cardiology Flashcards
Nishimura et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary. Circulation. 2014;129: 2440-2492
https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000000029
causes of broad QRS
Irregular irregular broad QRS
polymorphic ventricular tachycardia -Torsades des pontes .
AF with bundle branch block in which case there would be absent p waves .
AF with aberrant conduction pathway like in wolff parkinson white syndrome .-in which case AV nodal blocking agents /vasalva maneuver are contraindicated .
types of WPW syndrome
Treated with syn.DC cardioversion if unstable
Procainamide if stable
left sided pathway would create a Right axis deviation which is Type A
Right sided pathwy which is Type B and would create left axid deviation
Difference between early dumping syndrome and late dumping syndrome .
Both are complications of bariatric surgery
Early dumping occurs few hrs after eating resulting in vomiting/nausea and diarrhea
Late dumping results in post prandial hypoglycemia .
Both are compliactions of Rou-en-y and bariatric surgery.
Difference between chylothorax and pseudochylothorax
chylothorax -accumulation of triglycerides and chylomicons - causes include damaged thoarcic duct during surgery .
Important - chylothorax can occur in malignant melanoma .
pseudochylothorax - accumulation of cholesterol -causes include long standing fibrotic pleura
The prone position
Use of Nitric oxide
Use of Low tidal volume for ventilation
The three are good ,however only use of low tidal volume has motality benefits as published at the cochrane review .
Attributes of HSV Encephalitis
MRI features personalty change confusion seizures treated with 14 to 21 days of acyclovir IV
HSV meningitis
photophobia /nuchal rigidity /GCS remains 15
management is supportive
Autoimmune thrombocytopenic purpura like ITP
may be a manifestation of CLL
Drug causes of diarrhea
metformin via bile salt malabsorption
sertraline - via microscopic colitis with lymphocytic infiltration , less so for statins
calcium channel blockers are associated with diarrhea
Wellens syndrome
critical stenosis of the LAD
Seen as deep inversion of the T waves in v2 and v3
treat as stemi with urgent revascularization .
NIV indications
COPD with respiratory acidosis pH 7.25-7.35*
type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
cardiogenic pulmonary oedema unresponsive to CPAP
weaning from tracheal intubation
NIV bipap recommendations
Recommended initial settings for bi-level pressure support in COPD
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O back up rate: 15 breaths/min back up inspiration:expiration ratio: 1:3
Superficial siderosis
Accumulation of iron on brain neurons from
traumatic brain injuries
neurosurgery
presents with
profound bilateral hearing loss
anosmia
dementia
ataxia
no cure
lipid iron chelators may have some promise .
gradual progressive neurologic deterioration.
pyramidal signs (eg, spastic paraparesis, quadriparesis, etc.),
Even with successful surgical resection of the causative lesion (when that is identified), significant functional recovery cannot be anticipated.
Japanese encephalitis virus
Is transmitted by mosquitos
Confusion in a returning traveller from Asia- think JEV .
idiopathic pulmonary fibrosis
HRCT-for determining aetiology
FVC- for monitoring progression
Carbon monoxide transfer factor -for determining PROGNOSIS
investigating thyrotoxicosis
TSH R AB (TRAB)-if positive confirms graves
if negative -radonucleide uptake scan- diffuse uptake -Graves
poor uptake -thyroiditis
uneven uptake -prescence of nodules
Treatment of graves -carbimazole in the short term until surgery and radiotherapy done or carbimazole continued for the long term if radiotherapy and surgery are no options .
Features suspicious of malignancy -uss guided fine needle aspiration
TRALI
Associated with marked hypotension
No cardiomegaly
occurs few hrs after transfusion
most seen with transfusion of plasma products and less so with packed red cells
Pathergy
occurs in behcet
behcet is associated with HLA B51
Glucocorticoid induced osteoporosis
Osteoporosis: glucocorticoid-induced
We know that one of the most important risk factors for osteoporosis is the use of corticosteroids. As these drugs are so widely used in clinical practice it is important we manage this risk appropriately.
The most widely followed guidelines are based around the 2002 Royal College of Physicians (RCP) ‘Glucocorticoid-induced osteoporosis: A concise guide to prevention and treatment’.
The risk of osteoporosis is thought to rise significantly once a patient is taking the equivalent of prednisolone 7.5mg a day for 3 or more months. It is important to note that we should manage patients in an anticipatory, i.e. if it likely that the patient will have to take steroids for at least 3 months then we should start bone protection straight away, rather than waiting until 3 months has elapsed. A good example is a patient with newly diagnosed polymyalgia rheumatica. As it is very likely they will be on a significant dose of prednisolone for greater than 3 months bone protection should be commenced immediately.
