: contrast medium leakage in a barium meal or rectal filling; fluid collections and/or gas collections
Complications: abscess formation, peritonitis, SIRS, sepsis
Treatment
Revision surgery
Treating complications (e.g., by giving broad-spectrum antibiotics in the case of infection)
Endoluminal vacuum-assisted closure therapy
Initial management of renal colic
the BAUS recommend an NSAID as the analgesia of choice for renal colic
whilst diclofenac has been traditionally used the increased risk of cardiovascular events with certain NSAIDs (e.g. diclofenac, ibuprofen) should be considered when prescribing
the CKS guidelines suggest for patients who require admission: ‘Administer a parenteral analgesic (such as intramuscular diclofenac) for rapid relief of severe pain’
BAUS no longer endorse the use of alpha-adrenergic blockers to aid ureteric stone passage routinely. They do however acknowledge a recently published meta-analysis advocates the use of α-blockers for patients amenable to conservative management, with greatest benefit amongst those with larger stones
Nephrotoxicity due to contrast media
RF
Risk factors include
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
scabies features
Features
widespread pruritus
linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
in infants, the face and scalp may also be affected
secondary features are seen due to scratching: excoriation, infection
scabies Management
Management
permethrin 5% is first-line
malathion 0.5% is second-line
give appropriate guidance on use (see below)
pruritus persists for up to 4-6 weeks post eradication
Diclofenac CI when?
cvd increase the risk of major cardiovascular events (such as atrial fibrillation, ischaemic stroke, heart failure and myocardial infarction) in comparison to other painkillers such as paracetamol.
3 main frameworks in refusal for treatment
here are 3 main frameworks that are used in this scenario:
common law: used to treat patients in emergency scenarios
Mental Capacity Act: (MCA) used in patients who require treatment for physical disorders that affect brain function. Remember this may be delirium secondary to sepsis or a primary brain disorder such as dementia
Mental Health Act (MHA): used in patients who require treatment for mental disorders. For patients already admitted to hospital, a section 5(2) is used if there is not the time for a more formal section 2 or 3. A typical scenario would be a patient who has a mental health disorder attempting to discharge themselves, when it is thought this may result in harm
TIA management
Immediate antithrombotic therapy:
give aspirin 300 mg immediately, unless
1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team
acne treatment
A simple step-up management scheme often used in the treatment of acne is as follows:
single topical therapy (topical retinoids, benzoyl peroxide)
topical combination therapy (topical antibiotic, benzoyl peroxide, topical retinoid)
oral antibiotics:
a topical retinoid (if not contraindicated) or benzoyl peroxide should always be co-prescribed with oral antibiotics to reduce the risk of antibiotic resistance developing. Topical and oral antibiotics should not be used in combination
Gram-negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim is effective if this occurs
episcleritis
Features
red eye
classically not painful (in comparison to scleritis), but mild pain may be present
watering and mild photophobia may be present
in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move
phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
allergic bronchopulmonary aspergillosis
Oral glucocorticoids
The recommended initial management of otitis externa is:
The recommended initial management of otitis externa is:
topical antibiotic or a combined topical antibiotic with a steroid
if the tympanic membrane is perforated aminoglycosides are traditionally not used*
if there is canal debris then consider removal
if the canal is extensively swollen then an ear wick is sometimes inserted
Alendronic acid
= bisphosphate
accessing risk for osteoporosis
Consider assessment of fracture risk in all women aged 65 years and over and all men aged 75 years and over.
Use either FRAX (without a BMD value if a DXA scan has not previously been undertaken) or QFracture
Oral bisphosphonates for osteoporosis
Oral bisphosphonates (alendronic acid, ibandronic acid and risedronate sodium) are recommended as options for treating osteoporosis in adults only if: the person is eligible for risk assessment as defined in when to assess a person depending on age and sex and the 10-year probability of osteoporotic fragility fracture is at least 1%.
Delirium tremens
Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. peak 72 hours offer oral lorazepam1 as first-line treatment. If symptoms persist or oral medication is declined, offer parenteral lorazepam1 or haloperidol.
Spirometry findings in obstructive lung disease
Reduced FEV1 (<80% of the predicted normal) Reduced FVC (but to a lesser extent than FEV1) FEV1/FVC ratio reduced (<0.7)
Typical spirometry findings in restrictive lung disease include:
Typical spirometry findings in restrictive lung disease include:
Reduced FEV1 (<80% of the predicted normal) Reduced FVC (<80% of the predicted normal) FEV1/FVC ratio normal (>0.7)
Before starting azithromycin
do an ECG (to rule out prolonged QT interval) and baseline liver function tests
Factors that can increase an older person’s risk of developing anxiety or depression include
- morbidity
- losses: relationships, independence, work and income, self-worth, mobility andflexibility
- social isolation and lack of social support
Vitamin C deficiency presentation
ymptoms and signs include:
Follicular hyperkeratosis and perifollicular haemorrhage
Ecchymosis, easy bruising
Poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
Arthralgia
Oedema
Impaired wound healing
Generalised symptoms such as weakness, malaise, anorexia and depression
Psoriatic arthritis presentation
Linked the HLA-B38/B39 (peripheral PsA) and HLA-B27 (spondylitis PsA)
Inflammatory arthritis- i.e. painful, hot, swollen, erythematous joints
NB joints are usually less painful/tender than in rheumatoid
Joints are also more likely to present in a ‘ray’ distribution i.e. all the joints of one digits affected rather than the same joints of both hands (more typical of RA)
However, like RA, symptoms do worsen at rest/night and improve with movement
Pencil-in-cup deformity is the description given to one of the appearances on plain radiograph in psoriatic arthritis.
