Acute Care and Trauma Flashcards

Question 1

Q

Define acute kidney injury (AKI).

Answer

A

Acute kidney injury was previously known as acute renal failure (ARF). It is characterised by an ACUTE DECLINE IN RENAL FUNCTION. This leads to an increase in serum creatinine and a decrease in urine production/outflow.

Question 2

Q

Explain the aetiology/risk factors of acute kidney injury (AKI).

Answer

A

Sepsis Cardiovascular collapse Congestive heart failure Major surgery Nephrotoxins (such as antibiotics, intravenous contrast, or other drugs) Urinary outflow obstruction

Question 3

Q

Summarise the epidemiology of acute kidney injury (AKI).

Answer

A

Among people hospitalised in 2014 with AKI, 40% also had diabetes. In the intensive care unit (ICU), the incidence of AKI is higher. Acute tubular necrosis (ATN) accounts for 45% of cases of AKI.

Question 4

Q

Recognise the presenting symptoms of acute kidney injury (AKI). Recognise the signs of acute kidney injury (AKI) on physical examination.

Answer

A

Flank pain Haematuria Oedema Lethargy Uraemia Decreased urine output AKI can be asymptomatic and is usually defined by lab tests.

Question 5

Q

Identify appropriate investigations for acute kidney injury (AKI) and interpret the results.

Answer

A

Basic metabolic profile (including urea and creatinine). Ratio of serum urea to creatinine. Urinalysis. Urine culture FBC Fractional excretion of sodium Fractional excretion of urea Urinary eosinophil count Venous blood gases Fluid challenge Bladder catheterisation Urine osmolality Urine sodium concentration CXR, ECG

Question 6

Q

Generate a management plan for acute kidney injury (AKI).

Answer

A

Treat the underlying cause

Question 7

Q

Identify the possible complications of acute kidney injury (AKI) and its management.

Answer

A

- Hyperkalaemia - Heart failure Give calcium gluconate to stabilise the myocardium. Then give a bolus of insulin with 20% dextrose, 100ml.

- Uraemia - Metabolic acidosis Give dialysis.

Question 8

Q

Summarise the prognosis for patients with acute kidney injury (AKI).

Answer

A

Recovery for AKI is variable and depends on the cause of injury and the severity and duration of AKI.

Question 9

Q

Define acute respiratory distress syndrome.

Answer

A

Acute respiratory distress syndrome (ARDS) is a NON-CARDIOGENIC PULMONARY OEDEMA and DIFFUSE LUNG INFLAMMATION SYSTEM that often complicates critical illness.

Question 10

Q

Explain the aetiology/risk factors of acute respiratory distress syndrome.

Answer

A

Sepsis with pulmonary origin.

Other conditions associated with ARDS include aspiration, inhalation injury, acute pancreatitis, trauma, burns, pulmonary contusion, transfusion-related lung injury, cardiopulmonary bypass, fat embolism, disseminated intravascular coagulation, and drug overdose.

Critical illness, cigarette smoking, and alcohol use are predisposing factors for ARDS.

Question 11

Q

Summarise the epidemiology of acute respiratory distress syndrome.

Answer

A

Overall, 10% to 15% of patients admitted to the intensive care unit meet the criteria for ARDS, with an increased incidence among mechanically ventilated patients meeting the criteria for ARDS. Mortality is between 40% and 50%.

Question 12

Q

Recognise the presenting symptoms of acute respiratory distress syndrome.

Answer

A

SOB Fatigue Discolouration of nails Rapid resp rate Tachycardia Fever

Question 13

Q

Recognise the signs of acute respiratory distress syndrome on physical examination.

Answer

A

Low oxygen saturation Acute respiratory failure Dyspnoea Increased respiratory rate Pulmonary crepitations Low lung compliance Fever, cough, pleuritic chest pain (Frothy sputum)

Question 14

Q

Identify appropriate investigations for acute respiratory distress syndrome and interpret the results.

Answer

A

CXR - New onset of bilateral opacities that is not fully explained by effusions, lobar/lung collapse. ABG - A PaO₂/FiO₂ (inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O is part of the diagnostic criteria for ARDS. Sputum culture Blood culture Urine culture Amylase and lipase

Question 15

Q

Define adrenal insufficiency.

Answer

A

Addison's disease, or primary adrenal insufficiency, is a disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones (cortisol, aldosterone, and dehydroepiandrosterone).

Question 16

Q

Explain the aetiology/risk factors of adrenal insufficiency. Summarise the epidemiology of adrenal insufficiency.

Answer

A

TB is the most common cause worldwide, but in the UK, the most common cause is autoimmune disease. Less common causes are infections (e.g. Pseudomonas aeruginosa or meningococcus) or drugs (e.g. warfarin).

Question 17

Q

Recognise the presenting symptoms of adrenal insufficiency.

Answer

A

Fatigue Anorexia Weight loss Hyperpigmentation

Question 18

Q

Recognise the signs of adrenal insufficiency on physical examination.

Answer

A

Hypotension (can be Addisonian crisis). Nausea Vomiting

Question 19

Q

Identify appropriate investigations for adrenal insufficiency and interpret the results.

Answer

A

Serum electrolytes - hyponatraemia, hyperkalaemia, can rarely be hypercalcaemia Blood urea FBC - anaemia is present in 40% of patients. Morning serum cortisol - cortisol should be high in the morning.

Question 20

Q

Generate a management plan for adrenal insufficiency.

Answer

A

ACUTE IV Hydrocortisone 50-100mg for 1-3 days

STABLE Hydrocortisone: 15-30 mg/day orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.) OR Prednisolone: 2.5 to 5 mg orally once daily

AND

Fludrocortisone: 0.1 to 0.2 mg orally once daily

Question 21

Q

Identify the possible complications of adrenal insufficiency and its management.

