Pathology 6 Flashcards
(42 cards)
What defines a total anterior circulation infarct TACI
Contralateral hemiplegia or hemiparesis, AND
Contralateral homonymous hemianopia, AND
Higher cerebral dysfunction (e.g. aphasia, neglect)
A TACI involves the anterior AND middle cerebral arteries on the affected side.
A partial anterior circulation infarct (PACI) is defined by:
Two of
Contralateral hemiplegia or hemiparesis, AND
Contralateral homonymous hemianopia, AND
Higher cerebral dysfunction (e.g. aphasia, neglect)
A TACI involves the anterior AND middle cerebral arteries on the affected side.
OR
Higher cerebral dysfunction alone.
A PACI involves the anterior OR middle cerebral artery on the affected side.
A lacunar anterior circulation infarct (LACI) is defined by:
a pure motor stroke, pure sensory stroke, sensorimotor stroke, or ataxic hemiparesis.
There should be NO: visual field defect, higher cerebral dysfunction, or brainstem dysfunction.
A LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.
A posterior circulation infarct (POCI) is defined by:
Cerebellar dysfunction, OR
Conjugate eye movement disorder, OR
Bilateral motor/sensory deficit, OR
Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR
Cortical blindness/isolated hemianopia.
A POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).
Posterior stroke syndromes
Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death.
Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei.
Wallenberg’s syndrome (lateral medullary syndrome) causes ipsilateral Horner’s syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body.
Weber’s syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.
Stroke management
Acute management of ischaemic stroke
Patients should be approached in the DR ABCDE manner.
Airway protection (in patients presenting with depressed consciousness) and aspiration precautions (in patients presenting with swallowing impairment) are very important.
Subsequent stroke management depends on whether the stroke is ischaemic or haemorrhagic. CT head should be performed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke. The most sensitive test for confirming ischaemic infarct is a diffusion weighted MRI. This is generally used if the diagnosis is unclear but is not normally possible in the emergency setting due to logistical challenges.
Alteplase (tissue plasminogen activator) is indicated in patients presenting within 4.5 hours of symptom onset and with no contraindications to thrombolysis (e.g. recent head trauma, GI or intracranial haemorrhage, recent surgery, acceptable BP, platelet count, and INR).
Mechanical Thrombectomy can be performed in patients with anterior circulation strokes within 6 hours of symptom onset, provided that they have a good baseline functional status and lack of significant early infarction on initial CT scan. Mechanical Thrombectomy can also be performed in posterior circulation strokes up to 12 hours after onset.
If hyper-acute treatments are not offered, patients should receive aspirin 300 mg orally once daily for two weeks. If hyper-acute treatments are offered, aspirin is usually started 24 hours after the treatment following a repeat CT Head that excludes any new haemorrhagic stroke.
Stroke investigations (post-acute)
Investigations in the post-acute phase aim to further define the cause of the stroke and to quantify vascular risk factors.
Further investigations to determine the cause of the stroke include, for example:
In ischaemic stroke: carotid ultrasound (to identify critical carotid artery stenosis), CT/MR angiography (to identify intracranial and extracranial stenosis), and echocardiogram (if a cardio-embolic source is suspected). In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.
In haemorrhagic stroke: serum toxicology screen (sympathomimetic drugs e.g. cocaine are a strong risk factor for haemorrhagic stroke).
Further investigations to quantify vascular risk factors include: serum glucose (all patients with stroke should be screened for diabetes with a fasting plasma glucose or oral glucose tolerance test), serum lipids (to check for raised total cholesterol/LDL cholesterol).
Stroke management (chronic)
The key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:
Hypertension: studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.
Antiplatelet therapy: patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
Lipid-lowering therapy: patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
Tobacco: offer smoking cessation support.
Sugar: patients should be screened for diabetes and managed appropriately.
Surgery: patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
Causes of systolic vs diastolic heart failure
Causes of systolic heart failure Ischaemic heart disease Dilated cardiomyopathy Myocarditis Infiltration (e.g. in haemochromatosis or sarcoidosis) Causes of diastolic heart failure Hypertrophic obstructive cardiomyopathy Restrictive cardiomyopathy Cardiac tamponade Constrictive pericarditis
Causes of high output cardiac failure
Causes of high output cardiac failure can be remembered by the mnemonic AAPPTT: Anaemia Arteriovenous malformation Paget's disease Pregnancy Thyrotoxicosis Thiamine deficiency (wet Beri-Beri)
Left heart failure
Left heart failure causes pulmonary congestion (pressure builds up behind the left heart i.e. in the lungs) and systemic hypoperfusion (reduced left heart output).
