Pathology 7 Flashcards
Differentiating direct from indirect hernias
Differentiating direct from indirect hernias
Inguinal hernias are located superior and medial to the pubic tubercle.
Indirect inguinal hernias occur in young male patients, whereas direct inguinal hernias occur in elderly male patients.
Indirect inguinal hernias are typically congenital (caused by a patent processus vaginalis).Direct inguinal hernias are typically acquired (caused by factors that raise intra-abdominal pressure e.g. chronic cough in smokers, constipation, heavy lifting)
Indirect inguinal hernias may descend into the scrotum vs direct inguinal hernias rarely descend into the scrotum.
Following reduction of the hernia, pressure over the deep ring prevents reappearance of an indirect but NOT a direct inguinal hernia (an indirect hernia enters the femoral canal at the deep inguinal ring vs a direct hernia is emerging via a defect in the posterior wall medial to this point
Indirect inguinal hernias may strangulate vs direct inguinal hernias rarely strangulate.
Management
If the hernia is large and symptomatic, patients should be referred for surgical repair (typical open or laparoscopic mesh repair).
If the hernia is small and/or asymptomatic patients may be managed with watchful waiting, and advice on risk factor modification.
Cholecystitis and colicky pain
Features of biliary colic:
Colicky right upper quadrant pain Worse after eating No fever Murphy's sign negative A potential complication of biliary colic is obstructive jaundice which presents as jaundice, dark urine and pale stools.
Although if there is no obstruction no treatment is required, an elective cholecystectomy can be performed to relieve symptoms if they are recurrent or troublesome.
Features of Acute Cholecystitis
Key features of acute cholecystitis include:
Right upper quadrant/epigastric pain (radiating to right shoulder tip if the diaphragm is irritated)
Fever
Nausea and vomiting
Right upper quadrant tenderness
Murphy’s sign positive
If there is associated biliary obstruction the patient can also get jaundice with dark urine and pale stools, however this is not a key feature of cholecystitis.
Definition of Ascending Cholangitis
Ascending cholangitis is a bacterial infection of the biliary tree.
Clinical features
The most common predisposing factor is gallstones.
Charcot’s triad of (1/3 of patients) :
Right upper quadrant pain
Fever
Jaundice
Hypotension and confusion are also common symptoms if the sepsis is severe.
Causes of ascending cholangitis
Biliary calculi (stones) – 50%
Benign biliary stricture – 20%. These can be congenital, post-infectious, or inflammatory.
Malignancy – 10-20%. These can be due to tumour in the gallbladder, bile duct, ampulla, duodenum, pancreas.
Investigations
A basic blood panel will show raised LFTs with a raised CRP.
Initial imaging should be performed via US abdomen and can detect bile duct dilatation but is not very good at picking up stones in the mid/distal area of the biliary duct. CT scan gives you good anatomical detail of the biliary tree and may visualize radiopaque stones (although CT is poor at viewing radiolucent cholesterol stones which are the most common).
MRCP is the most accurate modality to determine disease including gallstones or strictures, and can view almost all causes of biliary tree blockage.
Once an aetiology has been determined, ERCP can be used as a therapeutic intervention.
Management
Resuscitation including intravenous fluids and antibiotics (according to local guidelines). Critical care may be required depending on the presence or severity of shock and organ failure
Biliary drainage may be required
Endoscopic drainage – ERCP (Endoscopic retrograde cholangiopancreatography). This may involve stent placement for strictures.
Percutaneous drainage – PTC (Percutaneous transhepatic cholangiography)
Surgical drainage
Assessment and management of predisposing cause – for example, if gallstones – consider cholecystectomy. If malignant stricture, this would need further investigation and management as appropriate.
Chronic Cholecystitis features
Features of chronic cholecystitis include:
Flatulent dyspepsia Vague abdominal pain Nausea Bloating Symptoms which are worse after a fatty meal. Sometimes colicky pain Gallstone Ileus features If a gallstone is able to erode through the gallbladder wall, a fistula can form between the gallbladder and small bowel (cholecystoenteric fistula).
If a large gallstone travels through this fistula it can get trapped in narrow areas of the bowel leading to small bowel obstruction. This most commonly occurs in the terminal ileum around the ileo-caecal valve.