Answer

A

Hyperkalaemia: Give calcium gluconate, bolus IV insulin and 20% dextrose, 100ml. Secondary Cushings’ syndrome: due to over-replacement of steroids. Osteoporosis due to long term use of steroids. Hypertension due to excessive mineralocorticoid replacement.

Question 22

Q

Summarise the prognosis for patients with adrenal insufficiency.

Answer

A

Patients are generally ok once they start treatment and stay on life-long replacement. Adherence is high since non-adherence results in uncomfortable symptoms.

Question 23

Q

Define alcohol withdrawal.

Answer

A

Alcohol withdrawal syndrome (AWS), commonly referred to as 'the shakes', occurs in patients with alcohol dependence when their daily alcohol consumption is decreased or stopped. The syndrome typically begins within 4 to 12 hours after the patient's last drink, and may progress to potentially fatal delirium tremens.

Question 24

Q

Explain the aetiology of alcohol withdrawal.

Answer

A

Chronic alcohol use results in up-regulation of postsynaptic NMDA receptors and down-regulation of post-synaptic GABA receptors. A decrease in blood ethanol concentration due to abrupt cessation in alcohol consumption results in an imbalance between stimulatory (NMDA) and inhibitory (GABA) systems in the central nervous system. Excessive stimulatory effect leads to the development of the clinical signs and symptoms of AWS.

Question 25

Q

Explain the risk factors of alcohol withdrawal.

Answer

A

Risk factors include having a history of AWS or delirium tremens, as well as sudden withdrawal of alcohol.

Question 26

Q

Summarise the epidemiology of alcohol withdrawal.

Answer

A

In the US, the 2016 National Survey on Drug Use and Health found that 5.2% of adults over 26 years, 10.7% of adults aged 18-25 years, and 2.0% of youths (aged 12 to 17 years) suffer from alcohol use disorder. It is estimated that of these alcohol-dependent patients, approximately 50% will experience symptoms of alcohol withdrawal upon reduced alcohol intake.

Question 27

Q

Recognise the presenting symptoms of alcohol withdrawal. Recognise the signs of alcohol withdrawal.

Answer

A

Hallucinations Change in mental status Tremor Nausea and vomiting Hypertension Seizures

Question 28

Q

Identify appropriate investigations for alcohol withdrawal and interpret the results.

Answer

A

Serum urea and creatinine Liver function tests Ethanol Electrolyte panel FBC CT of head CXR

Question 29

Q

Generate a management plan for alcohol withdrawal.

Answer

A

Benzodiazepine or clomethiazole (+ supportive care)

Adjunct: Phenobarbital Vitamin supplementation

Question 30

Q

Identify the possible complications of alcohol withdrawal and its management.

Answer

A

Over-sedation Delirium tremens Alcohol withdrawal seizures Status epilepticus Death

Question 31

Q

Summarise the prognosis for patients with alcohol withdrawal.

Answer

A

Patients may complain of persistent insomnia and autonomic symptoms for a few months after acute withdrawal phase. These symptoms usually last about 6 months. About 50% of patients remain abstinent for a year.

Question 32

Q

Define anaphylaxis.

Answer

A

An acute, systemic and life-threatening allergic response to a trigger caused by the release of immune and inflammatory mediators from basophils and mast cells. At least two organ systems are involved, such as the skin, the upper and lower airways, and the cardiovascular, neurological, and gastrointestinal systems, in this order of priority or in combination.

Question 33

Q

Explain the aetiology/risk factors of anaphylaxis.

Answer

A

Exposure to allergen in pre-sensitised individuals is the cause of immune-mediated anaphylaxis. Common allergens include drugs, foods, and insect stings, but exercise with or without the presence of an allergen may also be a trigger. Sometimes, a cofactor (such as an NSAID, alcohol, or another food) is required to provoke food-associated and exercise-induced anaphylaxis. The most common trigger (up to ⅓ of cases) is food.

Question 34

Q

Summarise the epidemiology of anaphylaxis.

Answer

A

Anaphylaxis is under-reported and it is difficult to estimate as study definitions and criteria are not always comparable. The incidence of food allergic reactions that are coded as anaphylaxis is highest in young children. In children, food allergy is most prevalent in the industrialised world and the emerging economies of southeast Asia, possibly due to an increased exposure to processed food.

Question 35

Q

Recognise the presenting symptoms of anaphylaxis.

Answer

A

Rapidly progressive upper airway obstruction Rash Bronchospasm Hypotension or cardiovascular collapse

Question 36

Q

Recognise the signs of anaphylaxis on physical examination.

Answer

A

The patient appears agitated, confused, and either flushed or pale. Neurological manifestations also include dizziness, visual disturbances, tremor, disorientation, syncope, and seizures. Wheezing, an over-inflated chest, the use of accessory muscles, and preference for the forward-leaning position point to bronchoconstriction. Cardiovascular collapse may occur in addition to hypotension. Nearly all adults will show skin manifestations of systemic mediator release, such as rash, erythema, or urticaria. These features might be overshadowed by the more dramatic respiratory and cardiovascular symptoms. Abdominal pain, nausea, vomiting, and diarrhoea are common symptoms.

Question 37

Q

Identify appropriate investigations for anaphylaxis and interpret the results.

Answer

A

During the anaphylactic shock, no investigations are useful as they take too long. Serum tryptase level.

Question 38

Q

Generate a management plan for anaphylaxis. Identify the possible complications of anaphylaxis and its management.

Answer

A

INITIAL Cardiorespiratory assessment + supportive measures IM adrenaline (epinephrine) Assess and secure airway IV normal saline

Cardiopulmonary arrest CPR and IV adrenaline (epinephrine)

Severe hypotension IV adrenaline (epinephrine) IV glucagon

Persistent respiratory symptom Inhaled beta-2 agonist

Symptomatic hives and rhinorrhoea H1 antagonist and H2 antagonist

Post-emergency stabilisation Corticosteroids

Question 39

Q

Summarise the prognosis for patients with anaphylaxis.

