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Y3 Content > Acute Care and Trauma > Flashcards

Acute Care and Trauma Flashcards

1
Q

Define ARDS.

A

A syndrome of acute and persistent lung inflammation with increased vascular permeability.

Characterised by:

  • acute onset
  • bilateral infiltrates consistent with pulmonary oedema
  • hypoxaemia
  • no clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure)
  • ARDS is the severe end of the spectrum of acute lung injury
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2
Q

What are the causes of ARDS?

A

Sepsis

Aspiration

Pneumonia

Pancreatitis

Trauma/burns

Transfusion

Transplantation (bone marrow and lung)

Drug overdose/reaction

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3
Q

What are the presenting symptoms of ARDS?

A

Rapid deterioration of respiratory function

Dyspnoea

Respiratory distress

Cough

Symptoms of CAUSE

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4
Q

What are the clinical signs of ARDS on examination?

A

Cyanosis

Tachypnoea

Tachycardia

Widespread inspiratory crepitations

Hypoxia refractory to oxygen treatment

Signs are usually bilateral but may be asymmetrical in early stages

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5
Q

What are the appropriate investigation for ARDS?

A

CXR - bilateral alveolar infiltrates and interstitial shadowing

Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture) -> plasma BNP < 100 pg/mL could distinguish ARDS from heart failure

Echocardiography - check for severe aortic or mitral valve dysfunction and low left ventricular ejection fractions = haemodynamic oedema rather than ARDS

Pulmonary Artery Catheterisation - check pulmonary capillary wedge pressure (PCWP)

Bronchoscopy - if the cause cannot be determined from the history

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6
Q

Define alcohol withdrawal.

A
  • symptoms that may occur when a person has been drinking too much alcohol on a regular basis and suddenly stops drinking
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7
Q

What are the presenting signs and symptoms of alcohol withdrawal?

A

- History of high alcohol intake

  • mild symptoms: insomnia and fatigue, tremor, mild anxiety/feeling nervous, mild restlessness/agitation, nausea and vomiting, headache, sweating, palpitations, anorexia, depression, craving alcohol
  • severe symptoms: hallucinations, withdrawal seizures (generalised tonic-clonic), delirium tremens (anxiety, tremor, sweating, vivid and terrifying visual and sensory hallucinations (usually of animals and insects)
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8
Q

What is the management plan for alcohol withdrawal?

A
  • Chlordiazepoxide - reduces symptoms of alcohol withdrawal
  • Barbiturates may be used if refractory to benzodiazepines
  • Thiamine - prevents progression to Wernicke-Korsakoff syndrome
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9
Q

Define anaphylaxis.

A
  • acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation
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10
Q

What are the common allergies that cause anaphylaxis?

A

Drugs (e.g. penicillin)

Latex

Peanuts

Shellfish

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11
Q

What are the presenting symptoms of anaphylaxis?

A

Wheeze

Shortness of breath and a sense of choking

Swelling of lips and face

Pruritus

Rash

History of other hypersensitivity reactions (e.g. asthma, allergic rhinitis)

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12
Q

What are the clinical signs of anaphylaxis on examination?

A

Tachypnoea

Wheeze

Cyanosis

Swollen upper airways and eyes

Rhinitis

Conjunctival infection

Urticarial rash

Hypotension

Tachycardia

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13
Q

What are the appropriate investigations for anaphylaxis?

A

- Clinical diagnosis

  • Serum tryptase, histamine levels or urinary metabolites of histamine may help support the clinical diagnosis
  • Following an attack -> allergen skin testing and IgE immunoassays (identifies food-specific IgE in the serum)
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14
Q

What is the management plan for anaphylaxis?

A

High flow oxygen

IM Adrenaline

Chlorpheniramine/anti-histamine

Hydrocortisone

If continued respiratory deterioration, may require bronchodilator therapy

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15
Q

What are the possible complications of anaphylaxis?

A
  • shock, organ failure due to shock, death
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16
Q

How much aspirin is toxic to adults?

A

10-20g causes moderate-sever toxicity in adults

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17
Q

What is the trauma triad of death?

A

Hypothermia Coagulopathy Acidosis

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18
Q

What questions are important to ask when dealing with aspirin overdose?

A

How much aspirin was taken?

When was it taken?

Were any other drugs taken?

Have you had any alcohol?

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19
Q

What are the presenting symptoms of aspirin overdose?

A
  • Patient may initially be asymptomatic
  • Early Symptoms: flushed, fever, sweating, hyperventilation, dizziness, tinnitus, deafness
  • Later Symptoms: lethargy, confusion, convulsions, drowsiness, respiratory depression, coma
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20
Q

What are the clinical signs of aspirin overdose on physical examination?

A

Fever

Tachycardia

Hyperventilation

Epigastric tenderness

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21
Q

What are the appropriate investigations for aspirin overdose?

A
  • Bloods: salicylate levels, FBC, U&Es to check for hypokalaemia, LFTs for high AST/ALT, clotting screen/high PT, other drug levels (e.g. paracetamol)
  • ABG - may show mixed metabolic acidosis and respiratory alkalosis
  • ECG = signs of hypokalaemia: flattened/inverted T waves, U waves, prolonged PR interval, ST depression
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22
Q

Define a burns injury.

A
  • tissue damage occurs by thermal, electrical or chemical injury
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23
Q

What are the clinical signs of a burns injury on examination?

A
  • depends on the severity
  • always check for inhalation injury as well as the site of the burn for severity and size
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24
Q

What are the clinical signs of an inhalation burns injury on examination?

A

Stridor

Dyspnoea

Hoarse voice

Soot in nose

Singed nose hairs

Carbonaceous sputum

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25
Q

How are burns injuries categorised?

A
  • partial thickness - splits into superficial and deep
  • full thickness = destruction of the epidermis and dermis
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26
Q

What are the clinical signs of a burns injury on examination of the injury site?

A
  • partial thickness - superficial = red, oedematous and painful skin
  • partial thickness - deep = blistering, mottling and painful skin
  • full thickness = charred leathery eschars, firm and painless with the loss of sensation
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27
Q

What are the appropriate investigations for a burns injury?

A
  • Bloods - sats, FBC, U&Es
  • ABG and carboxyhaemoglobin (if inhalational injury)
  • Investigations for electrical burns = serum CK, urine myoglobin (check for muscle damage), ECG
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28
Q

Define extradural haemorrhage.

A
  • bleeding and accumulation of blood in the extradural space
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29
Q

What is the usual cause of an extradural haemorrhage?

A
  • fracture of the temporal or parietal bones leading to rupture of the middle meningeal artery
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30
Q

What are the presenting symptoms of extradural haemorrhages?

A
  • Head injury with temporary loss of consciousness
  • Followed by lucid interval
  • Followed by progressive deterioration in conscious level
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31
Q

What are the clinical signs of an extradural haemorrhage on examination?

A
  • Scalp trauma or fracture
  • Headache
  • Deteriorating GCS
  • Signs of raised ICP - dilated, unresponsive pupil on the side of the injury
  • Cushing’s Reflex - hypertension, bradycardia, irregular breathing
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32
Q

What are the appropriate investigations foran extradural haemorrhage?

A
  • Urgent CT Scan
  • Check for a haematoma
  • Look for features of raised ICP (e.g. midline shift)
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33
Q

Define MODS.