X-ray demonstrating air in the biliary tree (pneumobilia) and dilated small bowel would heavily indicate gallstone ileus.
Cholangiocarcinoma
Cholangiocarcinoma is a relatively rare cancer with a high mortality rate (5 year survival is around 15 – 20%). It often presents late with metastases with vague symptoms of abdominal pain (not always in the right upper quadrant), jaundice, anorexia and weight loss. An abdominal mass may be felt in the right upper quadrant (Courvoisier sign).
The most common risk factor is a history of gallstones or chronic cholecystitis, but others include:
Porcelain gallbladder Smoking Obesity Primary sclerosing cholangitis Ulcerative colitis/Crohn's colitis Oestrogens Occupational exposure (pesticides, radiation, heavy metals, vinyl chloride) Several imaging modalities can be used including ultrasound and CT scan. However, ERCP can allow visualisation of the mass as well as obtain biopsies for histology and is therefore the most accurate investigation.
Bradycardia
Bradycardia is defined as a heart rate of <60 beats per minute
Initial management of acute bradycardia
According to the ALS adult bradycardia algorithm patients should first be assessed using DR ABCDE, ECG monitoring and any reversible causes should be identified and treated.
If there are any adverse features (shock, syncope, myocardial ischaemia or heart failure) then atropine 500 mcg IV is given.
Atropine blocks the vagus nerve activity on the heart, which increases the firing rate of the SA node.
Repeat boluses can be given up to 3mg
Pilonidal disease
Pilonidal disease is caused by insertion of hairs into the skin of the natal cleft, at the sacrococcygeal region. This causes a chronic inflammatory response, with formation of a discharging sinus. Infection of the region may precipitate abscess formation.
Presention
Pilonidal disease typically occurs in male patients age 15-40 and is more common in the presence of thick stiff body hair. Patients typically present with offensive discharge from the natal cleft and discomfort, especially when seated.
On physical examination sinus tracts may be visible around the natal cleft.
If superinfection occurs, there may be abscess formation which results in a tender fluctuant swelling and low-grade fever.
Coeliacs disease
Coeliac disease is a T cell-mediated inflammatory autoimmune disease affecting the small bowel in which sensitivity to prolamin results in villous atrophy and malabsorption.
Epidemiology
Coeliac disease is a common chronic condition and is estimated to affect approximately 0.5 to 1 percent of the general population in many parts of the world.
In Europe, the United States, and Australia, prevalence estimates range from 1:80 to 1:300 children.
Females are affected approximately twice as often as males.
Presentation is bimodal (in infancy and at age 50-60). It is more common in Irish populations.
Associations of coeliac disease
Associations include: positive family history, HLA-DQ2 allele, and other autoimmune disease (such as type 1 diabetes mellitus).
Gastrointestinal symptoms Abdominal pain Distension Nausea and vomiting Diarrhoea Steatorrhoea Systemic symptoms Fatigue
Weight loss or failure to thrive in children
General appearance: check for pallor (secondary to anaemia), short stature and wasted buttocks (secondary to malnutrition), and features of vitamin deficiency secondary to malabsorption (e.g. bruising due to vitamin K deficiency).
Dermatological manifestations: dermatitis herpetiformis (pruritic papulovesicular lesions over the buttocks and extensor surfaces of the arms, legs, and trunk).
Abdominal examination: there may be abdominal distension.
Features of severe disease are highlighted in bold.
Complications and associated diseases
Unexplained iron deficiency (complication)
B12 or folate deficiency (complication)
Osteoporosis (complication)
Type 1 diabetes (associated disease)
Autoimmune thyroid disease such as Graves disease or Hashimotos thyroiditis (associated disease)
Enteropathy associated T-cell lymphoma
Diagnostic tests
Stool culture is necessary to exclude infection.
The gold standard diagnostic test is with OGD and duodenal/jejunal biopsy. Patients should be referred for this after positive serological testing (or negative serological testing but high clinical suspicion). Ideally this should be carried out before gluten is withdrawn from the diet and repeated after gluten withdrawal (to demonstrate resolution).
Histology reveals sub-total villous atrophy, crypt hyperplasia, and intra-epithelial lymphocytes.