Answer

A

Individuals with previous reactions are at higher risk for recurrence. However, the severity of the previous reaction does not necessarily predict the severity of a subsequent reaction.

Question 40

Q

Define aspirin overdose.

Answer

A

Potentially fatal poisoning occurring as a result of ingestion or, rarely, topical exposure to salicylates. Can present acutely or indolently with more chronic exposure.

Question 41

Q

Explain the aetiology/risk factors of aspirin overdose.

Answer

A

The most common source of salicylate poisoning is aspirin (acetylsalicylic acid), which is rapidly hydrolysed to salicylate in the gastrointestinal tract and bloodstream.

Question 42

Q

Summarise the epidemiology of aspirin overdose.

Answer

A

In the UK, deaths by suicidal overdose of analgesics, including salicylates, were reduced by 22% in the year immediately after the introduction in 1998 of legislation limiting the pack size of analgesics that could be purchased.

Question 43

Q

Recognise the presenting symptoms of aspirin overdose. Recognise the signs of aspirin overdose on physical examination.

Answer

A

Nausea, vomiting, haematemesis, epigastric pain Fever and diaphoresis Shortness of breath Tachypnoea, hyperpnoea, Kussmaul's respirations Tinnitus and/or deafness Malaise and/or dizziness Movement disorders, asterixis, stupor Confusion and/or delirium (irritability, hallucinations) Coma and/or papilloedema Seizures

Question 44

Q

Identify appropriate investigations for aspirin overdose and interpret the results.

Answer

A

ABG Serum electrolyte panel Serum salicylate level Serum urea and creatinine Serum ketones Blood glucose FBC Serum LFTs Serum PT, activated PTT, INR Toxicology screen CXR ECG

Question 45

Q

Define asthma.

Answer

A

Asthma is a chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity.

Question 46

Q

Explain the aetiology/risk factors of asthma.

Answer

A

Patients' genetic make-up may predispose them to hyper-responsiveness to environmental aetiological triggers. Those triggers include viral infections (e.g. rhinovirus, respiratory syncytial virus, human metapneumovirus, and influenza virus), bacterial infections (e.g. Mycoplasma pneumoniae or Chlamydia pneumoniae), allergen exposure (e.g. tree, grass, or weed pollen; fungi; or indoor allergens), occupational exposures (e.g. animal or chemical), food additives and chemicals (e.g. metabisulfites), irritants, or aspirin in predisposed people.

Question 47

Q

Summarise the epidemiology of asthma.

Answer

A

Asthma affects approximately 30 million people in Europe and more than 25 million people in the US. The global burden is reported to be 300 million people, potentially increasing to 400 million by 2025. In 2010, overall asthma prevalence in the US was 8.4%.

Question 48

Q

Recognise the presenting symptoms of asthma.

Answer

A

Recurrent episodes of dyspnoea, chest tightness, wheezing, or coughing typically occur. The patient's medical history may help to identify allergen exposures that worsen asthma: for example, episodes may be exacerbated by exposure to irritants such as tobacco smoke or fumes from chemicals, such as bleach. Attacks may occur seasonally or upon exposure to cats in allergic patients. Exercise can also make the symptoms worse.

Question 49

Q

Recognise the signs of asthma on physical examination.

Answer

A

The examination may be normal in patients with bronchial asthma. Examination of the nasal passages may reveal nasal polyposis or nasal congestion. Chest auscultation may reveal expiratory wheezes. With more severe asthma, wheezes may be audible without the use of a stethoscope. In patients with severe exacerbations, the lung examination may be silent.

Question 50

Q

Identify appropriate investigations for asthma and interpret the results.

Answer

A

FEV1/FVC ratio - <80% of predicted FEV1 - 20% drop is indicative Peak expiratory flow rate (PEFR) CXR - normal or hyperinflated FBC - normal or raised eosinophils and neutrophils

Question 51

Q

Generate a management plan for asthma.

Answer

A

Salbutamol inhaler until in hospital. Once in hospital, administer 2.5mg salbutamol and oxygen as a nebuliser back to back (or 5mg in one dose but this increases the risk of tremor etc). Give IV hydrocortisone or oral prednisolone depending on how bad the patient is.

Question 52

Q

Identify the possible complications of asthma and its management.

Answer

A

IV magnesium sulfate in life-threatening exacerbation of asthma. Airway remodelling due to inflammation which leads to the airway resembling COPD.

Question 53

Q

Summarise the prognosis for patients with asthma.

Answer

A

People with asthma have the same life expectancy as normal people.

Question 54

Q

Define acute cardiac failure.

Answer

A

Heart failure is defined clinically as a syndrome in which patients have symptoms and signs resulting from an abnormality of cardiac structure and/or function. Acute heart failure refers to rapid onset or worsening of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment.

Question 55

Q

Explain the aetiology/risk factors of acute cardiac failure.

Answer

A

Decompensation of pre-existing chronic heart failure Other heart conditions such as aortic regurgitation Lack of compliance with medical treatment Volume overload Infections Severe brain insult After major surgery Reduction of renal function Drug abuse Phaeochromocytoma High output syndromes (Septicaemia, Thyrotoxic crisis, Anaemia, Shunt syndromes)

Question 56

Q

Summarise the epidemiology of acute cardiac failure.

Answer

A

Heart failure is the most common indication for hospitalisation in the US, and acute decompensated heart failure is the most common cause for hospitalisation among patients >65 years. The average age of people with heart failure in studies conducted in Europe is also older than 70 years, with slight predominance of men.

Question 57

Q

Recognise the presenting symptoms of acute cardiac failure.

Answer

A

Dyspnoea Decreased exercise tolerance Swelling of the legs Fatigue Generalised weakness

Question 58

Q

Recognise the signs of acute cardiac failure on physical examination.