Psoriatic arthritis extra art manifestations
Anterior uveitis SAPHO syndrome synovitis acne pustulosis hyperostosis osteitis
Management of Psoriatic arthritis
Management
NSAIDs are recommended for symptomatic treatment
Intra-articular steroids may be used second line. NB Oral corticosteroids should be avoided as psoriasis rash may rebound upon treatment withdrawal.
DMARDS
Early treatment with DMARDS should be considered for peripheral arthritis and enthesitis, +/- skin/nail disease.
Ideally treat both the skin and musculoskeletal symptoms (if both are present)
Methotrexate is often the best treatment for this reason
sarcoidosis.
differtating factor - high ACE levels
Reactive arthritis
hot joint + waxy yellow rash
time course
typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
around 25% of patients have recurrent episodes whilst 10% of patients develop chronic disease
arthritis is typically an asymmetrical oligoarthritis of lower limbs
dactylitis
symptoms of urethritis
eye
conjunctivitis (seen in 10-30%)
anterior uveitis
skin
circinate balanitis (painless vesicles on the coronal margin of the prepuce)
keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
osteoarthritis. how to diff
Heberden’s nodes and thumb symptoms is highly suggestive of osteoarthritis.
nerve most likely to be injured during knee arthroplasty
common peroneal nerve
osteoarthritis treatment
Osteoarthritis - paracetamol + topical NSAIDs (if knee/hand) first-line
ou are reviewing a patient who is complaining of hip pain. You suspect a diagnosis of osteoarthritis. Which of the following symptoms should prompt further investigations for an alternative diagnosis?
Morning stiffness lasting > 2 hours may be an indication of inflammatory arthritis. This would warrant further investigations.
Primary biliary cholangitis
Anti mitocondrial antibodies
middle-aged females (female:male ratio of 9:1). with itch
Clinical features
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
Primary sclerosing cholangitis presents with
p-ANCA
ass/w UC
Presents with cholestasis jaundice, pruritus raised bilirubin + ALP right upper quadrant pain fatigue
Primary sclerosing cholangitis investigation and management
nvestigation (MRCP prefered)
endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
p-ANCA may be positive
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’
Cholangiocarcinoma develops in around 10% of primary sclerosing cholangitis patients
Testicular cancer
is the most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer are germ-cell tumours.
Seminoma presentation.
Commonest subtype (50%) Average age at diagnosis = 40 Even advanced disease associated with 5 year survival of 73%
AFP usually normal
HCG elevated in 10% seminomas
Lactate dehydrogenase; elevated in 10-20% seminomas (but also in many other conditions)
Seminoma pathology
Sheet like lobular patterns of cells with substantial fibrous component. Fibrous septa contain lymphocytic inclusions and granulomas may be seen.
Non seminomatous germ cell tumours (42%) Teratoma Yolk sac tumour Choriocarcinoma Mixed germ cell tumours (10%) presentation
Younger age at presentation =20-30 years
Advanced disease carries worse prognosis (48% at 5 years)
Retroperitoneal lymph node dissection may be needed for residual disease after chemotherapy
AFP elevated in up to 70% of cases
HCG elevated in up to 40% of cases
Other markers rarely helpful
testicual cancer investigations and diagnosis
Diagnosis
Ultrasound is first-line!!
CT scanning of the chest/ abdomen and pelvis is used for staging
Tumour markers (see above) should be measured
Management
Orchidectomy (Inguinal approach)
Chemotherapy and radiotherapy may be given depending on staging
Abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node dissection.
Leptospirosis
what is this
Leptospirosis is caused by the spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae), classically being spread by contact with infected rat urine.