NB: Sometimes left sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases signs and symptoms of both left and right sided heart failure may be present.
Symptoms caused by pulmonary congestion
Shortness of breath on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Nocturnal cough (± pink frothy sputum)
Signs caused by pulmonary congestion
Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Signs caused by systemic hypoperfusion
Cyanosis
Prolonged capillary refill time
Hypotension
Less common signs of left heart failure
Pulsus alternans (an alternating strong and weak pulse)
S3 gallop rhythm (due to filling of a stiffened ventricle)
Features of functional mitral regurgitation
Right heart failure
Clinical features of right heart failure Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output). Symptoms caused by venous congestion Ankle swelling Weight gain Abdominal distension and discomfort, Anorexia/nausea. Signs caused by venous congestion Raised JVP Pitting ankle/sacral oedema Tender smooth hepatomegaly Ascites Transudative pleural effusions (typically bilateral)
Investigations in heart failure
ECG features
This may be normal or reveal clues as to the underlying cause of the heart failure (e.g. ischaemic changes or arrhythmias).
NT-proBNP interpretation
BNP is released by the ventricles in response to myocardial stretch.
BNP has a high negative predictive value, so if the BNP is not raised the diagnosis of congestive cardiac failure is highly unlikely.
If the BNP is raised, the patient should be referred for trans-thoracic echocardiogram.
If BNP>2000ng/L the patient needs an urgent 2 week referral for specialist assessment and an ECHO.
If BNP 400-2000ng/L the patient should get a 6 week referral for specialist assessment and an ECHO.
Echocardiogram interpretation
Echocardiogram will confirm the presence and degree of ventricular dysfunction.
Ventricular dysfunction is normally measured by the ejection fraction.
<40% = heart failure is reduced ejection fraction
Greater than 40% but raised BNP = Heart failure with preserved ejection fraction
Blood tests
U+Es to assess renal function (for medication) and to look for hyponatraemia
LFTs for hepatic congestion
TFTs to check for hyperthyroidism
Glucose and lipid profile to assess modifiable cardiovascular risk factors
BNP is significantly associated with a diagnosis of heart failuare
Chest Xray findings
Chest x-ray findings in heart failure can be remembered by the ABCDEF mnemonic:
A: Alveolar oedema (with ‘batwing’ perihilar shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio >0.5)
D: upper lobe blood diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure
Heart failure management
ACE-inhibitor and beta-blocker (these improve mortality)
Consider angiotensin receptor blocker (ARB) if intolerant to ACE inhibitors
Consider hydralazine and a nitrate intolerant to ACE-I and ARB.
Loop diuretics such as furosemide or bumetanide improve symptoms (but NOT mortality)
If symptoms persist and NYHA Class 3 or 4 consider:
Aldosterone antagonists such as spironolactone or eplerenone. These drugs also improve mortality.
Hydralazine and a nitrate for Afro-Caribbean patients
Ivabradine if in sinus rhythm and impaired ejection fraction
Angiotensin receptor blocker
Digoxin - useful in those with AF. This worsens mortality but improves morbidity.
Surgical/device management options
Cardiac resynchronisation therapy
ICDs are indicated if the following criteria are fulfilled:
QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
QRS interval 120-149ms without LBBB, NYHA class I-III
QRS interval 120-149ms with LBBB, NYHA class I
Initial Management of acute heart failure (pulmonary oedema)
Sit the patient up
Oxygen therapy (aiming saturations >94% in normal circumstances)
IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
Advanced management of acute heart failure (pulmonary oedema)
The following usually occurs in a high dependency or ITU setting.
CPAP - reduces hypoxia and may help push fluid out of alveoli
Intubation and ventilation
Furosemide infusion - continuous IV furosemide given over 24 hours to maximise diuresis
Dopamine infusion - Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility.
Intra-aortic balloon pump - if the patient is in cardiogenic shock
Ultrafiltration - If resistant to or contraindicated diuretics
Note that GTN infusion is no longer routinely used in acute heart failure
Adverse effects of heart failure medications
Common adverse effects for different medications are listed below
Beta blockers: Bradycardia, hypotension, fatigue, dizziness
ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema
Spironolactone: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido
Furosemide: Hypotension, hypoatraemia/kalaemia,
Hydralazine/nitrate: Headache, palpitation, flushing
Digoxin: Dizziness, blurred vision, GI disturbances
Ascites and Saag
Ascites describes the accumulation of fluid within the peritoneal cavity. It may be seen in patients with cirrhosis; though the mechanism is complex and not fully understood, it is thought to involve portal hypertension causing increased hydrostatic pressure leading to transudation of fluid.