Answer

A

Reduced cardiac output Tissue hypoperfusion Increased pulmonary pressure Tissue congestion Raised JVP

Question 59

Q

Identify appropriate investigations for acute cardiac failure and interpret the results.

Answer

A

ECG Echocardiogram CXR Hb TFT Troponin B-type natriuretic peptide (BNP)

Question 60

Q

Generate a management plan for acute cardiac failure.

Answer

A

Loop diuretic in order to get rid of oedema, and then ACEi after the patient stabilises. Treatment is generally with ACEi and beta blockers.

Question 61

Q

Identify the possible complications of acute cardiac failure and its management.

Answer

A

ARRHYTHMIAS Hypotension, hyperkalaemia and headaches may result from treatment.

Question 62

Q

Summarise the prognosis for patients with acute cardiac failure.

Answer

A

In hospital, mortality ranges from 2% to 20% depending on clinical factors found on admission. Predictors of adverse outcomes include: hypotension, renal dysfunction, older age, male sex, ischaemic congestive heart failure (CHF), previous CHF, respiratory rate on admission >30/minute, anaemia, hyponatraemia, elevated troponin, elevated B-type natriuretic peptide, and other comorbidities such as cancer.

Question 63

Q

Define burns injury.

Answer

A

Burns are very common injuries, predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current, or chemicals.

Question 64

Q

Explain the aetiology/risk factors of burns injury.

Answer

A

Thermal burns Electrical burns Chemical burns Non-accidental burns

Answer 65

A

In the UK, 250,000 people are injured by burns. Approximately 175,000 people visit accident and emergency departments with burn injuries. Around 13,000 of them are admitted to hospital for treatment.

Answer 66

A

Pain Redness

Answer 67

A

Full blood count Metabolic panel Carboxyhaemoglobin Arterial blood gas Fluorescein staining Computed tomography scan of head and spine Wound biopsy culture Wound histology

Answer 68

A

Sudden loss of cardiac systolic function. It is the result of 4 specific cardiac rhythm disturbances: ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), pulseless electrical activity, and asystole. Each of these rhythms may present in different clinical scenarios, though VT and VF are the most common causes of sudden cardiac arrest.

Answer 69

A

Myocardial ischaemia/infarction

Hypovolaemia

Hypoxia

Pulmonary embolism.

Other potential causes of cardiac arrest, all of which require emergent treatment, including hyperkalaemia, hydrogen ion excess (acidosis), hypothermia, hypo- or hyperglycaemia, trauma, tension pneumothorax,toxins, and cardiac tamponade.

Answer 70

A

In Europe, out-of-hospital cardiac arrest incidence for patients considered for resuscitation by emergency medical services has been reported as 84 per 100,000 population per year. Survival is estimated at <20% for patients presenting out-of-hospital with VF, and <10% overall for patients presenting with out-of-hospital cardiac arrest. In contrast, 36% of patients with VF/ventricular tachycardia (VT) and 11% of patients with pulseless electrical activity/asystole, presenting in-hospital, survive to discharge.

Answer 71

A

Family history of sudden cardiac arrest Pulmonary disease Chest pain Palpitations- possibility of pre-existing arrhythmias Syncope Tachycardia Unusual heart sounds

Answer 72

A

ECG FBC Serum electrolytes ABG Cardiac biomarkers Toxicology screen CXR Echocardiogram Coronary angiography

Answer 73

A

INITIAL CPR

ACUTE Shockable rhythms (pulseless ventricular tachycardia or ventricular fibrillation) CPR and defibrillation Adrenaline (epinephrine) Adjunct Magnesium Anti-arrhythmic

Non-shockable rhythms (pulseless electrical activity or asystole) CPR and adrenaline (epinephrine)

ONGOING Return of spontaneous circulation Post-resuscitation care No return of spontaneous circulation Continue or consider termination of resuscitation

Answer 74

A

Death

Rib and sternal fractures

Anoxic brain injury

Ischaemic liver injury (“shock liver”)

Renal acute tubular necrosis (ATN)

Recurrent cardiac arrest

Answer 75

A

The outcome of sudden cardiac arrest is generally poor. Early provision of CPR, including compression-only CPR by bystanders in out-of-hospital arrest increases the rate of survival from sudden cardiac arrest. The strongest predictor of survival is bystander CPR. Even those who do survive to hospital admission do not always survive to hospital discharge. Furthermore, those who do survive to hospital discharge often have neurological, pulmonary, cardiac, hepatic, renal, or musculoskeletal complications. Most important, the neurological outcome of the comatose survivors of sudden cardiac arrest must be carefully assessed. The following characteristics portend death or a poor neurological outcome: At 24 hours - loss of corneal reflex, lack of motor response, lack of withdrawal to pain, and loss of pupillary response. At 72 hours - lack of motor response.

Answer 76

A

A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The term “congestive heart failure” (CHF) is reserved for patients with breathlessness and abnormal sodium and water retention resulting in oedema.

Answer 77

A

Coronary artery disease Hypertension Valvular disease Myocarditis

Answer 78

A

The prevalence of CHF in the western world has been estimated at 1% to 2%, and the incidence is thought to approach 5 to 10 per 1000 people per year.

Answer 79

A

Tachycardia (heart rate >120 beats per minute) Chest discomfort Ankle oedema Night cough Fatigue, muscle weakness, or tiredness

Answer 80

A

Dyspnoea Neck vein distension S3 gallop Cardiomegaly Hepatojugular reflux Rales Hepatomegaly

Answer 81

A

ECG Echocardiogram CXR B-type natriuretic peptide (BNP)/N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels FBC Serum electrolytes (including calcium and magnesium) Serum creatinine, blood urea nitrogen BM LFT Thyroid function tests (especially thyroid-stimulating hormone [TSH]) Blood lipids Serum ferritin Transferrin saturation

Answer 82

A

In newly diagnosed patients with CHF, congestion and volume overload should be promptly treated with diuretics, which may be given intravenously in the initial phase. Loop diuretics used for the treatment of heart failure and congestion include furosemide, bumetanide, and torasemide.