A
  • a clinical syndrome characterised by the development of progressive and potentially reversible physiologic dysfunction of 2 or more organs or organ systems that is induced by a variety of insults, including sepsis
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34
Q

What can cause MODS?

A
  • Usually results from: infection, injury, hypoperfusion, hypermetabolism
  • Primary cause can trigger a systemic inflammatory response (sepsis or SIRS (systemic inflammatory response syndrome))
  • MODS is the final stage in a continuum beginning with SIRS + infection:

SIRS + infection –> sepsis –> severe sepsis –> MODS

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35
Q

What are the appropriate investigations for MODS?

A
  • Monitor vital signs
  • ABG may be necessary to look at hypoxaemia, lactic acidosis etc.
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36
Q

What are the presenting symptoms of opiate overdose?

A
  • Constipation (if chronic)
  • Nausea and vomiting
  • Loss of appetite
  • Sedation
  • Craving the next dose
  • Drowsiness (if acute overdose)
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37
Q

What are the clinical signs of opiate overdose on examination?

A
  • Respiratory depression
  • Hypotension and tachycardia
  • Pinpoint pupils
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38
Q

What are the appropriate investigations for opiate overdose?

A
  • Toxicology screen
  • Paracetamol blood level (should be considered in patients who have self-poisoned)
  • If in doubt, give a small test dose of naloxone
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39
Q

How much paracetamol causes hepatic necrosis?

A

12g

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40
Q

What are the risk factors for opiate overdose?

A
  • Mental health conditions
  • Alcoholics (due to liver damage)
  • Morphine toxicity at a lower dose due to: hepatic impairment, renal impairment, hypotension, hypothyroidism, asthma (decreased respiratory reserve)
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41
Q

What are the risk factors for paracetamol overdose?

A

Chronic alcohol abusers

Patients on enzyme-inducing drugs (e.g. anticonvulsants)

Malnourished

Anorexia nervosa

HIV

  • Commonly associated with ingestion of large amounts of alcohol
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42
Q

What are the presenting symptoms of paracetamol overdose?

A
  • 0-24 hrs = ASYMPTOMATIC, mild nausea/vomiting, lethargy, malaise
  • 24-72 hrs = RUQ pain, vomiting
  • 72+ hrs = increased confusion (encephalopathy), jaundice
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43
Q

What are the clinical signs of paracetamol overdose on examination?

A
  • 0-24 hrs = no signs
  • 24-72 hrs = liver enlargement and tenderness
  • 72+ hrs = jaundice, coagulopathy, hypoglycaemia, renal angle tenderness
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44
Q

What are the appropriate investigations for paracetamol overdose?

A
  • Measure paracetamol levels - peak paracetamol levels are 4 hrs after ingestion
  • Others: FBC, U&Es, Glucose, LFTs, Clotting Screen, Lactate and ABG
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45
Q

Define AKI.

A

An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.

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46
Q

What are the risk factors for AKI?

A

Age

Chronic kidney disease

Comorbidities (e.g. heart failure)

Sepsis

Hypovolaemia

Use of nephrotoxic medications

Emergency surgery

Diabetes mellitus

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47
Q

What are the presenting symptoms of AKI?

A

Oliguria/anuria - abrupt anuria suggests post-renal obstruction

Nausea/vomiting

Dehydration

Confusion

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48
Q

What are the signs of AKI on examination?

A

Hypertension

Distended bladder

Dehydration - postural hypotension

Fluid overload (raised JVP, pulmonary and peripheral oedema) heart failure, cirrhosis, nephrotic syndrome)

Pallor, rash, bruising (vascular disease)

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49
Q

What are the appropriate investigations for AKI?

A

o Bloods - FBC, Blood film, U&Es, Clotting, CRP, Immunology (serum immunoglobulins and protein electrophoresis for multiple myeloma, ANA and antidsDNA for SLE, anti-GBM antibodies for Goodpasture’s syndrome, antistreptolysin-O antibodies high after streptococcal infection), Virology (check for hepatitis and HIV)

o Urinalysis - Blood (nephritic cause), Leucocyte esterase and nitrites, Glucose, Protein, Urine osmolality

o Imaging - Ultrasound (post-renal cause and hydronephrosis), CXR (pulmonary oedema), AXR (renal stones)

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50
Q

What is the management plan for AKI?

A

- Treat the cause

  • 4 main components to management - Protect patient from hyperkalaemia (calcium gluconate), Optimise fluid balance, Stop nephrotoxic drugs, Consider for dialysis
  • Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
  • Renal Replacement Therapy (RRT) considered if hyperkalaemia refractory to medical management, pulmonary oedema refractory to medical management, severe metabolic acidaemia, uraemic complications
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51
Q

What are the possible complications of AKI?

A

Pulmonary oedema

Acidaemia

Uraemia

Hyperkalaemia

Bleeding

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52
Q

Define adrenal insufficiency.

A

Deficiency of adrenal cortical hormones (e.g. mineralocorticoids, glucocorticoids and androgens).

  • primary adrenal insufficiency = Addison’s disease
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53
Q

What are the causes/risk factors of adrenal insufficiency?

A

o Primary Adrenal Insufficiency - Addison’s disease (usually autoimmune)

o Secondary Adrenal Insufficiency - pituitary or hypothalamic disease

o Infections - TB, meningococcal septicaemia, CMV, histoplasmosis

o Infiltration - metastasis (mainly from lung, breast, melanoma), lymphomas, amyloidosis

o Infarction - secondary to thrombophilia

o Inherited - adrenoleukodystrophy, ACTH receptor mutation

o Surgical - after bilateral adrenalectomy

o Iatrogenic - sudden cessation of long-term steroid therapy

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54
Q

What are the presenting symptoms of chronic adrenal insufficiency?

A

o Symptoms tend to be VAGUE and NON-SPECIFIC

  • Dizziness
  • Anorexia
  • Weight loss
  • Diarrhoea and Vomiting
  • Abdominal pain
  • Lethargy
  • Weakness
  • Depression
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55
Q

What are the presenting symptoms of acute adrenal insufficiency?

A

Acute adrenal insufficiency

Major haemodynamic collapse

Precipitated by stress (e.g. infection, surgery)

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56
Q

What are the signs of adrenal insufficiency on examination?

A

Postural hypotension

Increased pigmentation

More noticeable on buccal mucosa, scars, skin creases, nails and pressure points

Loss of body hair in women (due to androgen deficiency)

Associated autoimmune condition (e.g. vitiligo)

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57
Q

What are the signs of an Addisonian crisis on examination?

A

Hypotensive shock

Tachycardia

Pale

Cold

Clammy

Oliguria

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58
Q

What are the appropriate investigations to confirm the diagnosis of adrenal insufficiency?

A

o To confirm the diagnosis

  • 9 am Serum Cortisol (< 100 nmol/L is diagnostic of adrenal insufficiency) - > 550 nmol/L makes adrenal insufficiency unlikely
  • Short Synacthen Test = IM 250 mg tetrocosactrin (synthetic ACTH) -> serum cortisol < 550 nmol/L at 30 mins indicates adrenal failure
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59
Q

What are the appropriate investigations to identify the cause of adrenal insufficiency?

A

o Autoantibodies (against 21-hydroxylase)

o Abdominal CT or MRI

o Other tests (adrenal biopsy, culture, PCR)

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60
Q

What are the appropriate investigations for Addisonian crisises?