Management of patients at risk of corticosteroid-induced osteoporosis
The RCP guidelines essentially divide patients into two groups.
- Patients over the age of 65 years or those who’ve previously had a fragility fracture should be offered bone protection.
- Patients under the age of 65 years should be offered a bone density scan, with further management dependent:
T score Management
Greater than 0 Reassure
Between 0 and -1.5 Repeat bone density scan in 1-3 years
Less than -1.5 Offer bone protection
The first-line treatment is alendronate. Patients should also be calcium and vitamin D replete.
Ascites
Ascites
The causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L as per the table below:
SAAG > 11g/L SAAG <11g/L
Indicates portal hypertension
Cirrhosis Alcoholic hepatitis Cardiac ascites Mixed ascites Massive liver metastases Fulminant hepatic failure Budd-Chiari syndrome Portal vein thrombosis Veno-occlusive disease Myxoedema Fatty liver of pregnancy Peritoneal carcinomatosis Tuberculous peritonitis Pancreatic ascites Bowel obstruction Biliary ascites Postoperative lymphatic leak Serositis in connective tissue diseases
Management
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone
loop diuretics are often added. Some authorities only add loop diuretics in patients who don't respond to aldosterone agonists whereas other authorities suggest starting both types of diuretic on the first presentation of ascites
drainage if tense ascites (therapeutic abdominal paracentesis)
large-volume paracentesis for the treatment of ascites requires albumin 'cover'. Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality
paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved'
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
Tips as a treatment for portal venous hypertension which presents with splenomegaly as a consequence .
Overdose and management
Severe iron toxicity presents with liver failure, gastrointestinal caustic damage and coagulopathy with raised APTT. Early hyperglycaemia and extensively haemolysed samples may also indicate significant iron burden
Important for meLess important
Iron is a surprisingly toxic drug. When taken in overdose symptoms may be expected to be seen at ingestions of 20mg/kg. 200mg/kg can be expected to be fatal. Symptoms of direct corrosion on the gastrointestinal tract may be seen within six hours of ingestion with abdominal pain, vomiting, diarrhoea and GI bleeding. Stool and vomitus may be black or grey unless frank bleeding predominates. During this interval, a hallmark of iron toxicity is a raised blood glucose; only a few drugs may cause this in overdose. Hypoglycaemia occurs later in presentation due to liver failure. Other early features may include a neutrophil leucocytosis and significant haemolysis of samples due to the high plasma iron burden. Arterial blood gases will show a significant metabolic acidosis with a high anion gap. Lactate may be elevated but not sufficiently to explain the anion gap. Coagulopathy develops rapidly but the APTT tends to be prolonged in iron toxicity compared to the prolongation of prothrombin time in a paracetamol poisoning. In the ensuing hours, iron deposition within the myocardium, brain and liver can be expected to cause rapid cardiac failure, encephalopathy and hepatocellular necrosis with liver failure respectively. Renal failure develops due to hypovolaemia and acute tubular necrosis. Unless treated, death may result from haemorrhagic volume loss or from hepatic failure, although in significant overdose, early death results from respiratory failure due to coma. Treatment for iron overdose is with decontamination of the bowel, including whole bowel irrigation if needed and chelation therapy with desferrioxamine.
Although paracetamol toxicity can be expected to cause fulminant hepatic failure with renal failure and coagulopathy, the INR would be expected to be significantly deranged if this was the culpable drug given the extent of other organ damage. Also hypoglycaemia would be expected due to liver failure.
Aspirin, when taken in significant overdose, causes a characteristic constellation of symptoms including metabolic acidosis (although alkalosis may be seen at lower dose intoxications), convulsions, tinnitus, hyperpyrexia and pulmonary oedema. Often ventricular arrhythmia occurs due to metabolic acidosis and intracellular anaerobic respiration. Rarely coagulopathy develops but usually in association with disseminated intravascular coagulation which is not the case here. Aspirin overdoses may present with hyperglycaemia however and along with iron and aminophylline, these agents should be considered when unexplained hyperglycaemia is seen.
Ibuprofen and other non-steroidals are of low toxicity unless taken in massive overdose. Gastrointestinal upset and occasional GI haemorrhaging may be seen but liver failure and coagulopathy is rare. In massive overdose, central nervous depression with cerebellar signs and global electrolyte imbalances may be seen with blood dyscrasias. Multi-organ failure may develop but individual organ dysfunction is less likely.
Venlafaxine, a noradrenaline and serotonin modulator, may cause serotonin syndrome and sympathomimetic symptoms, including arrhythmia, hyperpyrexia and respiratory failure. Hepatitis is rare.