In patients with low left ventricular ejection fraction (LVEF), in addition to diuretics, ACE inhibitors, beta-blockers, and aldosterone antagonists (e.g. spironolactone, eplerenone) should be added.

In unstable patients, beta-blockers should be initiated only after stabilisation, optimisation of volume status, and discontinuation of inotropes. Beta-blockers should be initiated at a low dose.

In patients with CHF and reduced LVEF who are hospitalised with exacerbation of heart failure, unless there is evidence of low cardiac output or haemodynamic instability or contraindication, both ACE-inhibitors and beta-blockers should be continued.

Answer 83

A

Pleural effusion Chronic renal insufficiency Anaemia Acute decompensation of chronic heart failure Acute renal failure Sudden cardiac death

Answer 84

A

The evaluation of a patient would be incomplete without an initial and periodic assessment of short- and long-term prognosis. However, the likelihood of survival can be determined reliably only in populations and not in individual patients. Haemoglobin A1c was also found to be an independent progressive risk factor for cardiovascular death, hospitalisation, and mortality, even in non-diabetic patients.

Answer 85

A

COPD is characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.

Answer 86

A

Tobacco smoking is by far the main risk factor for COPD. It is responsible for 40% to 70% of COPD cases and exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury. Air pollution and occupational exposure are other common aetiologies. Oxidative stress and an imbalance in proteases and antiproteases are also important factors in the pathogenesis of COPD, especially in patients with alpha-1 antitrypsin deficiency, who have panacinar emphysema that usually presents at an early age.

Answer 87

A

COPD is more common in older people, especially those aged 65 years and older. A retrospective study conducted in the UK between 1990 and 1997 estimated COPD prevalence to be 2% in men and 1% in women.

Answer 88

A

Cough Shortness of breath

Answer 89

A

Barrel chest

Hyperresonance on percussion

Distant breath sounds on auscultation

Poor air movement on auscultation

Wheezing on auscultation

Coarse crackles

Answer 90

A

Spirometry Pulse oximetry ABG CXR FBC ECG

Answer 91

A

Short-acting bronchodilator

Adjunct: Systemic corticosteroid Transition to inhaled corticosteroid Airway clearance techniques Supplemental oxygen

Answer 92

A

Cor pulmonale - Right-sided heart failure secondary to long-standing COPD. It is caused by chronic hypoxia and subsequent vasoconstriction in pulmonary vasculature that causes pulmonary hypertension and right-sided heart failure. Recurrent pneumonia Depression Pneumothorax Respiratory failure Anaemia Polycythaemia

Answer 93

A

COPD is a disease with an indeterminate course and variable prognosis. Its prognosis depends on several factors including genetic predisposition, environmental exposures, comorbidities, and, to a lesser degree, acute exacerbations.

Answer 94

A

Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment. It is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes mellitus.

Answer 95

A

In DKA, there is a reduction in the net effective concentration of circulating insulin along with an elevation of counter-regulatory hormones. The two most common precipitating events are inadequate insulin therapy and infection. Underlying medical conditions such as MI or stroke that provoke the release of counter-regulatory hormones are also likely to result in DKA in patients with diabetes. Drugs that affect carbohydrate metabolism, such as corticosteroids, thiazides, pentamidine, sympathomimetic agents (e.g. dobutamine and terbutaline), second-generation antipsychotic agents, and immune checkpoint inhibitors may contribute to the development of DKA.

Answer 96

A

In England, the incidence of hospital admissions for DKA among adults with type 2 diabetes increased 4.24% annually between 1998 and 2013; hospitalisations for DKA in adults with type 1 diabetes increased from 1998 to 2007, and remained static until 2013.

Answer 97

A

Polyuria Polyphagia Polydipsia Weight loss Weakness Nausea or vomiting Abdominal pain Sunken eyes

Answer 98

A

Dry mucous membranes Poor skin turgor Tachycardia Hypotension Kussmaul respiration Acetone breath Altered mental status

Answer 99

A

BM HbA1C FBC ABG Capillary or serum ketones Urinalysis Serum urea Serum creatinine Serum sodium Serum potassium Serum chloride Serum magnesium Serum calcium Serum phosphate Serum creatine phosphokinase Serum lactate LFT Serum amylase Serum lipase Serum osmolality

Answer 100

A

The main goals of treatment are:

<ul> <li>Restoration of volume deficits</li> <li>Resolution of hyperglycaemia and ketosis/acidosis</li> <li>Correction of electrolyte abnormalities (potassium level should be >3.3 mmol/L [>3.3 mEq/L] before initiation of insulin therapy; use of insulin in a patient with hypokalaemia may lead to respiratory paralysis, cardiac arrhythmias, and death)</li> <li>Treatment of the precipitating events and prevention of complications</li></ul>

The majority of patients present to the accident and emergency department, where treatment should be initiated. There are several important steps that should be followed in early management:

<ul> <li>Fluid therapy should be started immediately after initial laboratory evaluations.</li> <li>Infusion of isotonic solution of 0.9% sodium chloride at a rate of 1 to 1.5 L/hour should be used for the first hour of fluid therapy. </li></ul>

Answer 101

A

Hypoglycaemia Hypokalaemia Arterial or venous thromboembolic events Non-anion gap hyperchloremic acidosis Cerebral oedema/brain injury Acute respiratory distress syndrome (ARDS)

Answer 102

A

The mortality rate is 5% in experienced centres. Death is rarely caused by the metabolic complications of hyperglycaemia or ketoacidosis but rather relates to the underlying illness. The prognosis is substantially worsened at the extremes of age and in the presence of coma and hypotension.

Answer 103

A

DIC is an acquired syndrome characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors.