A

o Bloods - TFTs, FBC (neutrophilia –> infection), U&Es, high urea, low sodium, high potassium, CRP/ESR, calcium (may be raised), glucose

o Blood cultures and sensitivity

o Urinalysis

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61
Q

What are the possible complications of adrenal insufficiency?

A

o Hyperkalaemia

o Death during Addisonian crisis

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62
Q

What are the indications for an arterial blood gas?

A

o Respiratory failure - in acute and chronic states.

o Any severe illness which may lead to a metabolic acidosis - Cardiac failure, Liver failure, Renal failure, Hyperglycaemic states associated with diabetes mellitus, Multiorgan failure, Sepsis, Burns, Poisons/toxins,

o Ventilated patients

o Severely unwell patients from any cause - affects prognosis

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63
Q

What are the complications of ABGs?

A

Arteriospasm

Haematoma

Nevre damage

Fainting/Vasovagal response

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64
Q

Define asthma.

A

Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.

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65
Q

What are the risk factors/causes of asthma?

A
  • Genetic Factors = family history, atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens)
  • Environmental Factors = house dust mites, pollen, pets, cigarette smoke, viral respiratory tract infections, aspergillus fumigatus spores, occupational allergens
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66
Q

What is the epidemiology of asthma?

A

Affects 10% of children and 5% of adults

Prevalence appears to be increasing

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67
Q

What are the presetning symptoms of asthma?

A
  • Episodic history
  • Wheeze
  • Breathlessness
  • Cough (worse in the morning and at night)
  • Precipitating Factors = cold, viral infection, drugs (e.g. beta-blockers, NSAIDs), exercise, emotions
  • Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
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68
Q

What are the clinical signs of asthma on examination?

A
  • Tachypnoea
  • Use of accessory muscles
  • Prolonged expiratory phase
  • Polyphonic wheeze
  • Hyperinflated chest

o Severe Attack = PEFR < 50% predicted, Pulse > 110/min, RR > 25/min, Inability to complete sentences

o Life-Threatening Attack = PEFR < 33% predicted, Silent chest, Cyanosis, Bradycardia, Hypotension, Confusion, Coma

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69
Q

What are the appropriate investigations for asthma?

A

o Acute = Peak flow, Pulse oximetry, ABG, CXR - to exclude other diagnoses, FBC (infection if raised WCC), CRP, U&Es, Blood and sputum cultures

o Chronic = Peak flow monitoring, Pulmonary function test, Check for eosinophilia/IgE level/Aspergillus antibody titres, Skin prick tests to identify allergens

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70
Q

What is the treatment plan for an asthma attack?

A

o ABCDE plus resuscitation if required

o Monitor O2 sats, ABG and PEFR - normal PCO2 is a bad sign as patient should hyperventilate and blow CO2 off - if low it suggests the patient is fatiguing - think about anaesthesia and ventilation

o High-flow Oxygen

o Salbutamol nebulizer (5mg initially continously then 2-4 hourly)

o Ipratropium (0.5mg QDS)

o Steroids (100-200mg IV hydrocortisone then 40mg prednisolone for 5-7 days)

  • No imporvement = IV magnesium sulphate and consider IV aminophylline and/or IV sabutamol
  • Treat underlying cause
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71
Q

What is the long-term management of asthma?

A

o STEP 1 = Inhaled short-acting beta-2 agonist used as needed

o STEP 2 = Step 1 + regular inhaled low-dose steroids (400 mcg/day)

o STEP 3 = Step 2 + inhaled long-acting beta-2 agonist (LABA) -> If inadequate control with LABA, increase steroid dose (800 mcg/day) -> If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)

o STEP 4 = Increase inhaled steroid dose (2000 mcg/day) and add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet)

o STEP 5 = Add regular oral steroids, maintain high-dose oral steroids and refer to specialist care

  • Advice: teach proper inhaler technique, explain important of PEFR monitoring, avoid provoking factors
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72
Q

What are the possible complications of asthma?

A

Growth retardation

Chest wall deformity (e.g. pigeon chest)

Recurrent infections

Pneumothorax

Respiratory failure

Death

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73
Q

Define cardiac arrest.

A

Acute cessation of cardiac function.

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74
Q

What are the reversible causes of cardiac arrest?

A

o 4 Hs

  • Hypothermia
  • Hypoxia
  • Hypovolaemia
  • Hypokalaemia/Hyperkalaemia

o 4 Ts

  • Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))
  • Thromboembolic
  • Tamponade
  • Tension pneumothorax
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75
Q

What are the presenting symtpoms of cardiac arrest?

A

Management precedes or is concurrent to history

Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness

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76
Q

What are the signs of cardiac arrest on examination?

A

Unconscious

Not breathing

Absent carotid pulses

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77
Q

What are the appropriate investigations for cardiac arrest?

A

o Cardiac monitor - allows classification of the rhythm

o Bloods - ABG, U&E, FBC, X-match, clotting, toxicology screen, blood glucose

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78
Q

What is the treatment of a cardiac arrest?

A

o Safety is important - approach with caution as cause of arrest may pose a threat

o BLS - ABCDE, chest compressions, rescue breaths

o ALS - attach cardiac monitor/defibrillator to assess rhythm

  • If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms) - defibrillate once (150-360 J biphasic, 360 J monophasic) then resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF -> Administer adrenaline (1 mg IV) after second defibrillation and again every 3-5 mins -> If shockable rhythm persists after 3rd shock administer amiodarone 300 mg IV bolus (or lidocaine)

o If pulseless electrical activity (PEA) or asystole (non-shockable rhythms) - CPR for 2, and then reassess rhythm, administer adrenaline (1 mg IV) every 3-5 mins and atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm

o During CPR - check electrodes, paddle positions and contacts, secure airway and consider magnesium, bicarbonate and external pacing

o Stop CPR and check pulse only if change in rhythm or signs of life

o Treatment of reversible cause if known

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79
Q

Define cardiac failure.

A

Inability of the cardiac output to meet the body’s demands despite normal venous pressures.

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80
Q

What are the causes of low output, left heart failure?

A

Ischaemic heart disease

Hypertension

Cardiomyopathy

Aortic valve disease

Mitral regurgitation

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81
Q

What are the causes of low output, right heart failure?

A

Secondary to left heart failure (in which case it is called congestive cardiac failure)

Infarction

Cardiomyopathy

Pulmonary hypertension/embolus/valve disease

Chronic lung disease

Tricuspid regurgitation

Constrictive pericarditis/pericardial tamponade

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82
Q

What are the causes of low output, biventricular failure?

A

Arrhythmia

Cardiomyopathy (dilated or restrictive)

Myocarditis

Drug toxicity

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83
Q

What are the causes of high output cardiac failure?

A

Anaemia

Beriberi – caused by Vitamin B1 deficiency

Pregnancy

Paget’s disease

Hyperthyroidism

Arteriovenous malformation

84
Q

What are the presenting symptoms of left heart failure?

A

o Symptoms caused by pulmonary congestion = Orthopnoea, Paroxysmal Nocturnal Dyspnoea, Fatigue

o Dyspnoea - divided based on the New York Heart Association classification:

1 - no dyspnoea

2 - dyspnoea on ordinary activities

3 - dyspnoea on less than ordinary activities

4 - dyspnoea at rest

85
Q

What are the presenting symptoms of acute left ventricular failure?

A

o Dyspnoea

o Wheeze

o Cough

o Pink frothy sputum

86
Q

What are the presenting symptoms of right heart failure?