Overdose and poisoning: management
The table below outlines the main management for common overdoses:
Toxin Treatment
Paracetamol Management
activated charcoal if ingested < 1 hour ago N-acetylcysteine (NAC) liver transplantation
Salicylate Management
urinary alkalinization is now rarely used - it is contraindicated in cerebral and pulmonary oedema with most units now proceeding straight to haemodialysis in cases of severe poisoning haemodialysis
Opioid/opiates Naloxone
Benzodiazepines Flumazenil
The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.
Tricyclic antidepressants Management
IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias dialysis is ineffective in removing tricyclics
Lithium Management
mild-moderate toxicity may respond to volume resuscitation with normal saline haemodialysis may be needed in severe toxicity sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion
Warfarin Vitamin K, prothrombin complex
Heparin Protamine sulphate
Beta-blockers Management
if bradycardic then atropine in resistant cases glucagon may be used
Ethylene glycol Management has changed in recent times
ethanol has been used for many years works by competing with ethylene glycol for the enzyme alcohol dehydrogenase this limits the formation of toxic metabolites (e.g. Glycoaldehyde and glycolic acid) which are responsible for the haemodynamic/metabolic features of poisoning fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol haemodialysis also has a role in refractory cases
Methanol poisoning Management
fomepizole or ethanol haemodialysis
Organophosphate insecticides Management
atropine the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit
Digoxin Digoxin-specific antibody fragments
Iron Desferrioxamine, a chelating agent
Lead Dimercaprol, calcium edetate
Carbon monoxide Management
100% oxygen hyperbaric oxygen
Cyanide Hydroxocobalamin; also combination of amyl nitrite, sodium nitrite, and sodium thiosulfate
Miller fisher variant of Guillian Barre syndrome .
A 67 year-old woman presents to hospital after a collapse at home. One week earlier she had seen her own doctor after feeling generally unwell with fever, myalgia, and coryza. These symptoms were attributed to a viral infection and have now resolved. However, for the past few days she has felt unsteady on her feet and has had to hold on to the furniture whilst walking around the house. For the last two days in particular she has also noticed that her vision has deteriorated, and she has been seeing double. Today she tried to hold onto the sofa whilst walking around the room, but misjudged the distance and lost her grip, causing her to fall to the floor. Her daughter who is also present adds that she feels her mothers speech is slurred compared to normal, and has been so for the past three days.
Her past medical history includes hypertension, hypothyroidism, type 2 diabetes, hyperlipidaemia, angina, and recurrent urinary tract infection. She takes ramipril, amlodipine, doxazosin, laevoythyroxine, metformin, gliclazide, simvastatin, atenolol, nicorandil, and nitrofurantoin. She does not smoke but admits to enjoying a glass of sherry on most nights. Usually she is independently mobile, without aids. She lives on her own and is self-caring.
On examination, there are some bruises on the left shoulder where she fell, but no suggestion of any fracture. Observations are normal and she is afebrile. Cardiovascular, respiratory, and abdominal examination is unremarkable. She is fully alert and oriented. Pupils are equal and reactive to light. Eye movements are grossly impaired in all directions. There is no facial asymmetry. Muscle power is normal in all limbs, but finger-nose pointing is impaired and she is unable to walk in a straight line. Reflexes are unobtainable. Sensation is normal.
What is the most likely diagnosis?
Wernickes encephalopathy11% Viral cerebellitis20% Myasthenia gravis5% Miller Fisher syndrome51% Posterior circulation stroke13%
There has been a subacute deterioration in global cerebellar function, as suggested by gait ataxia, bilateral upper limb dysmetria, and dysarthria, progressing over a period of days. There is also complete ophthalmoplegia, and absence of reflexes. This combination of features occurring after a recent viral infection suggests a diagnosis of the Miller Fisher variant of Guillain-Barré syndrome. One might also expect to find descending weakness, which was not present in this case. Confirmation of the diagnosis is by lumbar puncture which demonstrates raised protein with normal cell count, and positive serum anti-GQ1b antibodies. Treatment is as for Guillain-Barré syndrome, with supportive care and intravenous immunoglobulin or plasmapheresis.
Wernickes encephalopathy presents with ataxia and ophthalmoplegia but also confusion, and typically occurs in malnourished alcoholics.
Viral cerebellitis is more common in children and would not explain the ophthalmoplegia and areflexia.
Myasthenia gravis would be unlikely to develop so rapidly, and though a cause of complex ophthalmoplegia, it would not explain the areflexia or the cerebellar signs.