Basic blood tests
FBC (this may show a microcytic anaemia due to iron deficiency, a normocytic anaemia due to chronic inflammation, or a macrocytic anaemia due to folate deficiency)
U&E and bone profile (vitamin D absorption may be impaired)
LFT (albumin may be low secondary to malabsorption)
Iron, B12, Folate
Serological blood tests
Anti-TTG IgA antibody is measured first line.
An IgA level should be measured in conjunction (2% of coeliac disease patients are IgA deficient so will have a false negative anti-TTG IgA).
Anti-TTG IgG can be measured if the patient is IgA deficient.
Anti-endomyseal antibody can be measured if IgA TTG is weakly positive (it is more specific but less sensitive).
Anti-gliadin is not recommended by NICE
Note that NICE do not recommend HLA-DQ2 testing in the non-specialist setting. It may be used in specialist settings e.g. in children who are not having a biopsy.
Management
The only management for Coeliac disease is life-long gluten free diet.
Patients often require education regarding what foods contain gluten, for example many patients do not realise that beer contains gluten.
Patients require regular monitoring to check adherence to a gluten-free diet and to screen for complications
Complications
Anaemia
Hyposplenism (and therefore a susceptibility to encapsulated organisms)
Osteoporosis (a DEXA scan may be required)
Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma).
The likelhood or aquiring this malignancy is directly proportional to the strength of overall adherence to a gluten free diet - i.e. the more a patient breaks adherence, the more likely they are to get EATL.
Glomerulonephritis
Damage to the glomerulus, including the glomerular basement membrane and glomerular capillaries, usually caused by inflammatory change.
Types of glomerulonephritis
Membranous glomerulonephritis
Minimal change disease
Focal segmental glomerulonephritis
IgA nephropathy
Rapidly progressing glomerulonephritis
Lupus nephritis
Post-infectious glomerulnephritis
Anti-glomerular basement membrane antibody (Anti-GBM) disease
Causes of glomerulonephritis
Infection e.g. group A streptococcus, hepatitis B and C, respiratory and gastrointestinal tract infections, endocarditis, HIV
Systemic inflammatory conditions e.g. lupus, rheumatoid arthritis, anti-glomerular basement membrane disease, microscopic polyangiitis, granulomatosis polyangiitis
Drugs, in particular non-steroidal anti-inflammatory drugs, gold, anabolic steroids
Metabolic disorders e.g. diabetes, hypertension and thyroid disease
Malignancy
Hereditary disorders e.g. Alport’s syndrome
Deposition diseases e.g. amyloidosis
Symptoms and signs
May be asymptomatic
Haematuria (macroscopic or microscopic)
Proteinuria
Oedema
Hypertension
Joint pain
Rash
Fever
Weight loss
Investigations
Urinalysis - may show haematuria, proteinuria
Urine microscopy
Urea and electrolytes - may show reduced glomerular filtration rate (GFR) or elevated creatinine
Full blood count - may have evidence of anaemia or inflammatory response
Metabolic profile - may reveal underlying diabetes
Lipid profile - may show hyperlipidaemia
C-reactive protein
Testing for specific systemic causes e.g. erythrocyte sedimentation rate (ESR), rheumatoid factor, complement, anti-nuclear antibody, anti-double-stranded DNA, antineutrophil cytoplasmic antibodies (ANCA), anti-glomerular basement membrane (GBM) antibodies
Renal tract ultrasound - to assess kidney size and any evidence of obstruction
Renal biopsy - definitive test for diagnosis of glomerulonephritis
Management
Management of glomerulonephritis depends on cause and may include
Antibiotics if infection
Angiotensin converting enzyme inhibitors (ACEi) to decrease proteinuria
Corticosteroids
Furosemide if hypertension and fluid overload
Immunosuppressant drugs
Plasmapheresis
Asthma
5.4 million people in the UK currently recieve some form of treatment for Asthma and one average three people die from an asthma attack each day. The NHS spends £1 billion a year treating Asthma.
Pathophysiology
Asthma occurs due to a reversible airway obstruction. The pathophysiology of asthma includes airway narrowing due to bronchial muscle contraction, inflammation caused by mast cell degranulation and increased mucus production.