A

o Swollen ankles

o Fatigue

o Increased weight (due to oedema)

o Reduced exercise tolerance

o Anorexia

o Nausea

87
Q

What are the signs of left heart failure on examination?

A

o Tachycardia

o Tachypnoea

o Displaced apex beat - due to cardiomegaly

o Bilateral basal crackles

o S3 gallop - due to rapid ventricular filling

o Pansystolic murmur - due to functional mitral regurgitation

88
Q

What are the signs of acute left ventricular failure on examination?

A

o Tachypnoea

o Cyanosis

o Tachycardia

o Peripheral shutdown

o Pulsus alternans = arterial pulse waveforms showing alternating strong and weak beats and signs of left ventricular systolic impairment (stronger systolic pulse)

o Gallop rhythm

o Wheeze (cardiac asthma)

o Fine crackles throughout lung

89
Q

What are the signs of right heart failure on examination?

A

Raised JVP

Hepatomegaly

Ascites

Ankle/sacral pitting oedema

Signs of functional tricuspid regurgitation

90
Q

What are the appropriate investigations for cardiac failure?

A

o Bloods = FBC, U&E, LFTs, CRP, glucose, lipids, TFTs

o CXR = Alveolar shadowing, Kerley B lines, Cardiomegaly, Upper Lobe Diversion, Pleural Effusion

o ECG = may be normal or show ischaemic changes (pathological q waves, t wave inversion), arrhythmia or left ventricular hypertrophy

o Echocardiogram = assess ventricular contraction, systolic dysfunction (LV ejection fraction < 40%), diastolic dysfunction (decreased compliance of the myocardium leads to restrictive filling defect)

o Swan-Ganz Catheter = allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures

o In Acute Left Ventricular Failure = ABG, Troponin, BNP (raised plasma BNP suggests diagnosis of cardiac failure or low plasma BNP rules out cardiac failure (90% sensitivity))

91
Q

What is the treatment for cardiogenic shock?

A

This is severe cardiac failure with low blood pressure

Requires the use of inotropes (e.g. dobutamine)

Managed in ITU

92
Q

What is the treatment for pulmonary oedema?

A

o Sit the patient up

o 60-100% Oxygen (and consider CPAP)

o Diamorphine (venodilator + anxiolytic)

o GTN infusion (venodilator –> reduced preload)

o IV furosemide (venodilator and later diuretic effect)

o TREAT THE CAUSE! (e.g. MI, arrhythmia)

93
Q

What is the treatment for chronic left ventricular failure?

A

o TREAT THE CAUSE (e.g. hypertension)

o TREAT EXACERBATING FACTORS (e.g. anaemia)

o ACE Inhibitors - slows progression of heart failure and improves survival

o Beta-Blockers - slows progression of heart failure and improves survival

  • benefits of ACE inhibitors and beta-blockers are additive

o Loop Diuretics/dietary salt restriction to correct fluid overload

o Aldosterone Antagonists - improves survival in patients with NYHA class III/IV symptoms on standard therapy

o Angiotensin Receptor Blockers

o Hydralazine and a Nitrate

o Digoxin - reduces hospitalisation/symptoms but does NOT improve survival

o N-3 Polyunsaturated Fatty Acids

o Cardiac Resynchronisation Therapy

94
Q

What are the possible complications of cardiac failure?

A

Respiratory failure

Cardiogenic shock

Death

95
Q

Define COPD.

A

A lung disease characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible.

96
Q

What are the risk factors for COPD?

A
  • Smoking
  • Asthma - especially if then exposed to tobacco fumes
  • Exposure to dust and/or chemicals
  • Exposure to fumes of burning fossil fuels
  • Being older
  • Genetics/Alpha-1 Anti-trypsin deficiency
97
Q

What are the presetnign symptoms of COPD?

A

o Shortness of breath, especially during physical activities

o Wheezing

o Chest tightness

o Having to clear your throat first thing in the morning, due to excess mucus in your lungs

o A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or greenish - depending on if infected or not

o Frequent respiratory infections

o Lack of energy

o Swelling in ankles, feet or legs

  • LAte on = Unintended weight loss
98
Q

What are the clinical signs of COPD?

A

o An expanded chest/barrel chest

o Wheezing during normal breathing

o Taking longer to exhale fully

o Decreased breath sounds or abnormal breath sounds such as crackles or wheezes.

o For assessing severity = use of “accessory” muscles, breathing through pursed lips, inability to complete full sentences without stopping to take a breath, bluish discoloration of the fingertips or nail beds (cyanosis), swelling in the legs or abdomen

99
Q

What are the appropriate investigations for COPD?

A
  • Spirometry
  • O2 Sats
  • ABG
  • CXR
  • FBC (may show signs of exacerbation, polycythaemia, anaemia or leucocytosis)
  • Alpha-1 Antitrypsin
  • Sputum Culture
100
Q

What are the possible complications of COPD?

A
  • Cor-pulmonale
  • Recurrent pneumonia
  • Depression
  • Pneumothorax
  • Respiratory failure
  • Anaemia
  • Polycythaemia
101
Q

What are the presenting signs and symptoms of DKA?

A

Nausea and vomiting

Abdominal pain

Polyuria, polydipsia

Drowsiness

Confusion

Coma

Kussmaul breathing

Ketotic breath

Signs of dehydration

102
Q

What are the appropriate investigations for DKA?

A

o Bloods = FBC (raised WCC without infection in DKA), U&Es (raised urea and creatinine due to dehydration), LFT, CRP, glucose, amylase

o Blood cultures

o ABG (metabolic acidosis with high anion gap)

o Blood/urinary ketones

103
Q

What is the treatment of DKA?

A

o 50 U soluble insulin in 50 mL of normal saline

o Use an insulin sliding scale until capillary ketones < 0.3, venous pH > 7.30, venous bicarbonate > 18 mmol/L before changing to SC insulin (keep insulin running for 1-2hrs after SC)

o 500 mL normal saline over 15-30 mins until SBP > 100

o Potassium replacement (because insulin drives potassium into cells)

o Monitor blood glucose, capillary ketones and urine output hourly

o Monitor U&Es and venous blood gas

o Broad spectrum antibiotics if infection is suspected

o Thromboprophylaxis

o NBM for at least 6 hrs

o NG tube if GCS is reduced

104
Q

Define DKA.

A

HIgh blood glucose with the presence of ketones in the blood and urine.

105
Q

What are the risk factors for DKA?

A
  • T1DM
  • Infection
  • Recent emotional or physical trauma
  • Smoking
  • Alcohol
  • Stress
106
Q

What are the possible complications of DKA?

A
  • Hypokalaemia -> heart arrhythmias and muscle weakness
  • Cerebral oedema
  • Pulmonary oedema
  • Damage to your kidney or other organs from your fluid loss
  • DEATH
107
Q

Define DIC.

A

A disorder of the clotting cascade that can complicate a serious illness.

o DIC can occur in TWO forms:

  • acute overt = there is bleeding and depletion of platelets and clotting factors
  • chronic non-overt = thromboembolism is accompanied by generalised activation of the coagulation system
108
Q

What are the risk factors/causes of DIC?