Thrombi may lead to vascular obstruction/ischaemia and multi-organ failure. Spontaneous bleeding may occur. Generalised bleeding, evidenced by at least 3 unrelated sites, is highly suggestive of DIC.

Answer 104

A

Disease states that trigger systemic activation of coagulation may lead to DIC. Causes include:

<ul> <li>Sepsis/severe infection, major trauma or burns</li> <li>Some malignancies (acute myelocytic leukemia or metastatic mucin-secreting adenocarcinoma)</li> <li>Obstetric disorders (amniotic fluid embolism, eclampsia, abruptio placentae, retained dead fetus syndrome)</li> <li>Severe organ destruction or failure (severe pancreatitis, acute hepatic failure)</li> <li>Vascular disorders (Kasabach-Merritt syndrome or giant haemangiomas, large aortic aneurysms)</li> <li>Severe toxic or immunological reactions (blood transfusion reaction or haemolytic reactions, organ transplant rejection, snake bite).</li></ul>

Answer 105

A

Many conditions can cause DIC; therefore, the overall incidence is difficult to determine. Age and sex are not good predictors. Mortality is high. For instance, the presence of DIC in patients with major trauma will result in a significant increase in overall mortality.

Answer 106

A

Oliguria Hypotension Tachycardia Purpura fulminans, gangrene, or acral cyanosis Delirium or coma Petechiae, ecchymosis, oozing, or haematuria

Answer 107

A

Platelet count Prothrombin time (PT) Fibrinogen D-dimer/fibrin degradation products Activated partial thromboplastin time (aPTT) Imaging studies or other tests

Answer 108

A

Encephalitis is defined as inflammation of the brain parenchyma associated with neurological dysfunction such as altered state of consciousness, seizures, personality changes, cranial nerve palsies, speech problems, and motor and sensory deficits.

Answer 109

A

It is the result of direct inflammation of the brain tissue, as opposed to the inflammation of the meninges (meningitis), and can be the result of infectious or noninfectious causes. An aetiological agent is only identified in around 50% of cases.

Answer 110

A

Age <1 or >65 years Immunodeficiency Post-infection Blood/body fluid exposure Organ transplantation Animal or insect bites Location Season Swimming or diving in warm freshwater or nasal/sinus irrigation

Answer 111

A

Around 2500 cases of encephalitis occur in England each year. Globally, the incidence of encephalitis is around 7 per 100,000 population per year. There is no specific gender predominance, but frequently a bimodal age distribution is seen with highest incidence in those under one year and over 65 years.

Answer 112

A

Fever Rash Altered mental state Focal neurological deficit Meningismus Cough Gastrointestinal infection

Answer 113

A

FBC Peripheral blood smear Serum electrolytes LFTs Blood cultures Throat swab Nasopharyngeal aspirate Sputum culture Chest radiography CT brain MRI brain EEG CSF analysis CSF culture CSF serology CSF polymerase chain reaction (PCR)

Answer 114

A

A disorder which causes seizures. There are many different forms of epilepsy and treatment depends on which form it is.

Answer 115

A

Age - The onset of epilepsy is most common in children and older adults, but the condition can occur at any age. Family history Head injuries Stroke and other vascular diseases Dementia Brain infections Seizures in childhood

Answer 116

A

Around 50 million people worldwide have epilepsy, making it one of the most common neurological diseases globally. Nearly 80% of people with epilepsy live in low- and middle-income countries. It is estimated that up to 70% of people living with epilepsy could live seizure-free if properly diagnosed and treated.

Answer 117

A

Symptoms range from generalised tonic-clonic seizures which are easily recognisable due to the whole body to absence seizures which is when people appear to lose focus for 5-10 seconds but otherwise appear perfectly normal and exhibit no other symptoms.

Answer 118

A

EEG MRI fMRI

Answer 119

A

The patient may hurt themselves during the seizure by falling. As well as this, prolonged seizures can cause brain damage. Breathing in food or saliva into the lungs during a seizure, which can cause aspiration pneumonia.

Answer 120

A

Prognosis depends on the type and severity of the epilepsy. There is no cure but it can be managed.

Answer 121

A

A contusion resulting in bleeding into the extradural space. This results in raised intracranial pressure and possibly compression of the brain resulting in neurological disorders and potential death.

Answer 122

A

This is usually caused by trauma with a lot of force.

Answer 123

A

Intracranial epidural hematoma occurs in approximately 2% of patients with head injuries and 5–15% of patients with fatal head injuries.

Answer 124

A

TRIPHASIC There is loss of consciousness followed by a LUCID INTERVAL before the patient’s condition declines again. LOC is followed by headache, progressive obtundation, and hemiparesis. Bleeding may eventually cause a “blown pupil” secondary to uncal herniation. The “blown pupil” will be ipsilateral and the hemiparesis will be contralateral.

Answer 125

A

CT scan - Will show characteristic bi-convex mass within the skull if there is an EDH is present (“lemon-shaped” as opposed to the typical “banana-shape” of subdural haemorrhages). MRI - Takes longer so is not suitable for first line but can be useful after surgery in order to determine if there is ischaemia of the brain.

Answer 126

A

Part of the myocardium dies due to lack of oxygen. This results in chest pain and reduced efficiency. It can be caused by a thrombus or an embolus.

Answer 127

A

Smoking Obesity Sedentary lifestyle Family history Hypertension

Answer 128

A

Epidemiology of ischaemic heart disease (IHD) Cardiovascular disease (CVD) is the most common cause of death in Europe, accounting for more than 4 million deaths each year. This corresponds to 45% of all deaths; 49% among women and 40% among men.