Symptoms
Symptoms:
Wheeze
Dyspnoea
Cough (may be nocturnal)
Chest tightness
Diurnal variation (symptoms often worse in the morning)
Note: a personal/family history of atopy may be present, and symptoms may worsen following exercise or NSAIDs/beta-blockers
Signs
Tachypnoea
Hyperinflated chest
Hyper-resonance on chest percussion
Decreased air entry (sign of severe illness: silent chest)
Wheeze on auscultation
Signs of a severe attack: inability to speak in complete sentences, respiratory rate >25, peak flow 33-50% predicted
Signs of a life-threatening attack: silent chest, confusion, bradycardia, cyanosis, exhaustion
Investigations in chronic asthma
The following investigations and their associated results point to a diagnosis of asthma.
Peak flow: variability >20%
Fractional exhaled nitric oxide (FeNO): >40 ppb in adults or >35 ppb in children
Spirometry: FEV1/FVC <0.7 (obstructive spirometry)
Bronchodilator reversibility tests: Improvement of FEV1 >12% after bronchodilator therapy is diagnostic
Investigations in acute asthma
The following investigations should be ordered more urgently in the context of an acute asthma attack.
ABG: type 2 respiratory failure (low PaO2 and high PaCO2) is a sign of a life-threatening attack.
Routine blood tests (including FBC, CRP): to look for precipitating causes of an asthma attack, such as an infection.
Chest x-ray: to exclude differentials and possibly identify a precipitating infection.
Management of an acute asthma attack
Ensure a patent airway
Ensure oxygen saturations of 94-98%
Nebulisers: Salbutamol, Ipratropium
Steroids: oral Prednisolone or IV Hydrocortisone (if severe)
IV Magnesium Sulphate: if severe
IV aminophylline: if severe and inadequate bronchodilatory response from nebulisers
If the patient does not improve following these measures, intensive care input will be required for consideration of an intensive care admission which may involve invasive ventilation.
Non-pharmacological management of chronic asthma
Non-pharmacological management:
Smoking cessation
Avoidance of precipitating factors (eg. known allergens)
Review inhaler technique
Pharmacological management of chronic asthma (stepwise approach based on BTS Guidelines)
Step 1: short-acting inhaled B2-agonist (eg. Salbutamol)
Step 2: add low-dose inhaled corticosteroid steroid (ICS)
Step 3: add long-acting B2-agonist (eg. Salmeterol). If no benefit, stop this and increase ICS dose; if benefit but inadequate control, continue and increase ICS dose.
Step 4: Trial oral leukotriene receptor antagonist, high-dose steroid, oral B2-agonist
Please note that the NICE guidance on Asthma differs at Step 3.
Asthma mimics
Acid Reflux
Acid reflux is when the acidic contents of the stomach are regurgitated into the oesophagus. This can result in a condition known as gastro-oesophageal reflux disease (GORD).
Risk factors that are associated with acid reflux include: obesity; smoking; alcohol and medications that relax the lower oesophageal sphincter tone (eg. calcium-channel blockers). Symptoms associated with GORD include dry cough, wheeze, shortness of breath, hoarse voice, dental erosion, chest pain. The cough, dyspnoea and wheeze can present like asthma.
Treatment includes over the counter antacids or alginates such as Gaviscon, in addition to proton pump inhibitors (eg. Omeprazole) or H2 blockers (eg. Ranitidine).
Churg-Strauss Syndrome
Churg-Strauss syndrome is a granulomatous vasculitis associated with adult-onset asthma and eosinophilia. Conditions associated with this syndrome include sinusitis, asthma, purpura, and peripheral neuropathy. Patients are pANCA +ve and have raised IgE levels. Treatment includes steroids and immunological agents in treatment-resistant cases such as Rituximab.
Allergic Bronchopulmonary Aspergillosis (ABPA)
ABPA is a type I and III hypersensitivity reaction to Aspergillus fumigatus. There is an association with both cystic fibrosis (up to 25% of patients) and 1% of patients with asthma.
Symptoms include wheeze, cough, dyspnoea, sputum production as well as reduced exercise tolerance.