A
  • Gram-negative sepsis
  • Obstetric Complications = missed miscarriage, severe pre-eclampsia, placental abruption, amniotic emboli
  • Malignancy = acute promyelocytic leukaemia (AML) - acute DIC, lung, breast and GI malignancy - chronic DIC
  • Severe trauma or surgery
  • Others: haemolytic transfusion reaction, burns, severe liver disease, aortic aneurysms, haemangiomas
109
Q

What are the presenting symptoms of DIC?

A

Severely unwell with symptoms of the underlying disease

Confusion

Dyspnoea

Evidence of bleeding

110
Q

What are the clinical signs of DIC on examination?

A

o Signs of underlying disease

o Fever

o Evidence of shock (hypotension, tachycardia)

o Acute DIC = petechiae, purpura, ecchymoses, epistaxis, mucosal bleeding, overt haemorrhage, signs of end organ damage, respiratory distress, oliguria due to renal failure

o Chronic DIC = signs of deep vein and arterial thrombosis or embolism, superficial venous thrombosis

111
Q

What are the appropriate investigations for DIC?

A

o Bloods = FBC, Low platelets, Low Hb, High APTT/PT, Low fibrinogen, High fibrin degradation products, High D-dimers

o Peripheral Blood Film = Schistocytes

112
Q

Define encephalitis.

A

Inflammation of the brain parenchyma.

113
Q

What are the risk factors for encephalitis?

A

o Most commonly due to VIRAL INFECTION - Herpes Simplex Virus - MOST COMMON in the UK, VZV, Mumps, Adenovirus, Coxsackie, EBV, HIV, Japanese encephalitis

o Non-Viral (RARE) - Syphilis, Staphylococcus aureus

o In immunocompromised patients - CMV, Toxoplasmosis, Listeria

o Autoimmune or Paraneoplastic - Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)

114
Q

What are the presenting symptoms of encephalitis?

A

In most cases, encephalitis is self-limiting and mild

Subacute onset (hours to days)

Headache

Fever

Vomiting

Neck stiffness

Photophobia

Behavioural changes

Drowsiness

Confusion

History of seizures

Focal neurological symptoms (e.g. dysphagia, hemiplegia)

A RECENT HISTORY OF TRAVEL

115
Q

What are the signs of encephalitis on examination?

A
  • Reduce consciousness
  • Deteriorating GCS
  • Seizures
  • Pyrexia
  • Signs of Meningism = neck stiffness, photophobia, Kernig’s test positive
  • Signs of raised ICP = Cushing’s Response: hypertension + bradycardia + irregular breathing, Papilloedema
  • Focal neurological signs
  • MMSE may reveal cognitive/psychiatric disturbance
116
Q

What are the appropropriate investigations for encephalitis?

A

o Bloods/ABG = FBC - high lymphocytes (indicates viral cause), U&Es - SIADH may occur as a result of encephalitis, Glucose, Viral serology

o MRI/CT = exclude mass lesion, HSV causes oedema of the temporal lobe on MRI

o Lumbar Puncture = high lymphocytes, high monocytes, high protein, glucose is usually normal, viral PCR

o EEG - may show epileptiform activity

o Brain biopsy (rarely needed)

117
Q

What are the indications for an epidural?

A
  • Surgery
  • Autonomic hyperreflexia
  • Myasthenia gravis
  • Pheochromocytoma
118
Q

What are the possible complications of an epidural?

A
  • Low blood pressure
  • Loss of bladder control
  • Feeling sick
  • Itchy skin
  • Headache
  • Temporary/Permanent nerve damage
  • Infection
  • Bradypnoea
  • Fits
  • DEATH
119
Q

What is the treatment of COPD?

A
  • Long or Short acting bronchodialtors
  • Patient education
  • Vaccination
  • Smoking cessation
  • Oxygen therapy
  • Theophylline or Aminophylline
120
Q

What are the indications for an unirnary catheter?

A
  • Acute/Chronic urinary retention
  • To protect the bladder
  • Surgery
  • Severly impaired continence
  • Neurogenic bladder
  • Spina bifida
121
Q

Define epilepsy.

A

A tendency to recurrent unprovoked seizures.

  • need to have >2 seizures for epilepsy to be diagnosed
122
Q

Define seizure.

A

Paroxysmal synchronised cortical electrical discharges.

123
Q

What are the risk factors for epilepsy?

A

o Most cases are IDIOPATHIC

o Primary epilepsy syndromes (e.g. idiopathic generalised epilepsy)

o Secondary Seizures = Tumour, Infection, Inflammation, Toxic/Metabolic, Drugs, Vascular/Haemorrhage, Congenital abnormalities, Neurodegenerative disease, Malignant hypertension or eclampsia, Trauma

124
Q

What is important to consider when taking a history of a potential epileptic?

A

Rapidity of onset

Duration of episode

Any alteration in consciousness?

Any tongue-biting or incontinence?

Any rhythmic synchronous limb jerking?

Any post-ictal abnormalities (e.g. exhaustion, confusion)?

Drug history (alcohol, recreational drugs)

125
Q

What are the presenting features of frontal lobe focal motor seizures?

A

Motor convulsions

May show a Jacksonian march (when the muscular spasm caused by the simple partial seizure spreads from affecting the distal part of the limb towards the ipsilateral face)

May show post-ictal flaccid weakness (Todd’s paralysis)

126
Q

What are the presenting features of temporal lobe seizures?

A

Aura (visceral or psychic symptoms)

Hallucinations (usually olfactory or affecting taste)

127
Q

What are the presenting symptoms of frontal lobe complex partial seizres?

A

Loss of consciousness

Involuntary actions/disinhibition

Rapid recovery

128
Q

What are the presenting symptoms of tonic-clonic seizures?

A
  • vague symptoms before attack (e.g. irritability)

o Tonic phase = generalised muscle spasm

o Clonic phase = repetitive synchronous jerks

  • Faecal/urinary incontinence
  • Tongue biting
  • post-ictal phase: impaired consciousness, lethargy, confusion, headache, back pain, stiffness
129
Q

What are the presenting symptoms of absence seizures?

A

Onset in CHILDHOOD

Loss of consciousness but MAINTAINTED POSTURE

The patient will appear to stop talking and stare into space for a few seconds

NO post-ictal phase

130
Q

What are the presenting symptoms of non-convulsive status epilepticus?

A

Acute confusional state

Often fluctuating

Difficult to distinguish from dementia

131
Q

What are appropriate investigations for epilepsy?

A

o Bloods/ABG - FBC, U&E, LFTs, glucose, calcium, magnesium, toxicology screen, prolactin (shows a transient increase shortly after seizures)

o EEG - to confirm diagnosis and classify the epilepsy

o CT/MRI - shows structural, space-occupying or vascular lesions

o Investigations if tumours, infection, haemorrhage etc is possible

132
Q

Define status epilepticus.

A

A seizure lasting > 30 mins or repeated seizure without recovery and regain of consciousness in between.

133
Q

What is the treatment of status epilepticus?

A

o Although the definition states that the seizure must last > 30 mins, treatment is usually initiated early (after around 5-10 mins)

o ABC approach

o Check GLUCOSE and give glucose if hypoglycaemic

o IV lorazepam OR IV/PR diazepam - REPEAT again after 10 mins if seizure does not terminate or consider IV phenytoin (an ECG monitor is required) or GAs (intubation and mechanical ventilation required)

o Treat the CAUSE (e.g. hypoglycaemia or hyponatraemia)

o Check plasma levels of anticonvulsants (because status epilepticus is often caused by lack of compliance with anti-epileptic medications)

134
Q

What is the treatment plan for newly diagnosed epilepsy?