Posterior circulation syndromes can cause acute cerebellar dysfunction but stroke of any sort is unlikely as this is a subacute presentation of neurological features not referable to one part of the brain.
Guillain-Barre syndrome
Guillain-Barre syndrome describes an immune mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)
Pathogenesis
cross reaction of antibodies with gangliosides in the peripheral nervous system correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated anti-GM1 antibodies in 25% of patients
Miller Fisher syndrome
variant of Guillain-Barre syndrome associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome anti-GQ1b antibodies are present in 90% of cases
Von hippel lindau syndrome
Von Hippel-Lindau syndrome
Von Hippel-Lindau (VHL) syndrome is an autosomal dominant condition predisposing to neoplasia. It is due to an abnormality in the VHL gene located on short arm of chromosome 3
Features
cerebellar haemangiomas: these can cause subarachnoid haemorrhages retinal haemangiomas: vitreous haemorrhage renal cysts (premalignant) phaeochromocytoma extra-renal cysts: epididymal, pancreatic, hepatic endolymphatic sac tumours clear-cell renal cell carcinoma
Turner syndrome
You are asked to review a 22-year-old female with a heart murmur. Her height is 4ft 7 inches and she reports having always been short for her year. She has been diagnosed with autoimmune hypothyroidism, for which she is taking levothyroxine replacement and is also taking ‘hormone replacement to protect her bones’ after her GP noted she had not started her periods by 19 years old.
On examination, you note short 4th metacarpals on both hands and lymphoedematous in her hands and feet. Auscultation of her precordium reveals an ejection systolic murmur at the left infraclavicular region. Her body mass index is 22.4 kg/m². The patient’s blood tests are as follows:
Hb 123 g/l
Platelets 380 * 109/l
WBC 6.5 * 109/l
Na+ 144 mmol/l K+ 4.8 mmol/l Urea 7.2 mmol/l Creatinine 110 µmol/l Adjusted calcium 2.40 mmol/l Phosphate 1.1 mmol/l PTH 9 mg/dl (8.5-10.2mg/dl)
What is the underlying unifying diagnosis?
Turner's syndrome55% Pseudohypoparathyroidism16% Pseudopseudohypoparathyroidism12% Noonan syndrome12% Down's syndrome5%
A syndromic presentation appears most likely in this patient. An acute infective endocarditis is unlikely for someone who is systemically well, a regurgitant murmur would also be more likely. The symptoms cannot be attributed to delayed puberty, defined as onset of puberty outside 95% of the normal population and typically before 18 years old. The combination of primary amenorrhoea, short stature, lymphoedema, shortened 4th metacarpal, autoimmune predisposition and an ejection systolic murmur suggestive of aortic coarctation should infer a diagnosis of Turner’s syndrome, a disorder caused by loss of an X chromosome.
Noonan syndrome, an autosomal dominant disorder, is a reasonable differential in a patient with short stature, lymphoedema and cardiac problems. However, patients with Noonan syndrome typically presents with learning difficulties, facial dysmorphisms and webbed neck. While valvular abnormalities are less common, hypertrophic cardiomyopathy is more commonly present.
Similar to Noonan syndrome, Down’s syndrome, caused by trisomy 21, also classically presents with facial dysmorphisms such as upslanting palpebral fissures, low-set ears and epicanthic folds. Cognitive impairment and learning difficulties are also common. However, similar to our patient, short stature, thyroid dysfunction and cardiac problems, predominantly ASD, VSD and PDA are frequently associated.
Pseudohypoparathyroidism is caused by normal parathyroid hormone release but end organ resistance to hormonal effects, resulting classically in round facies and shortened fourth and fifth metacarpals. The patient is commonly obese with possible learning difficulties.
Pseudopseudohypoparathyroidism presents with the phenotype of pseudohypoparathyroidism but with normal calcium chemistry.
Turner’s syndrome
Turner’s syndrome is a chromosomal disorder affecting around 1 in 2,500 females. It is caused by either the presence of only one sex chromosome (X) or a deletion of the short arm of one of the X chromosomes. Turner’s syndrome is denoted as 45,XO or 45,X.
Features
short stature shield chest, widely spaced nipples webbed neck bicuspid aortic valve (15%), coarctation of the aorta (5-10%) primary amenorrhoea cystic hygroma (often diagnosed prenatally) high-arched palate short fourth metacarpal multiple pigmented naevi lymphoedema in neonates (especially feet) gonadotrophin levels will be elevated hypothyroidism is much more common in Turner's horseshoe kidney: the most common renal abnormality in Turner's syndrome
There is also an increased incidence of autoimmune disease (especially autoimmune thyroiditis) and Crohn’s disease
