Acute Medicine Flashcards

0
Q

What is the initial assessment and management of ACS?

A
300mg PO aspirin
300mg PO clopidogrel
Diamorphine 2.5-10mg
Metoclopramide 10mg IV 
GTN spray two puffs 
High flow oxygen
Secure IV access
12 lead ECG
FBC, glucose, troponin, lipids
CXR to asses cardiac size and pulmonary oedema 
General examination
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1
Q

What conditions mimic pain in ACS?

A
Pericarditis
Aortic dissection
Pulmonary embolism
Oesophageal reflux, spasm, rupture
Biliary tract disease
Perforated peptic ulcer
Pancreatitis
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2
Q

What ECG changes are indicative of STEMI?

A

ST elevation
Pathological q waves (deep q waves) - indicate abnormal electrical conduction
ST depression is seen in leads reciprocal to the ST elevated leads
PR segment elevation/depression

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3
Q

When do serum Troponin levels rise and fall in STEMI?

A

Rise within 3-12 hours
Peak within 24-48 hours
Return to baseline over 5-14 days

Measure at presentation and at 10-12 hours after presentation

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4
Q

What are the indications for thrombolysis?

A

Cardiac pain within 12 hours and ST elevation in two contiguous ECG leads

Cardiac pain with new LBBB on ECG

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5
Q

Between what interval from the onset of chest pain should thrombolysis be administered?

A

Greatest benefit within four hours

Between 12-24 hours- thrombolysis if persisting symptoms and st elevation

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6
Q

What are common thrombolysis agents?

A

Streptokinase
Alteplase (rtPA) - use IV heparin as well
Reteplase
Tenecteplase

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7
Q

What are the complications and contraindications of thrombolysis?

A
Complications:
Bleeding
Hypotension
Allergic reactions
Intracranial haemorrhage 
Contraindications:
Internal bleeding
Suspected aortic dissection
Recent head trauma
Previous haemorrhage stroke
Trauma/surgery in last two weeks
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8
Q

What is the role of beta blockers and ACEI in STEMI?

A

Beta blockers:
Unless contraindicated
Use short acting agent IV eg metoprolol
Particularly of benefit in patients with tach arrhythmia, ongoing pain, hypertension

ACEI:
After aspirin, beta blockers and reperfusion, all patients with STEMI should receive ACEI in 24 hours

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9
Q

What is the gold standard for coronary reperfusion in STEMI?

A

PCI

Within 2 hours, 90 mins

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10
Q

What are the indications for PCI?

A

All patients with chest pain and st elevation or new LBBB

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11
Q

What is the difference between NSTEMI and unstable angina?

A

NSTEMI has evidence of myocardial damage, whereas unstable angina does not

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12
Q

How does NSTEMI/UA present?

A

Rest angina
New onset severe angina
Previously diagnosed angina which has become more frequent, longer in duration, or lower in threshold

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13
Q

How can NSTEMI/UA be diagnosed?

A

ECG changes:
ST depression
T wave inversion
Occasionally q waves or LBBB

Markers of cardiac injury:
A positive biochemical marker (CK, CKMB, troponin) with the aforementioned ECG changes is diagnostic of NSTEMI. If no changes in cardiac markers over 24-72 hours, UA is diagnosed

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14
Q

What agents are used to treat symptoms and for their anti-ischaemic effects in NSTEMI/UA?

A

Analgesia-Diamorphine 2.5-5mg IV- reduces pain and blood pressure

Nitrates - GTN infusion

B-blockers - start on presentation, shift acting metoprolol

Calcium antagonists- diltiazem/ verapamil to reduce hr and BP

Statins - atorvastatin - 80mg od

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15
Q

What anti platelet therapy is used in NSTEMI/UA?

A

Aspirin - 300mg administered indefinitely in emergency department - continue indefinitely

Clopidogrel - 300mg - continue on 75 mg for 12 months

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16
Q

What anti thrombotic therapy is used in NSTEMI/UA?

A

LMWH -
dalteparin/enoxaparin
Continue for 2-5 days after last episode of pain/ ECG changes?

Fondaparinux?

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17
Q

What are signs of severe haemodynamic compromise in bradyarrythmias?

And how should these be treated

A

Impending cardiac arrest
Severe pulmonary oedema
Blood pressure below 90
Depressed consciousness

Tachy - unsynchronised external defib
Brady - temporary pacing

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18
Q

How does atrial fibrillation typically present?

A
Palpitations
Chest pain
Breathlessness
Collapse
Hypotension
Embolus - stroke, peripheral
Asymptomatic
Occur in 10-15% patients post MI
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19
Q

What is the curb 65 scoring system for pneumonia, and what actions should be taken for the different scores?