A

o Only start anti-convulsant treatment after > 2 unprovoked seizures

  • focal seizure 1st line = lamotrigine or carbamazepine
  • generalised seizure 1st line = sodium valproate
  • start treatment with only ONE anti-epileptic drug
  • other anti-convulsants: phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin

o Patient EDUCATION - avoid triggers, seizure diaries, careful of drug interactions (e.g. AEDs can reduce the effectiveness of the oral contraceptive pill)

o Surgery may be considered for refractory epilepsy

135
Q

What are the possible complications of epilepsy?

A

o Fractures from tonic-clonic seizures

o Behavioural problems

o Sudden death in epilepsy (SUDEP)

o Complications of anti-epileptic drugs

136
Q

What are the presenting symptoms of ACS?

A

o Acute-onset chest pain which is central, heavy, tight, crushing pain

o Radiates to the arms, neck, jaw or epigastrium

o Occurs at rest

o More severe and frequent pain that previously occurring stable angina

o Breathlessness

o Sweating

o Nausea and vomiting

137
Q

What are the presenting symptoms of stable angina?

A

Chest pain brought on by exertion and relieved by rest

138
Q

What are the signs of stable angina on examination?

A
  • signs of risk factors
139
Q

What are the signs of ACS on examination?

A

o There may be NO CLINICAL SIGNS

o Pale

o Sweating

o Restless

o Low-grade pyrexia

o Check both radial pulses to rule out aortic dissection

o Arrhythmias

o Disturbances of BP

o New heart murmurs

Signs of complications (e.g. acute heart failure, cardiogenic shock)

140
Q

What are the appropriate investigations for IHD?

A

o Bloods

o ECG

o CXR

o Exercise ECG

o Radionuclide myocardial perfusion imaging

o Echo

o Pharmacological stress test

o Cardiac catherisation

o Coronary calcium scoring

141
Q

What is the treatment for stable angina?

A

o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)

o Aspirin 75 mg/day unless contraindicated

o Immediate symptom relief (e.g. GTN spray)

o Long-term management = beta-blockers unless contraindicated by acute heart failure, cardiogenic shock, bradycardia, heart block, asthma - so in these cases calcium channel blockers or nitrates

o Percutaneous coronary intervention (PCI) - performed in patients with stable angina despite maximal tolerable medical therapy

o Coronary artery bypass graft (CABG) - more severe cases (e.g. three-vessel disease)

142
Q

What is the treatment for unstable angina or NSTEMI?

A

o MONABASH for acute treatment

  • Morphine
  • Oxygen
  • Nitrates
  • Anti-coagulants - 300mg of aspirin and then 75mg + clopidogrel
  • Beta-blcokers
  • ACE inhibitors
  • Statins
  • Heparin (LMWH)

o admit to coronary care unit

143
Q

What is the treatment for a STEMI?

A

o MONABASH again with higher doses of clopidogrel

o Primary PCI with goal of < 90 mins

o Thrombolysis (tPa ect) if within 12 hours of chest pain and ECG changes and not contraindicated

o Secondary prevention

o Advised not to drive for 1 month

o CABG = for patients with left main stem or three-vessl disease

144
Q

What are the possible complications of IHD?

A

o DARTHVADE

Death

Arrhythmias

Rupture

Tamponade

Heart failure

Valve disease

Aneurysm

Dressler’s syndrome

Embolism

145
Q

Define meningitis.

A

Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection.

146
Q

What are the risk factors for meningitis?

A

Close communities (e.g. university/college halls)

Basal skull fractures

Mastoiditis

Sinusitis

Inner ear infections

Alcoholism

Immunodeficiency

Splenectomy

Sickle cell anaemia

CSF shunts

Intracranial surgery

147
Q

What are the presenting symptoms of meningitis?

A

o Severe headache

o Photophobia

o Neck or backache

o Irritability

o Drowsiness

o Vomiting

o High-pitched crying or fits (common in children)

o Reduced consciousness

o Fever

o Recent exposure to: rodents, ticks, mosquitoes, sexual transmitted disease or travel

148
Q

What are the signs of meningitis on examination?

A

o Signs of Meningism = Photophobia, Neck stiffness, Kernig’s Sign (with the hips flexed, there is pain/resistance on passive knee extension), Brudzinski’s Sign (flexion of the hips when the neck is flexed)

o Signs of Infection = Fever, Tachycardia, Hypotension, Skin rash, Altered mental state

149
Q

What are the appropriate investigations for meningitis?

A

o Bloods - 2 sets of blood cultures

o Imaging - CT scan to exclude mass lesion or raised ICP before LP

o Lumbar Puncture for MC&S

150
Q

What would the lumbar puncture results be for bacterial meningitis?

A

Cloudy CSF

High neutrophils

High protein

Low glucose

151
Q

What would the lumbar puncture results be for viral meningitis?

A

High lymphocytes

High protein

Normal glucose

152
Q

What would the lumbar puncture results be for TB meningitis?

A

Fibrinous CSF

High lymphocytes

High protein

Low glucose

153
Q

What is the treatment plan for meningitis?

A

o IMMEDIATE IV Antibiotics - first choice is 3rd generation cephalosporin (e.g. cefotaxime or ceftriaxone)

o Dexamethasone IV - given shortly before or with the first dose of antibiotics due to it being associated with a reduced risk of complications

o Resuscitation - manage in ITU, notify public health services

154
Q

What are the possible complications of meningitis?

A

Septicaemia

Shock

DIC

Renal failure

Seizures

Peripheral gangrene

Cerebral oedema

Cranial nerve lesions

Cerebral venous thrombosis

Hydrocephalus

Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)

155
Q

Define stroke.

A

Rapid permanent neurological deficit from cerebrovascular insult lasting >24hrs.

156
Q

What are the causes of infarction strokes?

A

o Thrombosis - can occur in small vessels (lacunar infarcts), larger vessels (e.g. middle cerebral artery) or in prothrombotic states (e.g. dehydration, thrombophilia)

o Emboli - from carotid dissection, carotid atherosclerosis, atrial fibrillation or occasionally venous blood clots that pass through a septal defect

o Hypotension - if the blood pressure is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories

o Others - vasculitis, cocaine (arterial spasm)

157
Q

What are the causes of haemorrhagic strokes?

A

Hypertension

Charcot-Bouchard microaneurysm rupture

Amyloid angiopathy

Arteriovenous malformations

Less common: trauma, tumours, vasculitis

158
Q

What are the presenting symptoms of strokes?

A

o Sudden onset

o Weakness

o Sensory, visual or cognitive impairment

o Impaired coordination

o Impaired consciousness

o Head or neck pain (if carotid or vertebral artery dissection)

o History of AF, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain

159
Q

What are the signs of lucnar infarct strokes on examination?

A

o Affecting the internal capsule or pons = pure sensory and/or motor deficit

o Affecting the thalamus = loss of consciousness, hemisensory deficit

o Affecting the basal ganglia = hemichorea, hemiballismus, parkinsonism

160
Q

What are the signs of an anterior cerebral artery stroke on examination?

A

Contralateral hemiplegia - leg more so than the arm or face - because the motor homunculus controlling the leg is more medial to the part controlling the arm

Disturbance of intellect, executive function and judgment (abulia – absence of willpower)

Loss of appropriate social behaviour

161
Q

What are the signs of a middle cerebral artery stroke on examination?