Answer 129

A

Chest pain Shortness of breath Epigastric discomfort Pain radiating to the jaw or arm Nausea/vomiting Perspiration (diaphoresis) Fatigue

Answer 130

A

Tachycardia S3 Mitral regurgitation murmur Bibasilar rales Aortic outflow murmur Carotid bruit Diminished peripheral pulses Signs of abdominal aortic aneurysm Retinopathy seen on fundoscopic examination Xanthomas or xanthelasma

Answer 131

A

CXR ECG Echocardiogram Troponin Creatine kinase BNP FBC Urea and serum creatinine LFT BM

Answer 132

A

Determine the cause of the ischaemic heart disease. Potentially give oxygen and anti-platelets in the acute phase.

Answer 133

A

Brain damage due to hypoxia. Decreased quality of life due to dyspnea during exercise.

Answer 134

A

Increased risk of further cardiac events in the future. The risk varies depending on personal factors.

Answer 135

A

Bacterial meningitis is a serious inflammation of the meninges caused by various bacteria.

Answer 136

A

Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib) are the predominant causative pathogens in both adults and children.

Answer 137

A

≤5 or ≥65 years of age Crowding Exposure to pathogens Non-immunised infants Immunodeficiency Cancer Asplenia/hyposplenic state Cranial anatomical defects Cochlear implants

Answer 138

A

The incidence of bacterial meningitis in Western countries and the US is 0.7 to 0.9 per 100,000 persons per year and has decreased by 3% to 4% in the past 10 to 20 years.

Answer 139

A

Stiff neck Photophobia Headache Fever Confusion Vomiting Non-blanching rash

Answer 140

A

LP FBC CRP Blood culture

Answer 141

A

Empirical antibiotic therapy

Plus: Supportive therapy Dexamethasone

Answer 142

A

Shock Elevated intracranial pressure Hydrocephalus Cognitive, academic, and behavioural problems Seizures Subdural effusion Hearing loss Brain abscess Septic deep vein thrombosis

Answer 143

A

Generally, with prompt and adequate antimicrobial and supportive therapy, the outcome after acute bacterial meningitis is excellent. However, prognosis does depend on multiple factors such as age, presence of comorbidity, causative pathogen, and severity at presentation.

Answer 144

A

Multi-organ dysfunction syndrome (MODS) is also known as multiple organ failure and is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

Answer 145

A

The condition usually results from infection, injury (accident, surgery), hypoperfusion and hypermetabolism. The primary cause triggers an uncontrolled inflammatory response. Sepsis is the most common cause of MODS and may result in septic shock.

Answer 146

A

Epidemiology is unknown.

Answer 147

A

Stage 1: The patient has increased volume requirements and mild respiratory alkalosis which is accompanied by oliguria, hyperglycemia and increased insulin requirements. Stage 2: The patient is tachypneic, hypercapnic and hypoxemic; develops moderate liver dysfunction and possible hematologic abnormalities. Stage 3: The patient develops shock with azotemia and acid-base disturbances; has significant coagulation abnormalities. Stage 4: The patient is vasopressor dependent and oliguric or anuric; subsequently develops ischemic colitis and lactic acidosis.

Answer 148

A

Investigations are to identify the cause of multi-organ dysfunction syndrome so there is a huge variety of tests you can do.

Answer 149

A

At present there is no drug or device that can reverse organ failure that has been judged by the health care team to be medically and/or surgically irreversible. Mortality varies from 30% to 100% where the chance of survival is diminished as the number of organs involved increases. Since the 1980s the mortality rate has not changed.

Answer 150

A

An opioid overdose occurs when larger quantities than physically tolerated are taken, resulting in central nervous system and respiratory depression.

Answer 151

A

Opioid abuse and dependence Recent abstinence in chronic users Chronic pain

Answer 152

A

Opioid abuse and overdose is a growing problem worldwide. In the US, from 1991 to 2015 the number of opioid-related deaths quadrupled.

Answer 153

A

Presence of risk factors Miosis Bradypnoea Altered mental status Dramatic response to naloxone Fresh needle marks Drug paraphernalia nearby Decreased gastrointestinal motility Old track marks on arms and legs

Answer 154

A

Therapeutic trial of naloxone Electrocardiogram (ECG)

Answer 155

A

Taking too much paracetamol which results in generation of hepatotoxic metabolites. Overdose may occur after an acute single ingestion of a large amount of paracetamol or paracetamol-containing medication, or repeated ingestion of an amount exceeding the recommended dosage.

Answer 156

A

Paracetamol is usually metabolised by glucuronidation, however, when these enzymes are saturated, the paracetamol is metabolised by the CYP450 system (specifically CYP3A4 and CYP2E1) which generates NAPQI which is a toxic metabolite.

Paracetamol overdose can be a suicide method due to its accessibility, however it seems that a lot of people are unaware of its harmful effects so is not a popular method by people attempting suicide. Death comes in the form of liver failure a few weeks later.

Answer 157

A

Paracetamol is easily accessible and often people take too much by accident by taking paracetamol along with other medication containing paracetamol.

Answer 158

A

Patients are often asymptomatic or have only mild gastrointestinal symptoms at initial presentation. Untreated paracetamol poisoning may cause varying degrees of liver injury over the 2 to 4 days following ingestion, including fulminant hepatic failure.

Rarely, massive overdose may initially present with coma and severe metabolic acidosis. Presentation with coma may also occur if a combination preparation of paracetamol and opioid is taken in overdose, or after an overdose of multiple drugs.

Hepatotoxicity is extremely rare in patients treated with acetylcysteine within 8 hours of an acute paracetamol overdose. The efficacy of acetylcysteine decreases subsequent to the first 8 hours following an acute paracetamol overdose, with a corresponding stepwise increase in hepatotoxicity with increasing treatment delays between 8 and 16 hours.

Answer 159

A

Serum paracetamol level Serum AST and ALT Arterial pH and lactate level Urea and electrolytes or tests of renal function Serum prothrombin time and INR - Used to monitor extent of hepatotoxicity

Answer 160

A

Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology.