A
Confusion - amts less than/equal to 8
Urea - >7mmol
Respiratory rate - greater than 30
BP - less than 90/60
Age - greater than 65

> 3- admit to hospital
2- increased risk of mortality- short inpatient stay
0-1- low risk, may be suitable for home treatment

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20
Q

What is the initial management and investigations for pneumonia

A
ABCDE
Venous access, arrange for CXR
Bloods- RBC, u+es, LFT, CRP
ABG- give 02 if necessary
Culture blood and sputum
Pain relief- paracetamol and NSAID 
More investigations if necessary 
Urine for legionella antigen
Pleural fluid aspiration
Mycoplasma cold agglutinins
Bronchoscope and lab age if fail to respond
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21
Q

What is the empirical management of mild, moderate, severe CAP?

A

Mild moderate- amoxicillin plus clarithromycin or doxycycline

Severe - coamoxiclav IV plus clarithromycin IV

Or

Cefuroxime/cefotaxime IV plus clarithromycin IV

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22
Q

What is the empirical treatment of hospital acquired pneumonia

A

Cefotaxime IV with or without metronidazole IV

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23
Q

What is the empirical management of aspiration pneumonia?

A

Cefuroxime and metronidazole

Or Benzylpenicillin and gentamicin and metronidazole

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24
Q

What is the initial management of acute severe asthma attack?

Monitor PEFR and ABG

A

Sit patient up in bed
PEF is 33-50% predicted
(PEF <33% is life threatening)
High percentage O2 via reservoir mask
Nebulisers bronchodilators- 5mg salbutamol, repeat every 15-3ins if required
Add ipratropium bromide 0.5mg 4-6 hourly if initial response to salbutamol is poor
IV access
Steroids 200mg hydrocortisone IV
Antibiotics if evidence of chest infection
Adequate hydration

Consider IV magnesium, aminophylline, salbutamol infusion

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25
Q

What are the features of a mild- moderate asthma attack and how is it managed?

A

No severe features, pef 51-75% of predicted

Administer nebulised salbutamol 5mg and oral prednisolone 30-60mg

Reassess after 30 mins, if worse, treat as per severe asthma, if no better, repeat nebs

Discharge on oral prednisolone 30-40mg is for 7 days
Inhaled corticosteroid, inhaled beta agonist

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26
Q

What investigations should be ordered for acute exacerbation of COPD?

A

U+Es - dehydration, RF
FBC- leucocytosis, anaemia, secondary polycythaemia
ABG and pulsox
Sputum and blood culture
Peak flow- compare to what is normal for patient
CXR
ECG- check for mi or arrhythmia causing breathlessness

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27
Q

What is the management of acute exacerbation if COPD

A

Venturi mask O2 - 24-28% O2
ABG
If type 2 resp failure, consider NiV - CPAP or BIPAP, especially if failure to respond to bronchodilator therapy

Nebulised salbutamol 5mg
Consider IV salbutamol or aminophylline
Nebulised ipratropium bromide 500mcg 6 hourly
Steroids - 200mg hydrocortisone IV or 30-40mg prednisolone PO

Physio may help to clear bronchial secretions

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28
Q

What is the role if mechanical ventilation in acute exacerbation of COPD?

A

Ventilation should be considered where respiratory failure is present (paO2 less than 7.3) regardless of CO2 levels, and in those who fail to respond to first line treatment including bronchodilator therapy

Check with ITU staff!

Good outcome if young, good exercise tolerance, acute resp failure

Poor outcome if old, comirbidities, on O2 therapy at home

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29
Q

What is adult respiratory distress syndrome?

A

A common clinical disorder in which damage to the alveolar epithelial and endothelial barriers of the lung, acute inflammation, and protein rich pulmonary oedema leads to acute respiratory failure.

Often occurs in the setting of multiple organ failure

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30
Q

What are the diagnostic criteria for ARDS?

A

Acute onset of respiratory failure with one or more of the risk factors

Hypoxaemia- ALI- paO2:fiO2 ratio <19mmHG with normal colloid oncotic pressure

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31
Q

What investigations are appropriate in ARDS?

A
CXR
ABG 
Blood, urine, sputum culture
ECG 
Pulmonary artery catheter to measure pulmonary capillary wedge pressure, cardiac output
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32
Q

Which disorders are most associated with ARDS? Direct and indirect lung injury

A
Direct lung injury
Aspiration
Inhalation of smoke/noxious gases
Pneumonia
Pulmonary contusions 
Drug OD- O2, opiates, bleomycin, salicytes
Indirect lung injury
Shock
Septicaemia
Pancreatitis
Burns/ trauma
Head injury and increased ICP
Liver failure
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33
Q

How and where is ARDS most appropriately managed?

A

Usually HDU/ICU

Identify and treat underlying cause

Respiratory support to improve gas exchange and correct hypoxia- High O2 conc or mechanical ventilation

Cardiovascular support- arterial line, inotropes, fluid resus

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34
Q

What are causes of pneumothorax?