ABPA patients characteristically react immediately upon exposure of the skin to Aspergillus fumigatus antigens. Raised IgE levels also raises suspicion of the diagnosis, but a proportion of patients do not exhibit this.
Treatment in acute episodes involves a Prednisolone regimen. Itraconazole may also be added to treatment regimes, and bronchodilators can be considered for patients with symptoms of asthma.
SIADH
Syndrome of Inappropriate ADH release (SIADH) is a euvolaemic hyponatraemia caused by inappropriate release of ADH leading to retention of water.
Causes
Causes of SIADH may be broken down into 4 types;
Hypoxia, such as;
Pneumonia
COPD
TB
CNS disease, such as;
Meningitis Stroke Subarachnoid haemorrhage (SAH) Head injury Brain tumours Acute psychosis Malignancy, such as;
Small cell lung cancer Pancreatic cancer Prostate cancer Thymoma Lymphoma Drugs, such as;
Carbamazepine SSRIs Opiates Anti-psychotics Other, such as;
Acute intermittent porphyria Trauma Major abdominal or thoracic surgery Symptomatic HIV Management Management revolves around offloading this excess water:
Fluid restriction (up to 750ml/day) and treat underlying cause ADH antagonists (e.g. tolvaptan, deomeclocycline) Oral sodium and furosemide If there is severe symptomatic hyponatraemia (e.g. confusion, seizures) the patient may require hypertonic saline and fluid restriction. This should be done by experienced staff, ideally in a critical care setting.
Delirium
Delirium or acute confusional state is a common condition affecting predominantly elderly people. It is seen in up to 30% of elderly inpatients.
Clinical features
It can present in a number of different ways, including:
Disorientation Hallucinations Inattention Memory problems Change in mood or personality Disturbed sleep Patients may be very agitated or very sedated and hypo-active.
Causes (Mnemonic: DELIRIUMS)
Common causes of delirium can be remembered using the mnemonic DELIRIUMS:
D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
E - Eyes, ears and emotional
L - Low Output state (MI, ARDS, PE, CHF, COPD)
I - Infection
R - Retention (of urine or stool)
I - Ictal
U - Under-hydration/Under-nutrition
M - Metabolic (Electrolyte imbalance, thyroid, wernickes
(S) - Subdural, Sleep deprivation
Investigations
A full physical examination and infection screen should be carried out in these patients.
Management
Management of delirium is predominantly to treat the underlying cause. Maintaining an environment with good lighting and frequent reassurance is helpful. In extremely agitated patients small doses of haloperidol or olanzapine may be considered.
Parkinson’s
Idiopathic Parkinson’s disease is the prototypical parkinsonian syndrome. It is a sporadic disease of adults >65 years, and presents with asymmetric tremor and bradykinesia. Familial variants, both dominant and recessive, of Parkinson’s disease also exist.
Epidemiology
Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. It affects 0.3% of the UK population.
Core features of Parkinson’s disease
Its core motor features include bradykinesia, asymmetric 3-5Hz “pill-rolling” tremor, and lead pipe rigidity.
The combination of lead pipe rigidity and tremor results in the phenomenon known as cogwheeling, a jerkiness felt when testing a patient’s tone.
These features combine together to give the classical parkinsonian gait and hypomimic facies. Key features of the gait in idiopathic parkinson’s disease include small, shuffling steps, slowness of movement (especially on initiation of movement and on turning), flexed posture, and asymmetric tremor.
Festination describes the tendency to pick up speed as a patient travels in a particular direction – this is also seen.
Postural instability is a late feature of idiopathic Parkinson’s disease, but is seen earlier in less common parkinsonian syndromes.
Non-motor features of idiopathic Parkinson’s disease
There are many non-motor features of idiopathic parkinson’s disease, some of which are common and highly suggestive of this diagnosis over other parkinsonian syndromes.
Autonomic involvement is almost universal with constipation, symptomatic orthostasis (postural hypotension) and erectile dysfunction being common features. This said, very prominent autonomic dysfunction should raise the suspicion of multiple system atrophy.
Olfactory loss is commonly seen in idiopathic parkinson’s disease, but is not seen in many of the parkinson’s plus syndromes. In this regard it represents an underutilised (probably because of lack of confidence with testing olfaction) discriminator.