A

Contralateral hemiplegia – arm and face more so than the leg

Hemisensory loss (sensory cortex)

Apraxia

Hemineglect (parietal lobe)

Receptive or expressive dysphasia (due to involvement of Wernicke’s and Broca’s areas)

Quadrantopia (if superior or inferior optic radiations are affected)

162
Q

What are the signs of a posterior cerebral artery stroke on examination?

A

Hemianopia

163
Q

What are the signs of an anterior inferior cerebellar artery stroke on examination?

A

Vertigo

Ipsilateral ataxia

Ipsilateral deafness

Ipsilateral facial weakness

164
Q

What are the signs of a posterior inferior cerebellar artery stroke on examination?

A

Vertigo

Ipsilateral ataxia

Ipsilateral Horner’s syndrome

Ipsilateral hemisensory loss

Dysarthria

Contralateral spinothalamic sensory loss

165
Q

What are the signs of a basilar artery stroke on examination?

A

Locked-In syndrome

  • cranial nerve pathology
  • impaired consciousness
166
Q

What are the signs of multiple lacunar infarct strokes on examination?

A

Vascular dementia

Urinary incontinence

Gait apraxia

Shuffling gait

Normal or excessive arm-swing

167
Q

What are the signs of a intracerebral stroke on examination?

A

Headache

Meningism

Focal neurological signs

Nausea/vomiting

Signs of raised ICP

Seizures

168
Q

What are the appropriate investigations for strokes?

A

o Bloods = clotting profile -> check for thrombophilia (especially in young patients)

o ECG = arrhythmias that may be the source of the clot

o Echocardiogram = identify cardiac thrombus, endocarditis and other cardiac sources of embolism

o Carotid Doppler Ultrasound = carotid artery disease (e.g. atherosclerosis)

o CT Head Scan = rapid detection of haemorrhages

o MRI-Brain = higher sensitivity for infarction but less available

o CT Cerebral Angiogram = detect dissections or intracranial stenosis

169
Q

What is the treatment of a hyperacute stroke (<4.5 hrs)?

A

Exclude haemorrhage using CT-head -> then thrombolysis may be considered

170
Q

What is the treatment for acute ischaemic strokes?

A

o Immediate = aspirin + clopidogrel to prevent further thrombosis (heparin anticoagulation considered if there is a high risk of emboli recurrence or stroke progression), formal swallow assessment (NG tube may be needed), GCS monitoring, thromboprophylaxis

o Secondary Prevention = aspirin and dipyridamole, warfarin/DOAC anticoagulation (atrial fibrillation), control risk factors: hypertension, hyperlipidaemia, treat carotid artery disease

o Surgical Treatment = carotid endarterectomy (removal of fatty deposits in carotid arteries)

171
Q

What are the possible conseqeunces of strokes?

A

Cerebral oedema (increased ICP)

Immobility

Infections

DVT

Cardiovascular events

Death

172
Q

What are the causes of subarachnoid haemorrhage?

A

85% - rupture of a saccular aneurysm at the base of the brain (Berry aneurysms)

10% - perimesencephalic haemorrhage

5% - arteriovenous malformations, bleeding diathesis, vertebral artery dissection

173
Q

What are the risk factors for subarachnoid haemorrhage?

A

o Hypertension

o Smoking

o Excess alcohol intake

o Saccular aneurysms are associated with: polycystic kidney disease, Marfan’s syndrome, Ehlers-Danlos syndrome

174
Q

What are the presenting symptoms of subarachnoid haemorrhages?

A

Sudden-onset ‘thunderclap’ headache ever

Nausea/vomiting

Neck stiffness

Photophobia

Reduced level of consciousness

175
Q

What are the signs of subarachnoid haemorrhages on examination?

A

o Meningism - neck stiffness, Kernig’s sign, pyrexia

o GCS to check for deterioration

o Signs of raised ICP - papilloedema, IV or III nerve palsies, hypertension, bradycardia

o Focal neurological signs (e.g. cranial nerve palsies)

176
Q

What are the appropriate investigations for subarachnoid haemorrhages?

A

o Bloods - FBC, U&Es, ESR/CRP, clotting

o CT Scan - hyperdense areas in the basal regions of the skull (due to blood)

o Angiography - detect source of bleeding

o Lumbar Puncture - increased opening pressure, increased red cells and xanthochromia (straw-coloured CSF due to breakdown of red blood cells)

177
Q

What are the classifications of subdural haemorrhages?

A

ACUTE: < 72 hrs

SUBACUTE: 3- 20 days

CHRONIC: > 3 weeks

178
Q

What are the presenting symptoms of subdural haemorrhages?

A

o Acute = history of trauma with head injury and reduced conscious level

o Subacute = worsening headache 7-14 days after injury, altered mental state

o Chronic = headache, confusion, cognitive impairment, psychiatric symptoms, gait deterioration, focal weakness, seizures

179
Q

What are the signs of subdural haemorrhages on examination?

A

o Acute = reduced GCS, ipsilateral fixed dilated pupil, pressure on brainstem causing reduced consciousness + bradycardia

o Chronic = neurological examination may be normal, focal neurological signs (e.g. 3rd nerve palsy)

180
Q

What are the appropriate investigations for subdural haemorrhages?

A

CT Head

MRI Brain - higher sensitivity than CT

181
Q

What is the treatment for subdural haemorrhages?

A

o Acute = ALS protocol, watch out for cervical spine injury, if raised ICP consider osmotic diuresis

o Conservative if small

o Surgical = prompt burr hole or craniotomy

o Chronic = if symptomatic a burr hole or craniotomy and drainage

o Children = younger children may be treated with percutaneous aspiration via an open fontanelle

182
Q

What are the possible complications of subdural haemorrhages?

A

Raised ICP

Cerebral oedema

Herniation

Post-Op - seizures, recurrence, intracerebral haemorrhage, brain abscess, meningitis, tension pneumocephalus

183
Q

What are the possible complications of urinary catheters?

A
  • Infection - UTI, sepsis, kidney etc
  • Allergic reaction to the material used in the catheter
  • Bladder stones
  • Blood in the urine
  • Injury to the urethra
  • Kidney damage (with long-term indwelling catheters)
184
Q

What is the cause of subdural haemorrhages?

A
  • Trauma (usually due to rapid acceleration and deceleration of the brain)
185
Q

Define pneumothorax.

A

Air in the pleural space - potential space between visceral and partietal pleura.

  • Haemothorax = Blood
  • Chylothorax = Lymph
186
Q

What are the causes and risk factors for pneumothorax?

A

o Spontaneous = Typically in tall, thin males - probably caused by the rupture of a subpleural bleb (bulla)

o Secondary = Patients with pre-existing lung disease (e.g. COPD, asthma, TB, pneumonia, lung abscess, sarcoidosis)

o Traumatic = Penetrating injury to the chest

o Risk Factors = Collagen disorders (e.g. Marfan’s syndrome, Ehlers-Danlos syndrome), Lung diseases, Being male

187
Q

What are the risk presenting symptoms of a pneumothorax?

A

o Asymptomatic if small

o Sudden-onset breathlessness

o Pleuritic chest pain

o Distress with rapid shallow breathing in tension pneumothorax

o Patients on ventilation may present with hypoxia or increase in ventilation pressures

188
Q

What are the clinical signs of pneumothorax on examination?