Diagnosis
There are a number of different causes of ascites. Though the cause is often indicated by the clinical picture, an ascitic tap can be performed to tell us more about the content of the ascitic fluid.
Serum ascites albumin gradient (SAAG)calculation
The serum ascites albumin gradient (SAAG) can help to determine the cause of ascites.
It is calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration.
Causes of a high SAAG
Cirrhosis
Heart failure
Budd Chiari syndrome
Constrictive pericarditis
Hepatic failure
A high SAAG (>1.1g/dL) suggests that the cause of the ascites is due to raised portal pressure. Raised hydrostatic pressure forces water into the peritoneal cavity whilst albumin remains within the vessels, thus resulting in a higher difference in the albumin concentration between the serum and ascitic fluid.
Causes of a low SAAG (<1.1g/dL)
Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome
COPD signs and symptoms
Chronic obstructive pulmonary disease (COPD) is characterised by irreversible obstruction of the airways. It comprises both chronic bronchitis, which involves hypertrophy and hyperplasia of the mucus glands in the bronchi, and emphysema, which involves enlargement of air spaces and destruction of alveolar walls. Symptoms Symptoms: Productive cough Wheeze Dyspnoea Reduced exercise tolerance Signs Accessory muscle use for respiration Tachypnoea Hyperinflation Reduction of the cricosternal distance Reduced chest expansion Hyper-resonant percussion Decreased/quiet breath sounds Wheeze Cyanosis Cor pulmonale (signs of right heart failure)
COPD investigations
Spirometry: FEV1 <80% of predicted; FEV1/FVC <0.7
Stage 1 Mild FEV1 ≥ 80% predicted
Stage 2 Moderate FEV1 50-79% of predicted
Stage 3 Severe FEV1 30-49% of predicted
Stage 4 Very Severe FEV1 <30% of predicted
Bloods: FBC (raised PCV; polycythaemia), ABG (reduced PaO2 +/- raised PaCO2 or type 2 respiratory failure)
ECG: P-pulmonale (right atrial hypertrophy) and right ventricular hypertrophy, if there is cor pulmonale
Chest x-ray:
Hyperinflated chest (>6 anterior ribs)
Bullae
Decreased peripheral vascular markings
Flattened hemidiaphragms
COPD management
Management of an acute exacerbation
Ensure a patent airway
Ensure oxygen saturations of 88-92%
Nebulisers: Salbutamol, Ipratropium
Steroids: oral Prednisolone or IV Hydrocortisone (if severe)
Antibiotics if any evidence of infection (fever or raised inflammatory markers)
If the patient does not improve following these measures, ITU input will be required and they may need to be started on non-invasive ventilation such as BiPAP. Further deterioration is an indication for invasive ventilation.
Non-pharmacological management of chronic COPD
Stop smoking
Nutritional support
Flu vaccinations
Pulmonary rehabilitation
Pharmacological management of chronic COPD
Starting with a Short acting B2 agonist (SABA)/ short acting muscarinic antagonist (SAMA). These are continued as the patient goes up the management steps.
Step 2
For patients with persistent exacerbations but no asthmatic features (e.g. asthma/atopy history, raised eosinophils, reduced FEV1 or diurnal variations in peak flow) or evidence of steroid responsiveness then add a long acting B2 agonist (LABA) AND a long acting muscarinic antagonist (LAMA).
For patients with persistent exacerbations with asthmatic features or evidence of steroid responsiveness increase management to long acting B2 agonist (LABA) and inhaled corticosteroid in combination (ICS).
Step 3
If patients on a LABA + LAMA combination are still getting daily symptoms that affect their activities of daily living then a 3 month trial of LAMA + LABA + ICS should be considered. If this does not work then it should be reverted back to LABA + LAMA.
If any patient on Step 2 is getting more than one severe or two moderate exacerbations in a year then LAMA + LABA + ICS should be started.
Step 4
If patients are still symptomatic consider specialist referral.
Indications for Long Term Oxygen Therapy
Long Term Oxygen Therapy (LTOT): A trial showed that maintaining oxygen above 8kPa for at least 15 hours a day improved mortality rates.
NICE guidelines state that LTOT can be prescribed for patients who:
Have a PaO2 <7.3kPa on two readings more than 3 weeks apart, and are non-smokers (but not absolutely contraindicated in smokers).