Answer 161

A

Hypertension Advanced age Male sex Asian, black and/or Hispanic Family history of haemorrhagic stroke Haemophilia Cerebral amyloid angiopathy Anticoagulation

Answer 162

A

Stroke is the third leading cause of death and a major cause of disability in the US and in England and Wales. Haemorrhagic strokes account for 15% of all strokes.

Answer 163

A

Neck stiffness History of atrial fibrillation History of liver disease Visual changes Photophobia Sudden onset Altered sensation Headache Weakness Sensory loss Aphasia Dysarthria Ataxia

Answer 164

A

Non-infused head CT Chemistry panel FBC Clotting tests ECG Platelet function test Urine drug screen Pregnancy test in women of childbearing age Liver function test Intracerebral haemorrhage (ICH) Score

Answer 165

A

Neurosurgical and neurocritical care evaluation

Plus: Admission to neuroscience ICU or stroke unit Airway protection Aspiration precautions

Answer 166

A

Deep venous thrombosis Infection Seizures Delirium Aspiration pneumonia Hydrocephalus

Answer 167

A

Mortality is significantly higher than for ischaemic stroke, in the range of 35% to 40%. Only 20% to 30% of all patients are well enough to live independently by 3 to 6 months.

Answer 168

A

Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology.

Answer 169

A

Older age Family history of stroke Hypertension Smoking Diabetes mellitus Atrial fibrillation Comorbid cardiac conditions Carotid artery stenosis Sickle cell disease Dyslipidaemia

Answer 170

A

The most common type of stroke. Stroke is the third leading cause of death and a major cause of disability in the US and in England and Wales.

Answer 171

A

Vision loss or visual field deficit Weakness Aphasia Impaired coordination (ataxia) Sudden onset of symptoms Negative symptoms (i.e., loss of function) Altered sensation Headache Diplopia Sensory loss Dysarthria Gaze paresis Arrhythmias, murmurs, or pulmonary oedema

Answer 172

A

CT head MRI brain Serum glucose Serum electrolytes Serum urea and creatinine Cardiac enzymes ECG FBC Prothrombin time and PTT (with international normalised ratio)

Answer 173

A

Alteplase (recombinant tissue plasminogen activator or r-tPA)

Adjunct: Aspirin 24 hours after r-tPA Endovascular intervention (stent retriever) Plus: Supportive care Swallowing assessment VTE prophylaxis + early mobilisation

Answer 174

A

Aspirin

Plus: Supportive care Swallowing assessment Adjunct: VTE prophylaxis + early mobilisation

Answer 175

A

Deep venous thrombosis (DVT) Seizure Haemorrhagic transformation of ischaemic stroke r-tPA-related orolingual oedema Brain oedema and elevated intracranial pressure Depression Aspiration pneumonia

Answer 176

A

In 2013, a total of 3.3 million individuals died of ischaemic stroke worldwide. Between 1990 and 2010, ischaemic stroke mortality decreased 37% in high-income countries and 14% in low- and middle-income countries.

Answer 177

A

Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space and is an emergency. The most common cause of non-traumatic SAH is intracranial aneurysm. Aneurysmal SAH causes substantial morbidity and mortality. When a cerebral aneurysm ruptures, blood flows into the subarachnoid space, sometimes seeping into brain parenchyma and/or ventricles. The sudden increase in intracranial pressure, as well as the destructive and toxic effects of blood on brain parenchyma and cerebral vessels, accounts for most complications.

Answer 178

A

Rupture of an intracranial saccular aneurysm is the leading cause of non-traumatic SAH, accounting for approximately 80% of cases. The remaining 20% are attributed to non-aneurysmal perimesencephalic SAH, arteriovenous malformations, arterial dissections, use of anticoagulants, and other rare conditions.

Answer 179

A

The incidence of SAH in most populations is between 6 and 8 cases out of 100,000 per year. In the UK, just over 9000 cases were reported in 2012-2013. SAH accounts for about 5% of all strokes.

Answer 180

A

Headache Photophobia Loss of consciousness

Answer 181

A

CT - May also show subdural or parenchymal haematoma, hypodensities, hydrocephalus, and sometimes the aneurysm(s) if large or thrombosed. FBC Clotting profile Serum electrolytes Troponin I ECG

Answer 182

A

A contusion or haemorrhage in the subdural space of the brain.

Answer 183

A

The primary aetiology of both acute and chronic subdural haematomas is trauma. Less commonly, subdural haematomas are associated with rupture of a cerebral aneurysm or vascular malformation (i.e., arteriovenous malformation or dural fistula). There are also case reports in the literature of spontaneous subdural haematomas associated with cerebral hypotension and malignancy.

Answer 184

A

The exact incidence of subdural haematoma is unknown. Acute subdural haematoma is found in about 11% to 20% of patients admitted to hospital with mild to severe traumatic brain injury. Chronic subdural haematomas occur most commonly in older people (age >65 years), and are frequently associated with a history of falls or anticoagulant use.

Answer 185

A

Evidence of trauma Headache Nausea/vomiting Diminished eye response Diminished verbal response Diminished motor response Confusion

Answer 186

A

Non-contrast CT scan - The subdural fluid collection is usually crescentic in shape and can cross suture lines. The age of the haematoma determines the density of the lesion. There may be effacement of the underlying sulci or midline shift, effacement of cisterns or other signs of herniation, or a skull fracture or other intracranial haematomas.

There is no advantage of using an MRI or x-ray. An MRI may be useful after surgery in order to determine the extent of ischaemia and x-ray may be used in order to identify skull fractures which may be due to trauma.

Answer 187

A

All patients on anticoagulation should have their antiplatelet or anticoagulant agent stopped and/or reversed. All patients require serial prothrombin time, partial thromboplastin time, international normalised ratio, and platelet and fibrinogen levels followed. In order to reduce ICP, consider raising the head or surgical intervention if it’s severe.

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Acute Care and Trauma Flashcards

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