A

o There may be no signs if the pneumothorax is small

o Signs of respiratory distress

o Reduced expansion on affected side

o Hyper-resonance to percussion on affected side

o Reduced breath sounds on affected side

189
Q

What are the clinical signs of a tension pneumothorax?

A

o Severe respiratory distress

o Tachycardia

o Hypotension

o Cyanosis

o Distended neck veins

o Tracheal deviation away from the side of the pneumothorax

o Increased percussion note, reduced air entry/breath sounds on affected side

190
Q

What are the appropriate investigations for a pneumothorax?

A

o CXR = Dark area of film with no vascular markings

  • Fluid level may be seen if there is any bleeding

o ABG = Check for hypoxaemia

191
Q

What is the management plan for a tension pneumothorax?

A

o Maximum O2

o Needle decompression - Insert large bore needle into 2nd intercostal space MCL on affected side, just above the 3rd rib to avoid neurovascular bundle below rib - Stop if patient coughs or resistance is felt before starting again

o Follow-up CXR 2 hrs and 2 weeks later

192
Q

What is the management plan for a pneumothorax?

A

o < 2cm - Primary = Discharge and repeat CXR in 2 weeks

o < 2cm - Secondary = Aspiration and admit for 24hrs

o >2cm - Primary = Aspiration, if unsuccesful repeat and then a chest drain if still not working

o > 2cm - Secondary = Chest drain

o Recurrent pneumothoraces = chemical pleurodesis or surgical pleurectomy

o Advice = Avoid driving and air travel until follow-up complete

193
Q

What are the possible complication of a pneumothorax?

A

o Recurrent pneumothoraces

o Bronchopleural fistula

194
Q

Define pneumonia.

A

Infection of the distal lung parenchyma - causing a shadow on a CXR.

195
Q

What are the risk factors for pneumonia?

A

o Age

o Smoking

o Alcohol

o Pre-existing lung disease (e.g. COPD)

o Immunodeficiency

o Contact with patients with pneumonia

196
Q

What are the presenting symptoms of pneumonia?

A

o Fever

o Rigors

o Sweating

o Malaise

o Dyspnoea

o Cough

o Purulent Sputum

o Haemoptysis - rare

o Pleuritic chest pain

o Weight loss

o Confusion (in severe cases or in the elderly)

o Atypical Pneumonia Symptoms = Headache, Myalgia, Diarrhoea/abdominal pain, Dry cough

197
Q

What are the clinical signs of pneumoina on examination?

A

o Pyrexia

o Respiratory distress

o Tachypnoea

o Tachycardia

o Hypotension

o Cyanosis

o Signs of consolidation = Decreased chest expansion, Dull to percuss over affected area, Increased tactile vocal fremitus/vocal resonance over affected area, Bronchial breathing over affected area, Coarse crackles on affected side

o Chronic suppurative lung disease (empyema, abscess) –> clubbing

o Confusion and may be hypothermic – elderly

198
Q

What are the appropriate investigations for pneumonia?

A

o Bloods = FBC (raised WCC), U&Es, LFT, CRP, Blood cultures, ABG (assess pulmonary function), Blood film (Mycoplasma causes red cell agglutination)

o CXR = Lobar or multilobar (patchy) shadowing, Pleural effusion or cavitation, May detect complications (e.g. lung abscess)

o Sputum/Pleural Fluid = MC&S

o Urine = Pneumococcus and Legionella antigens – in severe cases, check for Legionella (sputum culture, urine antigen)

o Atypical Viral Serology

o Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia (immunocompromised) is suspected, or if pneumonia fails to resolve

199
Q

What is the management plan for pneumonia?

A

o CURB-65 = 0-1: home treatment if possible, 2: hospital therapy, 3+: severe pneumonia so consider ICU

o Start empirical antibiotics - use sensitivity results when back

  • Mild = oral amoxicillin
  • Moderate = IV/oral amoxicillin + clarithromycin
  • Severe = IV co-amoxiclav + clarithromycin

o Supportive treatment = Oxygen, IV fluids, CPAP, BiPAP or ITU care for respiratory failure

o Surgical drainage may be needed for lung abscesses and empyema

o Prevention = Pneumococcal vaccine, Haemophilus influenzae type B vaccine - if patient is in a high risk groups (e.g. elderly, splenectomy)

200
Q

What are the possible complications of pneumonia?

A

o Pleural effusion

o Empyema

o Localised suppuration (e.g. abscess) - symptoms of abscesses = swinging fever, persistent pneumonia, copious/foul-smelling sputum

o Septic shock

o ARDS

o Acute renal failure

o Pericarditis

o Myocarditis

o Extra complications of Mycoplasma pneumonia = Erythema multiforme, Haemolytic anaemia, Meningoencephalitis, Transverse myelitis, Guillain-Barre

201
Q

Define PE.

A

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site.

202
Q

What are the risk factors for a PE?

A

o Surgical patients

o Immobility

o Obesity

o OCP

o Heart failure

o Malignancy

o Thrombophilia

o Pregnancy

o Previous PE

o AF

203
Q

What are the presenting symptoms of a PE?

A

o Small may be asymptomatic

o Moderate = Sudden-onset SOB, Cough, Haemoptysis, Pleuritic chest pain

o Large (or proximal) = Severe central pleuritic chest pain, Shock, Collapse, Acute right heart failure, Sudden death

o Multiple Small Recurrent = Symptoms of pulmonary hypertension

204
Q

What are the clinical signs of a PE on examination?

A

Small = Often no clinical signs - may be some tachycardia and tachypnoea

o Moderate = Tachypnoea, Tachycardia, Pleural rub, Low O2 saturation, Pyrexia, Hypotension

o Massive PE = Shock, Cyanosis, Signs of right heart strain (Raised JVP, Left parasternal heave, Accentuated S2 heart sound)

o Multiple Recurrent PE = Signs of pulmonary hypertension, Signs of right heart failure

205
Q

What are the appropriate investigations for a PE?

A

o Well’s Score

  • 4 or less = D-dimer - if negative exclude PE if raised do a CTPA
  • >4 = CTPA and start on LMWH

o Spiral CT Pulmonary Angiogram = Gold standard

o Bloods = ABG (low PaO2 and PaCO2), thrombophilia screen

o ECG = May be normal, May show tachycardia, right axis deviation or RBBB or right ventricular strain (inverted T in V1-V4), May show S1Q3T3 pattern (S waves in lead I, Q waves in III, Inverted T waves in III)

o CXR = Often normal but helps exclude other diagnoses

o Ventilation-Perfusion (VQ) Scan

o Pulmonary Angiography - rarely required

o Doppler US of Lower Limb - allows assessment of venous thromboembolism

o Echocardiography = May show right heart strain

206
Q

What is the management plan for a PE?

A

o Primary Prevention = Compression stockings, Heparin prophylaxis for those at risk, Good mobilisation and adequate hydration

o If haemodynamically stable = O2, Anticoagulation with LMWH or rivaroxaban and then oral warfarin for at least 3 months (maintain INR 2-3), Analgesia

o If haemodynamically unstable (massive PE) = Resuscitate, O2, IV fluids, Thrombolysis with tPA may be considered if cardiac arrest is imminent

o Surgical or radiological = Embolectomy, IVC filters - sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated

207
Q

What are the possible complications of a PE?

A

o Pulmonary infarction

o Pulmonary hypertension

o Right heart failure

o Death

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