Or have a PaO2 of 7.3-8kPa alongside one of the following: nocturnal hypoxia, polycythemia, peripheral oedema and pulmonary hypertension.
LTOT can also be prescribed for patients with terminal illness.
Indications for surgery in COPD
Patients with severe COPD who remain breathless despite maximal medical therapy should be considered for lung volume reduction surgery if:
They have upper lobe predominant emphysema
FEV1 >20% predicted
PaCO2 below 7.3 kPa
TlCO above 20% predicted.
Retinal detachment
Retinal detachment refers to a separation of the retina from the retinal pigment epithelium (RPE).
There are different types of retinal detachment, but the most common is rhegmatogenous retinal detachment which is commonly caused by trauma.
Clinical features
Patients may present painlessly with floaters, photopsia, reduced visual acuity and visual field impairment depending on the area of detachment. The danger is that if the detachment progresses to the macula, sight may be irreparably lost.
Management
There are various surgical and non-surgical treatments available depending on the extent of the detachment. These include laser therapy, cryotherapy, vitrectomy, scleral buckling and pneumatic retinopexy.
Amaurosis fugax
Amaurosis fugax can present with a so called curtain but normally resolves and would not be associated with flashes.
5%
Enteric arthropathy
Patterns of joint disease in enteric arthropathy
In enteropathic arthritis, joint involvement may present before, during or after a diagnosis of IBD. There are various patterns of joint disease.
Axial arthritis:
Gradual onset of lower back pain and stiffness, worse in the morning, improves with exercise
Peripheral arthritis of IBD:
Asymmetric, oligoarticular arthritis, predominantly of the lower limbs
Often transient and migratory joint inflammation
Enthesopathy of IBD:
Severe localised pain in specific areas of tendon insertion
Achilles tendonopathy, patellar tendonopathy, plantar fasciitis
Peripheral arthritis of IBD:
Asymmetric, oligoarticular arthritis, predominantly of the lower limbs
Often transient and migratory joint inflammation
Extra-articular manifestations of inflammatory bowel disease
These may useful clues in the vignette
Bowel symptoms to include abdominal pain, diarrhoea, weight loss, blood/ mucus in faeces
Pyoderma gangrenosum and erythema nodosum
Aphthous ulcers in the mouth
Anterior uveitis
Systemic symptoms including fever in a flare of disease
Blood tests in enteric arthropathy
Inflammatory markers will likely be raised due to inflammation.
Seronegative spondylarthropathies should all be rheumatoid factor negative.
Seronegative spondylarthropathies are all associated with HLA-B27. A positive test can support the diagnosis, but not confirm or exclude it.
Radiology in enteric arthropathy
Affected joints do not generally show changes on X-ray.
Pelvic X-rays may show sacroiliitis, and spinal X-rays may show squaring of vertebrae and syndesmophytes creating a “bamboo spine”, as in ankylosing spondylitis
Hepatitis
Hepatitis means inflammation of the liver and may be caused by a range of infectious and non-infectious etiologies.
All infectious hepatitis cases are notifiable diseases in the UK.
Most common causes of viral hepatitis in the UK are hepatitis A, B and C viruses. These can all cause acute disease, but HBV and HCV can also cause chronic infection. The latter can lead to liver fibrosis, and hepatocellular carcinoma.
Other causes of viral hepatitis include:
Hepatitis D Virus (can cause chronic hepatitis)
Hepatitis E Virus
CMV
EBV
Adenovirus
Clinical Features
Malaise and fatigue
Nausea and vomiting
Right upper quadrant pain
diarrhoea (may have pale stools and dark urine)
Jaundice
Hepatomegaly
Splenomegaly and lymphadenopathy
Liver failure: characterized by hepatic encephalopathy, jaundice, ascites and abnormal clotting.
Other causes of acute hepatitis include drugs, toxins, alcohol, EBV, CMV, hepatitis E, leptospirosis, and malaria.
Hepatitis A
Hepatitis A (Virus type and transmission route)
RNA picornavirus, transmitted by fecal-oral route (occasionally through food sources or through anal sex)
Epidemiology of Hepatitis A
Prevalence is high in developing countries.
Increasing age is the only real determinant of disease severity, with the greatest morbidity and mortality in those over 50 years old.
Travelers and those at risk can be offered immunization
Presentation of Hepatitis A
Flu-like symptoms followed by jaundice, pale stools (in some), dark urine and abdominal pain.