REM behavioural disorder, in which a patient performs violent reenactments of their dreams during REM phase sleep may be seen in PD, so too may obstructive sleep apnoea.
Finally, psychiatric features including depression and anxiety are more common in the PD population (over and above what would be expected for chronic disease-related psychological issues). Hallucinations may also occur, and in the later stages patients may develop cognitive abnormalities. Early and prominent cognitive dysfunction should raise the suspicion of dementia with lewy bodies.
Pharmacological treatment of idiopathic Parkinson’s disease
Once a secure diagnosis of idiopathic parkinson’s disease has been made, the choice of long term treatment is dependent primarily on the effect that the motor symptoms are having on the patient’s quality of life.
New data from the PD MED study has found that all patients with significant functional impairment should be started on levodopa.
For patients with clinical features of Parkinson’s disease, but in whom there is no functional impairment, the guidance is less clear and patients should be considered for either levodopa, dopamine agonists and monoamine oxidase inhibitors as directed by a specialist.
Adjunctive therapies to help with side effects (including drug-induced dyskinesias) include anticholinergic drugs and the anti-influenza drug amantadine.
Monoamine oxidase inhibitors and COMT inhibitors, which reduce dopamine breakdown may also be used.
Side effects of L-dopa
Levodopa is a medication used most commonly in the treatment of Parkinson’s disease and other movement disorders (e.g. dopa-responsive dystonia).
It should be remembered an absolute failure to respond to 1-1.5g of levodopa daily virtually excludes a diagnosis of idiopathic parkinson disease, though a response to levodopa does not confirm the diagnosis (as many primary parkinsonian syndromes may also respond).
Common side effects include:
Hypotension
Restlessness
Gastrointestinal upset
In rare cases, dopamine excess can result in psychiatric reactions including acute psychosis.
Peripheral side effects are reduced by the co-administration of a peripheral dopa decarboxylase inhibitor, such as carbidopa.
With time, and as the underlying disease progresses, levodopa may become a less effective and patients may report end-of-dose effects, where motor activity progressively declines as the previous dose wears off, and on-off phenomena, which manifest as seemingly random fluctuations in drug effect.
One of the most disabling side effects are the drug-induced dyskinesias, writhing and uncoordinated movements of the limbs associated with poorly organised dopaminergic control of motor activity.
HIV
Primary HIV infection is the period immediately after exposure to virus. It can range from a mild glandular fever to an evolving encephalopathy
Clinical features
Classically, patients present with fever and lymphadenopathy. The second most common feature of infection is a maculopapular rash, found commonly on the upper chest and the third most common feature are mucosal ulcers.Onset of symptoms within 3 weeks of infection that last for longer than 2 weeks or that involve the CNS are associated with a rapid progression to AIDS.
Asymptomatic infection may also occur.
Syphilis must be excluded, along with any other sexually transmitted infections. Contact tracing is also required, along with assessing suitability for cART if a diagnosis of HIV is confirmed.
Neutropenic sepsis
Neutropenic sepsis
Definition
Temperature >38.5 degrees, or two consecutive readings over 38 degrees, in a patient with a neutrophil count of less than 0.5x109 (or expected to fall below this level in the next 48 hours).
Most commonly arises in patients receiving cytotoxic chemotherapy, and is often the only indication of a severe infection.
Risk Factors
Patients at high risk:
Have sustained, significant neutropenia that is expected to last more than 7 days. Are clinically unstable Have an underlying malignancy and are being treated with high-intensity chemo Have significant co-morbidities Pathogens involved Gram-negatives: can all produce extended-spectrum beta-lactams E.coli Klebsiella Enterobacter spp. - can get carbapenem-resistent strains (CRE) Pseudomonas aeruginosa Acinetobacter Gram-positives: Coagulase-negative staphylococci (e.g. staph epidermidis) Staphylococcus aureus (including MRSA) Enterococcus (including VRE) Viridans group strep Strep pneumo Group A streptococci Fungal: Candida Aspergillus Assessment History:
Type and timing of chemo regimen and any other immunosuppressive medication being taken.
