Week 3 Flashcards
Uses of Thiazides vs Loop diuretics? (2)
Eg indapamide vs furosemide
Thiazides relieve oedema from chronic heart failure and lower doses reduces blood pressure.
Loop diuretics are used in pulmonary oedema due to left ventricular failure and chronic heart failure.
Posterior stroke syndromes (4)
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-vertigo, nystagmus, dysphagia, hiccups, ipsilateral clumsiness/slouch, (Wallenberg) ipsilateral Horner’s sweating, contralateral lack of pain and temp.
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.
Acute treatment of stroke (7)
Acute management of ischaemic stroke
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.
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.
Chronic stroke management (5/6)
Stroke management (chronic)
The key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:
Hypertension: 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, Rivaroxaban or Apixiban is initiated 2 weeks post-stroke.
Lipid-lowering therapy: patients should be prescribed high dose atorvastatin 20-80 mg once nightly
Tobacco, Sugar and Surgery
Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
Threatened miscarriage (2) When and what signs?
Threatened miscarriage typically occurs between 6-9 weeks.
There would be painless bleeding and cervical os would be closed.
Complete miscarriage, signs (2)
Complete miscarriage is when the products of conception have finished being expelled. There would be cramping abdominal pain or period pain due to the uterus contracting to empty and light bleeding, which may continue for several days. Cervical os would be closed.
Trophoblastic disease - when, signs, confirmation (3)
Trophoblastic disease is when trophoblast cells grow inside the uterus after conception. It classically presents after 14 weeks of pregnancy and symptoms include vaginal bleeding and vomiting due to the high levels of human chorionic gonodotrophin (b-HCG), which has a thyroid-stimulating hormone-like activity. The uterus is larger for dates and the ultrasound classically shows a “snowstorm” appearance with hyperechogeneity reflecting molar disease. The diagnosis is confirmed with histological study of the products of conception.
Placental abruption, signs, risk factors (3)
Placental abruption is separation of the placenta from the uterine wall and it presents in third trimester with sudden abdominal pain and vaginal bleeding, though, vaginal bleeding can be absent in 20% of cases. Risk factors include maternal hypertension smoking, and previous history of placental abruption. It is an emergency resulting in significant maternal haemorrhage causing significant maternal and foetal mortality and morbidity.
Giant cell arteritis, presentation, complications, investigations, management (7)
Giant Cell Arteritis
Giant cell arteritis, also known as temporal arteritis, is where the arteries, particularly those at the side of the head (the temples), become inflamed.
Presentation:
Temporal headache
Jaw claudication (pain on chewing food)
Amaurosis fugax (transient monocular blindness, often described as a dark curtain descending vertically)
Thickened, tender temporal artery on examination. It may be pulseless
Scalp tenderness
The onset can be acute or insidious. In addition, GCA and polymyalgia rheumatica (PMR) often occur together, and so symmetrical proximal muscle weakness and an oligoarthritis may occur.
Complications
Permanent monocular blindness
Stroke
Investigations
ESR, FBC and LFTS. Patients often have a normochromic normocytic anaemia, and about ⅓ have mildly abnormal LFTs.
The definitive investigation is temporal artery biopsy. If negative on the side with symptoms, the asymptomatic side may also be biopsied.
3-5cm of the artery should be biopsied due to skip lesions. Might also do angiography.
Management
60mg OD prednisolone to prevent blindness and stroke.
Once symptoms resolve, prednisolone is gradually tapered, usually over a long period of 1-2 years, because relapses can occur when tapering too quickly.
Sparing agents may be used to lower the dose such as azathioprine.
Due to the prolonged high corticosteroid dose bisphosphonates and proton pump inhibitors may be warranted to prevent osteoporosis and gastric ulcers.
Low dose aspirin is usually also given to further reduce the risk of stroke and blindness.