A

Primary/spontaneous- tall young men who smoke- rupture if apical subpleural blend

Secondary/spontaneous- pleural rupture due to underlying lung disease: emphysema, fibrosis etc

Infection- cavitating pneumonia

Trauma- chest trauma in RTA

Iatrogenic- mechanical ventilation, pleural biopsy, subclavian vein cannulation

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35
Q

What are signs of tension pneumothorax?

A

Distressed patient
Tachypnoeic with cyanosis
Profuse sweating
Marked tachycardia and hypotension

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36
Q

How may acute upper GI bleed present?

A

Haematemesis- bright red, dark clots, coffee grounds
Malaena- from anywhere proximal to caecum
Weakness, sweating, palpitations
Postural dizziness, fainting
Collapse or shock

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37
Q

What are causes of acute upper GI bleeding?

A
Peptic ulcer
Gastroduodenal erosions
Oesophagitis
Varices
Malory Weiss tear
Upper GI malignancy
Vascular malformations
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38
Q

What factors indicate a high risk of death in acute upper GI bleed, and what scoring system incorporates these?

A

Rockall scoring system

Age greater than 60
Shock - SBP 100
Comorbidities- cardiac, renal, liver, malignancy
Diagnosis of GI tract malignancy
Blood in upper GI tract
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39
Q

What is the initial management of acute upper GI bleeding?

A

Position patient on side to protect the airway
Secure IV access
Take FBC and U+E, platelets and LFTs, clotting and crossmatch
Fluid resus
Monitor urine output
IV PPI - 80mg omeprazole bolus, followed by 8mg/hr infusion
Contact on call endoscopy team and surgeons

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40
Q

What general measures can be taken to stop bleeding in acute upper GI bleed?

A

Platelet count below 50,000/mm3 requires platelet support
If on anticoagulants, give FFP and vitamin k
Serum calcium may drop after blood units given, replace with calcium gluconate
Tranexamic acid may be helpful

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41
Q

How does biliary obstruction present?

A
Jaundice
RUQ pain and tenderness
Fever 
Itching
Dark urine and pale stools
Septic shock
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42
Q

What investigations are indicated in biliary obstruction, and what may they show?

A
Wcc- increased
U+es- renal failure
LFTs- increased bilirubin, alp, ggt, and amylase if concomitant pancreatitis
Blood cultures
CRP
USS - dilates ducts and gallstones
AXR- aerobilia may be due to gas forming organism
ERCP- stones in CBD
MRCP
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43
Q

What may cause biliary obstruction?

A
Gallstones
Malignancy 
Postoperative stricture
Primary sclerosing cholangitis
Primary biliary cirrhosis
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44
Q

How is biliary obstruction managed?

A

Analgesia
Antibiotics if septic

If dilated ducts:
Indicates gallstones
ERCP to decompress biliary system

If not dilated ducts:
Autoantibodies- pANCA, AMA
When stable, consider ERCP, liver biopsy

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45
Q

What is a differential for ascites?

A

Ovarian cyst
Obesity
Pregnancy
Abdominal mass

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46
Q

What are causes of ascites?

A
Cirrhosis and portal hypertension
Malignancy
Congestive cardiac failure
Pancreatic ascites
Nephrotic syndrome
Hypothyroidism
Infection eg TB
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47
Q

What investigations are indicated in ascites?

A

U+es, glucose, FBC, pregnancy test, LFTs, blood cultures, amylase
Ascitic tap unless malignant cause!
USS, axr, ct scan?
Urine sodium, 24hr protein

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48
Q

After treating the cause, how is ascites treated?

A

Restrict salt intake to 90mmol a day
Paracentese- if tense or moderate. Replace albumin afterwards
Start spironolactone at 100mg a day

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49
Q

How can AKI be defined?

A

Abrupt (within 48 hours) reduction in kidney function

Absolute increase in serum creatinine of >/= 26mmol
Or
>50% relative increase inn serum creatinine
Or
Reduction in urine output - less than 0.5 ml/kg per hour for more than six hours

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50
Q

How does AKI present?

A
Asymptomatic
Incidental finding on biochemical screening
Oliguria
Malaise, confusion, seizures, coma
Nausea, anorexia, vomiting
Haematuria
Vasculitic rash
Multi organ failure
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51
Q

What are pre renal causes of AKI?

A
Hypovolaemia
Hypotension
Renal artery emboli
Renal artery stenosis and ACEI 
Hepatorenal syndrome
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52
Q

What are post renal causes of AKI

A
Renal vein thrombosis 
Increased intrabdominal pressure 
HIV drugs
Ureteric stones
Prostatic hyper trophy
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53
Q

What are renal causes of AKI?

A
Vasculitis eg SLE
Glomerulonephritis
Acute tubular necrosis- due to ischaemia, septicaemia, gentamicin, radio contrast, malaria
Scleroderma crisis
Calcium/urate oxalate overload
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54
Q

What investigations are indicated in AKI?