Incubation period of 2-6 weeks
Complete recovery can take up to 6 months.
Investigations of Hepatitis A
IgM and IgG antibodies to HAV.
Management of Hepatitis A
Mangement is largely supportive
Hepatitis B
Hepatitis B Virus type
dsDNA virus of Hepadnaviridae family
Hepatitis B Virus Epidemiology
Most common cause of hepatitis globally
High prevalence regions include sub-Saharan Africa, Asia and the Pacific Islands.
Decline of disease in children and adolescents in the UK is due to routine vaccination
- Incubation period usually 60-90 days.
Hepatitis B Virus transmission
Transmission is via infected blood or body fluids
Vaginal/anal intercourse
Transfusion
Vertical transmission (in 90% of pregnancies where the mother is HBeAg positive, and 10% where this is negative).
In developing countries, infection is mostly in childhood through vertical or horizontal transmission. In areas of low endemicity (such as the UK), infections are mostly acquired in adulthood.
Hepatitis B Infection
Only 5% of children have jaundice and severe symptoms, but the majority cannot clear the infection and develop chronic disease.
30-50% of adults experience jaundice, fever, malaise, and darkening of urine and lightening of stool. Some develop fulminant liver failure with decompensation (ascites, encephalopathy etc.). Risk of developing chronic disease is low (<5%).
Serology of Hepatitis B
HBsAg is detected 3-5 weeks after infection. If present for >6 months, this defines carrier status (5-10% of infections).
In carriers, HBeAg-positive patients are the most infectious. If HBeAg-negative (and anti-HBe-antibody positive), they have lower infectivity.
Antibodies to HBsAg (anti-HBs) indicate previous vaccination
Antibodies to hep B core antigen (anti-HBc) indicate past infection.
Patients with chronic infection who are HBeAg -ve may get immune escape phase when the virus mutates despite anti-HBe antibodies being present. These patients are the main pool for the spread in the UK, and so all chronically infectious patients need yearly screens to identify this.
Patients with acute infection have raised IgM to HBcAg, while this is negative in chronic infection.
Management of Hepatitis B
Only adults who are HBsAg-positive, have compensated liver disease, are pregnant or of young age may be referred for treatment
Peginterferon alfa-2a is the first line, with tenofovir and entecavir as second-line alternatives.
Hepatitis C
Hepatitis C Virus type
RNA virus of the Flaviviridae family, with 6 major genetic types (genotypes 1 and 3 are most common in the UK, and genotype 1 is associated with longer treatment and worse prognosis).
Hepatitis C Virus transmission
Transmitted via exchange of blood and bodily fluids:
Intravenous drug use
Blood transfusion
Haemodialysis (rare in the UK)
Sexual transmission (less than 1% per year of relationship, but rate higher if co-infected with HIV)
Needlestick injuries in healthcare facilities - 3% risk of transmission.
Perinatal infection from infected mother.
Incubation period of 6-9 weeks.
Acute and Chronic Hepatitis C Infection features
Most infections are asymptomatic, and only 15-25% clear the virus. 75% go on to develop chronic infection
Patients with chronic infection have persistently high LFTs, and cirrhosis develops in 20-30%.
1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure.
Investigations of Hepatitis C
Anti-HCV serology - 90% are positive 3 months after infection but it may take many months to become positive for some.
HCV RNA - if positive for more than two months then need to be treated.
Management of Hepatitis C
Symptomatic treatment in the early stages of the disease
Drug therapy should be considered for all patients and depends on the genotype of the virus. Nucleoside analogs are generally preferred e.g. Sofosbuvir and often lead to undetectable viral loads
Antivirals of proven benefit in basically every patient irrespective of the amount of cirrhosis and fibrosis
Manage any underlying cirrhosis
Antigen screen result for someone hep B vaccinated
HbSAg negative, Anti-HbS positive, Anti-HbC negative result for someone hep B vaccinated
Twin to twin transfusion syndrome
TTTS is a serious condition that can occur in 10-15% of twins sharing one placenta (identical)
Aetiology
Twin to twin transfusion syndrome is caused by anastomoses of umbilical vessels between the two foetuses in the placenta of monochorionic twins.
Risks
Both foetuses are at risk of developing heart failure and hydrops. The donor suffers high output cardiac failure as a consequence of severe anaemia and the recipient suffers fluid overload.
Management
Untreated, TTTS has a high mortality rate for both twins, with the donor more likely to survive. Treatment is now available at specialist centres and is by laser transection of the problem vessels in-utero.