Localizing symptoms e.g right lower-quadrant pain associated with neutropenic enterocolitis
Recent infections and antibiotics used
Latent infections are known to reactivate (e.g. TB), sick contacts, blood transfusions
Co-morbidities
Any intravascular devices
Examination:
DRABCDE Systems-based examinations ENT Fundoscopy DO NOT perform DRE until antibiotics given) Investigations:
2 sets of blood cultures Swabs from any indwelling lines Blood tests from complete blood cell count, WCC, inflammatory markers, renal and liver function. CXR Serology and PCR for viruses e.g. CMV Sputum, urine, stool samples, CT scans etc. where clinically indicated. Management DRABCDE approach
If low risk can give oral antibiotics (quinolone + co-amoxiclav)
Features suggesting low risk: Hemodynamically stable Doesn't have acute leukemia No organ failure No soft tissue infection No indwelling lines For most patients, they need empirical IV treatment with piperacillin and tazobactam (tazocin), with added coverage for MRSA or gram-negatives if thought at risk. A macrolide should also be added if diagnosed with pneumonia (to cover atypical organisms)
Daily measures of fever and baseline bloods until the patient is apyrexial and neutrophil count above 0.5x109
When the neutrophil count is normal, has been afebrile for 48 hours and blood tests have normalized, antibiotics can be stopped.
Prophylaxis with a fluoroquinolone can be offered
Hyperthyroidism
Fine tremor
Finger clubbing
Sweating
Pretibial myxoedema
Head and Neck Features
Goitre (depending on cause)
Thyroid bruit
Eye Features Lid retraction Lid lag Exophthalmos (Graves' disease) Periorbital oedema (Graves' disease) Opthalmoplegia (Graves' disease)
Cardiac Features
Atrial fibrillation
High output heat failure (if severe and prolonged
Gastrointestinal Features
Diarrhoea
Neurological Features
Muscle wasting
Proximal weakness
Primary Causes of Hyperthyroidism (i.e. caused by thyroid dysfunction)
Graves disease
Toxic thyroid adenoma
Multinodular goitre
Silent thyroiditis
De Quervain’s thyroiditis (painful goitre)
Radiation
Secondary Causes of Hyperthyroidism (i.e. not caused by thyroid dysfunction)
Amiodarone
Lithium
TSH producing pituitary adenoma
Choriocarcinoma (beta-hCG can activate TSH receptors)
Gestational hyperthyroidism
Pituitary resistance to thyroxine (i.e. failure of negative feedback)
Struma ovarii (ectopic thyroid tissue in ovarian tumours)
Management of Hyperthyroidism - Symptom Relief
Propranolol
Management of Hyperthyroidism - Medical
Either ‘titration-block’ or ‘block and replace’ regimens
Carbimazole
Propylthiouracil
Pregnancy considerations in thyroid disease
Carbimazole – contraindicated in pregnancy
Propylthiouracil – Treatment of choice in first trimester pregnancy/thyroid storm
Radio-iodine indications and contra-indications
Definitive management for multinodular goitre and adenomas
Contraindicated in Graves eye disease because it may worsen symptoms
Thyroidectomy indications and complications
Indicated for recurrence, goitres that obstruct other structures, potential cancer.
May lead to hypoparathyroidism, hypocalcaemia,laryngeal nerve damage and bleeding.
Thyroid Storm Management
IV propranolol
IV digoxin
Propylthiouracil through NG tube followed by Lugol’s iodine 6 hours later
Prednisolone/hydrocortisone
Complications of Hyperthyroidism
Thyroid storm (often precipitated by surgery, trauma or infection)
This may present as high fever, tachycardia, confusion, nausea and severe vomiting
Atrial fibrillation
High output heart failure
Osteopenia/osteoporosis
Upper airway obstruction due to a large goitre
Corneal ulcers/visual loss in Graves’ eye disease
Gastric cancer
Gastric cancer
Epidemiology
Over 7,000 new stomach cancers are diagnosed each year in the UK.
A full time GP is likely to diagnose approximately 1 person with stomach cancer every 3-5 years.
Five year survival is approximately 20%.