A
UandEs
FBC- anaemia suggests chronic RF
Coagulation- to detect DIC, SLE 
LFTs- hepatitis, paracetamol OD
Blood cultures
Immunology- antigens etc 
CRP - raised in Vasculitis
Protein strip- for para proteins, BJ proteins
Urine dipstick, Micro and culture
Renal USS
CXR to assess heart size, pulmonary oedema
ECG - hyperkalaemia
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55
Q

How is AKI managed?

A

Treat hyperkalaemia- calcium gluconate, glucose and insulin, salbutamol nebs, dialysis?

Treat metabolic acidosis- 50-100ml of 8.4% bicarbonate via central line

Treat pulmonary oedema
Oxygen, CPAP?, IV GTN, IV furosemide, Diamorphine

Assess hydration and fluid balance- if depleted, fluid challenge with saline

Treat infection
Stop nephrotoxic drugs
Identify intrinsic renal disease
Relieve obstruction

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56
Q

What are common causes of acute confusion?

A

Pain or discomfort- urinary retention, constipation

Hypoxia

Infection- systemic/localised

Metabolic disorders- renal failure, liver failure, acidosis, hypercalcaemia

Endocrine disease- thyrotoxicosis,

Addison’s disease, DM

Cardiac- MI, CCF, endocarditis

Neuro- head injury, subdural haematoma, cns infection

Drugs- benzodiazepines, opiates, digoxin, cimetidine, steroids, anticholinergics, recreational

Alcohol/drug withdrawal

57
Q

What are the initial symptoms of acute alcohol withdrawal?

A
Peaking at 12-30hr, subside by 48hr:
Anxiety
Tremor
Hyperactivity
Sweating
Nausea and retching
Tachycardia
Hypertension

Tonic clonic seizures may occur later

58
Q

What are features of delirium tremens?

A

Coarse tremor, agitation, delusions, hallucinations
Fever, sweating, tachycardia
Rarely lactic acidosis, ketoacidosis
Hypoglycaemia, wernicke korsakoff psychosis

59
Q

How is acute alcohol withdrawal managed?

A

Rehydrate, monitor urine output and blood glucose

IV pabrinex 8 hourly five days or thiamine 100mg PO bd for a week

Chlordiazepoxide

60
Q

What is the triad of wernickes disease?

A

Opthalmoplegia- nystagmus, VI nerve palsy
Ataxia
Confusion state

Diagnosed by reduced red cell transketolase activity

61
Q

Can DKA occur in patients with type 2 diabetes?

A

DKA predominantly occurs in insulin dependent diabetes. It does not usually occur in non insulin dependent diabetes, but is increasingly being seen in type 2 diabetics, particularly of afrocaribbean origin

62
Q

What are the clinical features of DKA?

A
Polyuria
Polydipsia
Weight loss
Weakness
SOB with kussmauls (sighing) breathing
Abdominal pain
Vomiting
Confusion and coma
63
Q

What may precipitate DKA?

A

Infections
Non compliance with treatment
Newly diagnosed diabetes

64
Q

What investigations are indicated in DKA?

A
Blood glucose - may not be high!
ABG
U+Es
Urinalysis - ketones
FBC - increased WBC
Urine and blood cultures
Plasma ketones
CXR to investigate infection
Amylase- may be high in absence of pancreatitis, although pancreatitis may occur in DKA 

Ketoacidosis requires positive urinary or plasma ketones and ph <= 7.30

65
Q

What is the management if DKA?

A

Consider HDU/ICU, central line, arterial line, urinary catheter if sever acidosis, hypotension, oliguric

Insulin- 50u soluble insulin in 50ml NaCl at rate of 6-7units/hr

Fluids- 500 saline over 15-30mins until SBP is greater than 100. Then 1l two hourly for six hours and 1l three hourly for nine hours

Potassium replacement in second bag of fluid

Monitor blood glucose, capillary ketones and urine output hourly

Potassium replacement and glucose replacement when potassium and glucose drop

66
Q

What is the presentation of HONK?

A

Usually previously unknown diabetes in an elderly patient
Severe dehydration
Impaired consciousness
Respiration is usually normal
Patient is at risk of venous and arterial thromboses and may present with stroke, seizures or MI

67
Q

What may precipitate HONK?

A
Infection
MI or CVA
GI bleed
Poor compliance with oral anti diabetic agents 
Diuretics, beta blockers, antihistamines
68
Q

Investigations in honk?

A
High glucose
U+es show dehydration- hypernatraemia
ABG - relatively normal compared to DKA 
FBC - polycythaemia or leucocytosis
ECG- mi or ischaemia
CXR - look for signs of infection 
Urinalysis and mc&s
69
Q

How is honk managed?

A

Insulin infusion at 2-4u per hour. When blood glucose reaches 15mmol/l, commence 5% glucose infusion

IV fluid- 1l saline over first hour, the. 1l two hourly for 4 hrs,

Potassium replacement

Treat underlying cause

Thromboprophulaxis!