Epidemiology
leptospirosis is commonly seen in questions referring to sewage workers, farmers, vets or people who work in an abattoir
however, on an international level, leptospirosis is far more common in the tropics so should be considered in the returning traveller
Leptospirosis features
Features
the early phase is due to bacteraemia and lasts around a week
may be mild or subclinical
fever
flu-like symptoms
subconjunctival suffusion (redness)/haemorrhage
second immune phase may lead to more severe disease (Weil’s disease)
acute kidney injury (seen in 50% of patients)
hepatitis: jaundice, hepatomegaly
aseptic meningitis
Leptospirosis investigations and management
Investigation
serology: antibodies to Leptospira develop after about 7 days
PCR
culture
growth may take several weeks so limits usefulness in diagnosis
blood and CSF samples are generally positive for the first 10 days
urine cultures become positive during the second week of illness
Management
high-dose benzylpenicillin or doxycycline
clinical features aortic stenosis
Clinical features of symptomatic disease chest pain dyspnoea syncope murmur an ejection systolic murmur (ESM) is classically seen in aortic stenosis classically radiates to the carotids this is decreased following the Valsalva manoeuvre
Features of severe aortic stenosis narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure
metformin CI
Contraindications
chronic kidney disease: NICE recommend that the dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)
metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration
iodine-containing x-ray contrast media: examples include peripheral arterial angiography, coronary angiography, intravenous pyelography (IVP); there is an increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter
alcohol abuse is a relative contraindication
Papillary carcinoma
Usually contain a mixture of papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare
Follicular adenoma
Usually present as a solitary thyroid nodule
Malignancy can only be excluded on formal histological assessment
Follicular carcinoma
May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease raree
Medullary carcinoma
C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.
Anaplastic carcinoma
Most common in elderly females
Local invasion is a common feature
Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective
severe asthma management
Supplementary oxygen should be given to all hypoxaemic patients with severe acute asthma to maintain an SpO2 level between 94–98%. Do not delay if pulse oximetry is unavailable.
First-line treatment for acute asthma is a high-dose inhaled short-acting beta2 agonist (salbutamol or terbutaline sulfate) given as soon as possible.
If response poor - consider continuous nebulisation with an appropriate nebuliser
adequate dose of oral prednisolone.
Nebulised ipratropium bromide may be combined with a nebulised beta2 agonist in patients with severe or life-threatening acute asthma,
. A single intravenous dose of magnesium sulfate may be considered in patients with severe acute asthma (peak flow
intravenous aminophylline in asthma
Monitoring
• ECG – Cardiac side effects include: Arrhythmias, Hypotension, Tachycardia
• Neurology – if convulsions are seen call a ‘MET call’
• U+E’s – Hypokalaemia
Therapeutic Drug monitoring
• Take levels 4- 6 hours after starting infusion then daily thereafter
• Therapeutic range 10 - 20mg/L
Post op pain: check epidural sensory block level
patient must be monitored every 15mins for at least 1 hour 1 hourly for 4 hours 2 hourly thereafter If stable commence 4 hourly observations (or as per NEWS frequency)
COMPLICATIONS ASSOCIATED WITH EPIDURAL ANALGESIA
Respiratory depression- Inform Anaesthetist/ DR have Naloxone ready. Nausea and vomiting - Give anti emetic.
Hallucinations
Pruritis
Urinary retention
MANAGEMENT OF HYPOTENSION in epidural block
1) Stop epidural infusion if patient is symptomatic
2) Place patient supine or in the lateral recovery position if there is any concern about the patient’s airway or level of consciousness is depressed.
3) Rapidly infuse 250-500mls of colloid?
4) Give 100% O2 by face mask
5) Have EPHEDRINE at patient’s bedside (with 10 mls water for injection)
6) Get Medical Assistance, i.e. ward doctor and/or on-call anaesthetist Bleep 1130
7) Monitor the following: blood pressure, pulse, respiratory rate, AVPU (conscious level) every 5 minutes until there is sustained improvement in blood pressure and level of consciousness.
symtoms and signs of CKD
Symptoms
Frequently asymptomatic in early stages Anorexia & nausea Fatigue & weakness Muscle cramps Pruritus Dyspnoea Oedema Signs
Pallor (secondary to anaemia) Hypertension Fluid overload (e.g. raised JVP, peripheral & pulmonary oedema) Skin pigmentation Excoriation marks Peripheral neuropathy
Investigations may be used to help diagnose, monitor and assess for complications of CKD.
Urine
Urine dipstick Urine microscopy ACR (spot test) ACR (24-hour collection) Electrophoresis (e.g. myeloma) Bloods
FBC U&Es (inc. eGFR) Bone profile PTH Bicarbonate LFTs Lipid profile Autoimmune screen (e.g. ANCA, ANA) Myeloma screen Imaging
Renal ultrasound
Magnetic resonance angiography
Echocardiogram
ECG (high risk of CVS disease)
complications of CKD
normocytic normochromic anaemia is typical of CKD (decreased erythropoietin)
Hyperkalaemia
ypocalcaemia, hyperphosphataemia and hyperparathyroidism = bony pathology adynamic bone disease, osteomalacia, osteoporosis and osteitis fibrosa cystica
hypervolaemia and patients may have evidence of peripheral oedema, ascites, raised JVP, gallop rhythm and bilateral pleural effusions.
low bicarbonate levels
management of CKD complications
Hypocalcaemia: dietary supplements and calcitriol.
Hyperphosphataemia: dietary restriction and phosphate binders.
Hyperparathyroidism: calcimimetics or surgery.
fluid restriction reduced sodium intake and the use of oral diuretics (e.g. furosemide)
oral sodium bicarbonate therapy. .