Subtypes of gastric cancer
Gastric carcinoma can be split up into two types of cancer:
Intestinal
Associated with H. pylori, tobacco smoking, achlorhydria and chronic gastritis
Commonly on lesser curvature of the stomach
Diffuse
Not associated with H. pylori
Associated with signet cells
Specific forms or precancerous forms of gastric cancer
Menetrier’s disease (pre-cancerous)
There is hyperplasia of the gastric mucosa – the cause is unknown
There are large, gastric folds on the body and stomach associated with increased mucus production
Associated with parietal cell atrophy and hence reduced acid production
Krukenberg tumour
It is known as a ‘signet ring’ tumour, due to the pathological appearance of these cells.
These cells readily secrete mucin and readily metastasize to the ovaries.
Patients often present with abdominal bloating, ascites or pain during intercourse.
The most common primary site is the stomach and the colon, with breast, lung and contralateral ovary being less common.
Sister Mary Joseph nodule
Subcutaneous peri-umbilical metastasis associated with intestinal type of gastric cancer
Linitis plastica
Muscles of the stomach wall become thicker and more rigid. The stomach holds less food as it cannot stretch and transition of food is slower due to decreased relaxation of the stomach
It is sometimes known as leather bottle stomach
Associated with diffuse type of stomach cancer
Risk factors for gastric cancer
Smoking
Pernicious anaemia
H. pylori infection
High alcohol intake (> 6 units per day)
Dietary nitrosamines (found in smoked foods and gastric cancer has higher incidence in Japan)
Atrophic gastritis
Blood group A
Adenomatous polyps
Achlorhydria (as seen in Menetrier’s disease)
Although GORD does not increase the risk of gastric cancer, it does increase the risk of oesophageal adenocarcinoma via Barrett’s oesophagus.
Presentation of gastric cancer Anaemia (iron deficient) Loss of weight Anorexia (early satiety) Recent onset/progression of symptoms Melaena/haematemesis Swallowing difficulty (dysphagia) Indications for Urgent Referral for OGD Current guidelines include urgent referral (within 2 weeks) for patients with:
Dysphagia (at any age)
Aged 55 and over with weight loss AND –
Upper abdominal pain OR reflux OR dyspepsia
Upper abdominal mass consistent with stomach cancer
Indications for Non-Urgent Referral for OGD
Non-urgent (within 6 weeks is required for) –
Haematemesis (at any age)
Aged 55 and over with either –
Treatment-resistant dyspepsia
Upper abdominal pain and low haemoglobin
Raised platelet count AND any of the following –
Nausea, vomiting, reflux, weight loss, dyspepsia epigastric pain
Nausea or vomiting AND any of the following –
Weight loss, reflux, dyspepsia, epigastric pain
Investigations for gastric cancer post-endoscopy
After endoscopy, the tumour must be staged to assess whether it is resectable. A tumour is not resectable if there is extensive local spread or any distant metastases. There are several methods to assess this.
CT chest, abdomen and pelvis is the first tool used. It is important to assess the size of the tumour and is very good at identifying local spread and lymph node spread. It will also identify any visceral metastases to the liver or lungs. It is the first-line investigation after endoscopy.
MRI is very accurate for identifying metastatic spread to the liver and if there is advanced local disease. It is less accurate for early localized spread and hence a CT scan is preferred.
Endoscopic ultrasound is useful to assess whether a tumour is amenable for resection (i.e. ensuring there is no invasion into surrounding structures such as the heart or lungs). It is the most accurate method of local staging of oesophageal cancer. But due to limited penetration of ultrasound waves, will not inform us about metastatic spread.
Treatment
As a general rule of thumb, operative tumours that can be cured tend to be those that have only locally invaded which usually include stages T0 – T3. T4 usually indicates a tumour that has invaded local structures which means that operative intervention is needed. Nodal spread can be treated surgically but depends on the site of spread. Metastatic cancer is usually inoperable.
In gastric cancer, locally invasive disease is managed with partial or total gastrectomy. Moreover, neoadjuvant chemotherapy has been shown to improve outcomes in those undergoing surgery. There is no scope for radiotherapy alone, however when used in combination with chemotherapy (fluorouracil) can be used as a potential curative in a non-surgical candidate.
In advanced cases, palliation can be managed with:
Surgery – To relieve obstruction or haemorrhage
Chemotherapy – Improves quality of life
Prognosis is poor with a 10 year survival rate of 11%