70
Q

How does hypoglycaemic coma present? Hint: more than just coma

A
Sympathetic overactivity (glucose <2.6)
Confusion
Slurred speech
Focal neurological defect
Coma
71
Q

What investigations should be made in hypoglycaemic coma?

A

Blood glucose- for obvious reasons
U&Es - hypoglycaemia is more common in diabetic nephropathy

Take blood prior to glucose administration

72
Q

What are causes of hypoglycaemia?

A

Insulin
Sulphonylurea
Alcohol
Salicylates

Hypopituitarism
Acute liver failure
Adrenal failure
Myxoedema
Sepsis
Malaria
73
Q

How is hypoglycaemic coma treated?

A

If patient conscious and cooperative- oral glucose 50-100ml, or 3 glucose tablets

If reduced level of consciousness- 50ml of 50% glucose IV, or 1mg glucagon IM if no venous access

74
Q

What factors comprise the wells score for DVT assessment?

A

Active cancer (including treatment up to six months previously)
Paralysis/immobilisation of leg
Recently bedridden for >3 days or major surgery within four weeks
Localised tenderness along distribution of deep venous system
Entire limb swollen
Calf swelling >3cm relative to other leg
Pitting oedema
Dilated collateral superficial veins

Subtract two points if:
Alternative diagnosis at least as likely as DVT

75
Q

What investigations should be taken in DVT?

A

Venous compression ultrasonography- usually 90% accurate
D-dimers- to exclude PE

Consider coagulation screen, screen for malignancy eg ultrasound/ct abdomen and pelvis

76
Q

Which patients should be anticoagulated with DVT? Based on wells score

A

Wells >/=1: performed dimer:
If negative, exclude DVT
If positive, perform USS - if positive, treat as DVT

Wells >/=2: perform d dimer and USS
If USS positive, treat
If d dimer positive but USS negative repeat USS in one week

77
Q

What anticoagulants are used in DVT management?

A

LMWH- once daily SC injection

Warfarin- always use LMWH first!
Anticoagulated for three months

Consider thrombolysis for recurrent extensive, proximal thromboses

78
Q

What are the symptoms of PE?

A

Sudden onset pleuritic chest pain
Breathlessness
Haemoptysis
Postural dizziness or syncope

Massive PE may present as cardiac arrest

79
Q

What are the signs of PE?

A
Tachycardia
Tachypnoea
Cyanosis (large PE)
Pleural rub or effusion
Thrombophlebitis in lower limbs
Mild fever may be present

Signs of raised right heart pressures and cor pulmonale- raised jvp, tricuspid regurgitation, paras thermal heave

80
Q

What investigations are indicated in PE?

A

ABG - may show low O2 and low CO2 due to tachpnoea
ECG - sinus tachycardia and non specific ST and T wave changes. Cor pulmonale - RAD and RBBB
CXR- may be normal- this is suggestive of PE if respiratory compromise!
Blood tests - neutrophil leucocytosis
D dimer
VQ or CTPA

81
Q

What is the management of PE?

A

Cardiac monitor, pulse, BP, resp rate, O2 sats
High flow oxygen
Venous access and start IV fluids
LMWH for all patients with High or intermediate risk of PE until diagnosis confirmed
NSAIDs for analgesia

If positive diagnosis:
Anticoagulate with warfarin- target INR 2-3 for four weeks at least

82
Q

What are the presentations of paracetamol overdose, and when do these occur after ingestion?

A

Within 24 hours
- generally asymptomatic- possibly nausea, vomiting, anorexia,

24-36 hours
Hepatic necrosis- jaundice, RUQ pain, vomiting? Confusion

Over 72 hours
Encephalopathy, renal failure, lactic acidosis

83
Q

What are some complications of paracetamol overdose

A

Acute liver failure- GI bleeds, hypoglycaemic , cerebral oedema

Pancreatitis

Lactic acidosis

Acute tubular necrosis- renal failure

84
Q

What investigations should be done in paracetamol overdose?

A
Paracetamol - at four hours!
UandEs- renal failure
FBC - thrombocytopenia
Glucose
LFTs
Prothrombin
ABG lactic acidosis
85
Q

What is the management of paracetamol overdose?

A

Activated charcoal 50g or gastric lavage if presents within one hour

Treat with NAC if 4h paracetamol places above treatment line on graph

First infusion over 15min, second over 4h, third over 16h

If allergic, give methionine

If high risk lower threshold for treating with NAC- high risk if: phenytoin, carbamazepine, rifampicin, high alcohol, anorexic or AIDS

If present before 8 hours - paracetamol levels before acetylcysteine

If present after 8 hours - give acetylcysteine straight away

86
Q

What is a differential for cardiogenic shock?

A
MI
Aortic dissection
Arrhythmia
Valvular disease
Overdose of cardiac depressant
Myocarditis
87
Q

What is a differential for anaphylactic shock?