Dilated cardiomyopathy: age, causes, signs, investigations (4)
Epidemiology of Dilated Cardiomyopathy
Age between 30-60
Causes of Dilated Cardiomyopathy
Post-myocardial infarction ischemia
Hypertensive
Genetic and congenital
Toxin-related - excessive alcohol - > myocardial dysfunction, Cocaine -> ischaemia, anthracycline chemotherapy Doxorubicin, Cyclophosphamide, antiretroviral Zidovudine, Chloroquine and Clozapine.
Infiltrative - haemochromatosis, amyloidosis and sarcoidosis
Peripartum
Thyrotoxicosis
Infectious- HIV, Lyme disease and Chagas disease
Takotsubo cardiomyopathy
Clinical features of Dilated Cardiomyopathy
poor ventricular contraction - ejection fraction < 40%
Exertional + night time + lying down dyspnoea
Peripheral oedema
Arrhythmia (atrial fibrillation or ventricular tachycardia)
Conduction disturbances
Sudden cardiac death.
Displaced apex beat
S3 gallop rhythm (rapid ventricular filling)
Murmur of mitral regurgitation (due to displacement of the valve leaflets)
Signs of heart failure (such as oedema, hepatomegaly, ascites, raised JVP).
Investigations of Dilated Cardiomyopathy
ECG may show poor R-wave progression. Echocardiography is diagnostic.
Hypertrophic cardiomyopathy cause, consequences, symptoms, signs, diagnostic (7)
Hypertrophic cardiomyopathy
The condition arises as a result of a mutation in one of several myocyte sarcomere genes such as myosin and troponin, causing myocyte hypertrophy and disarray.
Inheritance is autosomal dominant, however half of cases are as a result of sporadic mutations where the parents do not carry a disease-causing mutation.
Consequences Left ventricular outflow tract obstruction (LVOTO) Diastolic dysfunction Ischaemia Mitral regurgitation
Symptoms of Hypertrophic cardiomyopathy
Many patients have little to no symptoms and the initial presenting condition can sometimes be presyncope, syncope or sudden death. Others may experience exertional dyspnoea, fatigue or chest pain which may be anginal or atypical.
Signs of Hypertrophic cardiomyopathy "Jerky" pulse Double apex beat Harsh ejection systolic murmur Apical thrill ECG findings of Hypertrophic cardiomyopathy
ECG typically demonstrates:
Abnormal Q waves
Deeply inverted T waves
Left ventricular hypertrophy
Ecocardiography diagnoses.
Restrictive cardiomyopathy, causes, features, diagnostic (4)
Restrictive cardiomyopathy involves non-dilated non-hypertrophied ventricles with impaired ventricular filling.
Causes of restrictive cardiomyopathy Familial non-infiltrative cardiomyopathy Amyloidosis Sarcoidosis Gaucher disease Hurler syndrome Fatty infiltration Haemochromatosis Fabry diseas Glycogen storage disorders Diabetic cardiomyopathy Scleroderma Radiation Chemotherapy
Clinical features of restrictive cardiomyopathy
Presentation is often that of heart failure or sometimes similar to that of constrictive pericarditis. Up to 75% of patients will have associated atrial fibrillation.
Diagnosis is usually based on Echocardiogram (which shows thickened ventricular walls and valves) and cardiac MR (which is useful for distinguishing between restrictive cardiomyopathy and constrictive pericarditis).
Retinal detachment, common type, features, risk, management (5)
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
Laser therapy, cryotherapy, vitrectomy, scleral buckling and pneumatic retinopexy.
Ascites, causes of high SAAG, low SAAG, management (5)
Ascites describes the accumulation of fluid within the peritoneal cavity. Involves portal hypertension causing increased hydrostatic pressure leading to transudation of fluid.
Diagnosis
An ascitic tap -> serum ascites albumin gradient (SAAG)calculation. 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
Management
Address the underlying cause
Salt restricted diet
Fluid restriction
Spironolactone
furosemide may be needed if spironolactone is insufficient.
Paracentesis, whereby the fluid is drained from the abdomen over a few