A

Recent drug therapy
Food allergy
Insect stings

88
Q

What is a differential for Hypovolaemia shock?

A
GI haemorrhage
Aortic dissection
AAA rupture
Fluid losses- diarrhoea, vomiting, burns
Third spacing
Adrenal failure
89
Q

What is a differential for distributive shock?

A
Sepsis
Liver failure
Drug overdose- calcium antagonists
Adrenal failure
Neurogenic shock
90
Q

What is a differential for obstructive shock?

A

Cardiac tamponade
Pulmonary embolus
Tension pneumothorax

91
Q

Within what timeframe must broad spectrum antibiotics be administered in septic shock?

A

Within one hour

92
Q

What are signs of anaphylaxis?

A
Skin redness
Urticaria
Conjunctival injection
Angiooedema
Rhinitis
Laryngeal obstruction- choking, cough, stridor
Bronchospasm
Tachycardia
Hypotension
93
Q

What is the immediate management of anaphylaxis?

A

Maintain airway- consider intubation or emergency cricothyroidotomy if necessary
Give 100% oxygen
Give IM adrenaline 0.5-1mg- or IV if venous access
Establish venous access if not - fluid bolus/challenge
Give Hydrocortisone 200mg, chlorphenamine 10mg

94
Q

How may Hyponatraemia present?

A

Mild Hyponatraemia is usually asymptomatic

Severe Hyponatraemia presents with disturbed mental state, restlessness, confusion, irritability, seizures and coma

95
Q

What investigations are necessary in Hyponatraemia

A

Serum osmolarity
Urinary sodium
Assessment of patients volume assessment

96
Q

What are causes of Hyponatraemia in hypovolaemic patients?

A

Renal losses (High urinary sodium)
Diuretics
Addison’s
Nephropathy

Non renal losses ( low urinary sodium)
GI losses- N+V
Burns
Fluid sequestration- peritonitis, pancreatitis

97
Q

What are causes of normovolaemic Hyponatraemia?

A

Syndrome of inappropriate anti diuretic hormone - due to trauma, malignancy, Vasculitis, infection, lung disease

SIADH also caused by opiates, haloperidol, amitriptyline, cyclophosphamide, thiazides, vincristine

98
Q

What is SIADH?

A

Excessive ADH secretion- ADH increases water absorbed in the kidneys

This results in high urine osmolarity and low serum osmolarity

99
Q

How is Hyponatraemia typically managed?

A

Exclude pseudohyponatraemia- calculate osmolar gap

If volume depleted start IV normal saline. Do not correct by more than 10mmol in first 24 hrs

If SIADH, restrict fluid intake to 750ml per ???

100
Q

How does subarachnoid haemorrhage typically present?

A

Sudden and severe thunderclap headache, radiating from the occiput with associated neck stiffness

Often occurs on bending/lifting heavy objects

Time to peak onset is usually less than a few seconds

Nausea, vomiting, dizziness

Reduces gcs

Seizures are uncommon but may occur

Herald bleed- unusually severe headache days or weeks before main bleed

101
Q

Within what timeframe should a patient with suspected SAH be scanned?

A

Within 24h- 95% correct

102
Q

When is Lumbar puncture indicated in SAH investigation?

A

Not usually required
Consider when ct scan is normal but history is highly suggestive

Xanthochromia if positive

103
Q

What is the immediate management of SAH?

A

Protect airway, give oxygen
Treat seizures with drugs
Correct hypotension if necessary- nifedipine if diagnosis established to reduce vasospasm

ECG monitoring and treat dysrhythmias
Venepuncture for clotting screen and UandEs (Hyponatraemia from SIADH)

Arrange urgent cr head and lp if necessary

Analgesia

Regular neurological observations

Refer to neurologists for clipping/coil

104
Q

What is status epilepticus?

A

Continuous tonic clonic convulsions lasting 30mins or longer, or convulsions so frequents that each attack begins before the previous convulsion ends

105
Q

What are causes of status epilepticus?

A
Cerebral tumour
Hypoglycaemia
Head injury
Low sodium, calcium, or magnesium
Drug overdose
Drug/alcohol withdrawal
Hypoxia eg post cardiac arrest
Anti epileptic non compliance
106
Q

What is the management of status epilepticus

A

Open the airway
Give oxygen
Take blood for UandEs, glucose, calcium, magnesium, LFTs, FBC, toxicology if required

Anti epileptic therapy
Lorazepam
Diazepam as alternative to lorazepam
Start infusion if phenytoin - req ECG monitoring

If seizures continue, give phenobarbitol

If lasts greater than 60 mins, transfer to intensive care

107
Q

What conditions may mimic a stroke?

A

Cerebral tumour- if presents over days
Brain abscess- pyrexial
Focal migraine
Subdural haematoma- variable consciousness
Post seizure (todds paresis)- although seizures occur in 5-10 percent of strokes
Hypoglycaemic attack
Encephalitis

108
Q

When should patients suspected of stroke have a CT head?

A

All patients suspected of stroke should be scanned within 24h to detect if haemorrhagic stroke

Urgent CT if:
Depressed level of consciousness
History of anticoagulant treatment
No available history
Features suggestive of- SAH, SDH, space occupying lesion, cerebral infection
Indications for thrombolysis
109
Q

What are the indications for thrombolysis in acute stroke? And when should it be administered?

A

Give 300mg aspirin
IV alteplase, within three hours of onset of symptoms
Patient must have measurable neurological deficit
BP must be maintained below 180/105

Exclude if:
MI, stroke, head trauma within three months
LP within seven days
Major operation within 14 days
Previous GI, intracranial bleed
110
Q

How does a total anterior (carotid) circulation infarct present?

A

Contralateral hemiplegia and hemianaesthesia in two contiguous areas (face, upper/lower limb)

Homonymous hemianopia

Higher cerebral dysfunction:
If left sided- global dysphasia
If right sided- unilateral neglect of contralateral space

111
Q

How does a partial anterior (carotid) circulation infarct present?

A

Usually present with two out of the three components of the TACI subtype

112
Q

How does lacunar infarction present?

A

Infarcts in small penetrating vessels- often due to hypertension

Pure motor or sensory stroke
Ataxic hemiparesis

113
Q

How does posterior cerebral artery infarction present?

A

Contralateral homonymous hemianopia (or quadrantinopia)
Mild contralateral hemiparesis/hemisensory loss
Dyslexia
Memory impairment

114
Q

What scoring system assesses risk of stroke following a TIA?

A

ABCD2

Age- >60
BP- >140/90
Clinical features- unilateral weakness or speech disturbance 
Duration of symptoms- >60mins 
Diabetes
115
Q

What investigation can be done to confirm vascular territory/pathology in Suspected TIA

A

MRI

Ct if MRI contraindicated

116
Q

How does opiate overdose present?

A

Pinpoint pupils
Resp depression and cyanosis
Possibly low BP
Hypotonia

117
Q

How is opiate overdose managed?

A

Monitor RR (and depth), O2 sats, ECG for arrhythmias
Give oxygen
IV access
UandEs, CPK
Any comatose/respiratory signs requires CXR for infection, emboli, non cardiogenic pulmonary oedema
Naloxone, given IV in blouses until patient is rousable and resp depression corrected
Start infusion to avoid resedation!

118
Q

What are complications of opiate overdose?

A

Non cardiogenic pulmonary oedema- may require CPAP or mechanical ventilation

Rhabdomyolysis may occur in opiate induced coma

IV drug users may develop right sided endocarditis and septic pulmonary emboli

Paracetamol containing preparations, such as codydramol, may cause renal or hepatic failure

119
Q

How does tricyclic antidepressant overdose present?

A

Anticholinergics features such as dry mouth, dilated pupils, blurred vision, sinus tachycardia, urinary retention, myoclonic jerking and hallucinations may occur

Cardiac arrhythmias and coma may occur later

120
Q

What are other complications of TCA overdose?

A

Severe toxicity - coma with respiratory depression, hypoxia, metabolic acidosis

Neurological signs of toxicity include loss of oculocephalic and oculo vestibular reflexes, ophthalmoplegia.

Hypothermia, skin blistering, rhabdomyolysis are also reported

121
Q

What is the management of TCA antidepressant?

A

If CNS depression, monitor in ICU/HDU
Lavage/charcoal if within one hour
ECG should be recorded to asses arrhythmia/qrs prolongation
Resp failure may require intubation and ventilation
Alkalinization with boluses of bicarbonate if long qrs, metabolic acidosis, hypotension, or arrhythmias
Treat hypotension with glucagon or vasopressors, and fluid resus
Tricyclic coma may last 24-48hr, and require sedation

122
Q

What is the management of AF in haemodynamically unstable patients?

A

Hypotensive patients- external defibrillation using synchronised shock, unless chronic AF

If DC shock fails:
IV amiodarone
Correct hypokalaemia
Attempt further dc shock

123
Q

How should AF be managed in haemodynamically stable patients?

A

Rate control, and then rhythm control if appropriate

AF > 2 days duration:
Control rate with - digoxin/b-blocker/verapamil/diltiazem/amiodarone
Start LMWH 
Restore SR with amiodarone
Consider DC cardioversion

AF <2 days duration:
Attempt chemical cardioversion: flecainide, amiodarone
If cardioversion unsuccessful, consider rate control as for AF greater than 2 days

124
Q

How does aortic dissection present?

A

Chest pain- abrupt onset severe, anterior chest pain most commonly radiating to the inter scapular region. Usually tearing in nature and most severe at its onset

Sudden death or shock- due to aortic rupture or cardiac tamponade

Congestive cardiac failure- due to aortic incompetence

Patients may present with signs of occlusion of the branches of the aorta- renal failure, stroke, acute limb ischaemia, mi

125
Q

What signs may be found in examination in aortic dissection?

A

May be normal
Usually hypertensive on presentation- but may be hypotensive

Aortic valve regurgitation
Neurological deficits due to carotid artery dissection or compression or spinal artery occlusion

126
Q

What investigations are indicated in aortic dissection?

A

ECG- may be normal or non specific
CXR- may be normal, or show wide mediastinum, aortic knuckle enlargement
Bloods- FBC, UandEs, cardiac enzymes, crossmatch
Echocardiography - esp transoesophageal- first line!
MRI angiography - gold standard!
Spiral ct with contrast

127
Q

What is the immediate management of aortic dissection?

A
Resus/ITU 
Cannulas
FBC, UandEs, crossmatch
Arterial line
Morphine
 Correct BP

Ascending aorta (type a)- surgical repair and BP control

Descending aorta (type b)- medical management with aggressive BP control

128
Q

How does pericarditis present?

A

Central chest pain, also pleuritic, relieved by sitting forward
May be SOB

Other symptoms may reflect underlying disease- fever, cough, arthralgia, rash, faintness

Venous pressure rises if effusion develops. Look for signs of cardiac tamponade

129
Q

What are causes of acute pericarditis?

A
Idiopathic
Infection- viral, bacterial, TB
Dressers syndrome 
Malignancy- breast, bronchus, lymphoma
Uraemia
SLE, RA, wegeners, sarcoidosis
Hypothyroidism
Trauma
Radiotherapy
Hydralazine, procainamide, isoniazid
130
Q

What investigations are indicated in acute pericarditis?

A

ECG- saddle shaped ST segment, some t wave inversion, PR segment depression
Usually all leads involved

Echocardiography- may demonstrate pericardial collection
Enables assessment of LV function

FBC, UandEs, CRP, cardiac enzymes, CXR

Where appropriate- viral titres, blood cultures, autoantibodies, TFTs, diagnostic pericardial tap

131
Q

Acute pericarditis management?

A

Consider admission
Analgesia- NSAIDs
Steroids- if pain does not settle- prednisolone
Colchicine
Pericardiocentesis- if serious or signs of tamponade
Antibiotics if infection suspected

132
Q

How does acute pancreatitis present?

A

Abdominal pain- epigastric or generalised, of rapid onset, dull constant and boring. May radiate to the back it between the scapular, may be relieved by leaning forward.

Nausea and vomiting
Peritonitis with epigastric tenderness
Localised rebound tenderness or general abdominal rigidity. No BS

Grey turners (flank) or cullens (umbilical)

133
Q

What investigations should be ordered in acute pancreatitis?

A
Amylase
FBC- leucocytosis 
UandEs- urea may be raised
Glucose- may be raised
LFTs- AST and bilirubin raised
Hypocalcaemia
CRP- elevated
ABGs- hypoxia and metabolic acidosis
AXR
CXR - pleural effusion
USS - gallstones
Ct abdomen- pancreatic necrosis
134
Q

What is the management of acute pancreatitis?

A

IV access
Fluid replacement if necessary
Oxygen if necessary
Keep NBM
Monitor blood glucose and treat with insulin if needs be
Pethidine- causes least sphincter of oddi spasm
Octreotide- suppresses pancreatic enzymes
Liaise with surgeons
Antibiotic prophylaxis with cefuroxime

135
Q

After head injury, which risk factors suggest that ct head should be performed within one hour?

A

Any one of:
GCS <15 at two hours after injury on assessment
Suspected open or depressed skull fracture
Signs of basal skull fracture
Post traumatic seizure
Focal neurological deficit
More than one episode of vomiting since head injury

136
Q

What clinical features are part of the wells DVT scoring system?

A

Active cancer- treatment ongoing or within six months

Paralysis, paresis or recent plaster immobilisation of legs

Recently bedridden for three days or more or major surgery within 12 weeks

Entire leg is swollen

Calf swelling by more than three cm compared with asymptomatic leg (measured 10cm below ischial tuberosity)

Putting oedema of symptomatic leg

Collateral superficial veins

Previously documented DVT

One point for each, subtract two points for equally likely alternative diagnosis, greater than two points indicates high risk of DVT

137
Q

When is an ankle X-ray indicated according to the Ottawa ankle rules?

A

Only if pain in the malleolar zone and any one of:

Bone tenderness at posterior edge or tip of lateral malleolus
Bone tenderness at posterior edge or tip of medial malleolus
Inability to weight bear both immediately and in casualty department

138
Q

What are the components of the trauma triad of death? And what is it’s significance?

A

Hypothermia
Acidosis
Coagulopathy

Seen in patients who have sustained severe traumatic injuries, and results in a significant rise in the mortality rate

139
Q

What factors may cause coagulopathy in a trauma patient?

A

Hypothermia
Massive transfusion
Or both