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MANCHESTER YEAR 3 > TCD Cases 1-12 > Flashcards

TCD Cases 1-12 Flashcards

1
Q

What are the causes of myocardial ishaemia? (HINT there’s 6)

A
  1. Coronary artery disease (main cause)
  2. Aortic stenosis
  3. Hypertrophic cardiomyopathy
  4. Cocaine use
  5. Anaemia
  6. Thyrotoxicosis
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2
Q

What are the non-ishaemic causes of cardiac chest pain? (hint there’s 2)

A

Aortic dissection and pericarditis

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3
Q

What are the 4 upper GI causes of chest pain?

A

GORD
Gallstones
Peptic ulcer
Pancreatitis

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4
Q

What are the 4 respiratory causes of chest pain?

A

Pulmonary embolism
Pneumothorax
Pneumonia
Pleurisy

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5
Q

What are the 2 musculoskeletal causes of chest pain?

A

chostochondritis

herpes zoster

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6
Q

What does it suggest if chest pain radiates to the left arm/both arms/jaw/neck?

A

ACS

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7
Q

What does it suggest if chest pain radiates to the right shoulder?

A

cholecystitis

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8
Q

What does it suggest if chest pain radiates to the intrascapular region/back?

A

Aortic dissection, GORD, pancreatitis, peptic ulcer, ACS

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9
Q

What does it suggest if chest pain radiates to the epigastrium?

A

Pancreatitis, peptic ulcer, gallstones, ACS

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10
Q

Define angina.

A

Discomfort in the chest and or adjacent areas (jaw, shoulder, back, arm) caused by MI. Most commonly due to CAD.

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11
Q

What are the 3 characteristics of typical angina?

A
  1. Constricting discomfort in front of chest, or neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest/GTN within about 5 minutes
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12
Q

What is atypical angina?

A

Only meets 2 of the characteristics of typical angina

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13
Q

What are the risk factors for developing CAD? (HINT there’s 6)

A 
Age
Gender
Diabetes
Hyperlipidaemia
Smoking
Hypertension
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14
Q

What factors can provoke angina? (HINT theres 4)

A

Physical exertion
Emotional stress
Exposure to cold
Eating a heavy meal

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15
Q

What 3 interventions should NOT be offered to manage stable angina?

A
  1. transcutaneous electrical nerve stimulation
  2. enhanced external counterpulsation
  3. acupuncture.
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16
Q

Does a normal ECG exclude an acute coronary syndrome (ACS)?

A

no

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17
Q

What tests, after a normal ECG, are used to exclude ACS?

A

Cardiac troponin testing

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18
Q

What treatment is given for suspected ACS?

A

loading dose of aspirin 300mg

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19
Q

What are the various clinical presentations of ACS?

A
  1. Prolonged chest pain (>20 min) at rest
  2. New onset angina pectoris
  3. Worsening of existing angina
  4. Angina following myocardial infarction
  5. Atypical presentations are common over 75 years of age
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20
Q

What 3 reasons could result in a normal ECG in ACS?

A
  1. ischaemia in circumflex territory
  2. isolated RV ischaemia
  3. transient episodes of bundle branch block
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21
Q

What are the common ECG changes for CAD to be present? (hint there’s 3 points)

A
  1. Pathological Q waves indicate current/prev MI
  2. LBBB (broad QRS, deep S wave V1, no Q wave in v5/6)
  3. ST segment and T wave abnormalities (ST depression and T wave flattening/inversion)
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22
Q

What are the 6 types of non invasive imagine used in NSTEMI ACS?

A
  1. 12 lead ECG
  2. Transthoracic (TTE) echocardiography
  3. Stress echocardiography
  4. Cardiac Magnetic Resonance (CMR)
  5. Nuclear myocardial perfusion imaging
  6. CT coronary angiography
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23
Q

What do troponins reflect? What are the 2 gold standard troponins?

A

Reflect myocardial cellular damage

I and T are gold standard

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24
Q

What invasive imaging is used in ACS?

A

Coronary angiography

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25
Q

What are the 3 categories of drug treatments for ACS?

A
  1. anti-ischaemic = b blockers, nitrates, ca channel block, nicorandil, ivabradine, ranolazine
  2. antiplatelet = aspirin, P2Y12 receptor inhibitors, clopidogrel, prasugrel, ticagrelor
  3. anticoagulation = LMWH, fondiparinux, apixaban, rivaroxaban
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26
Q

Name 2 risk scoring systems commonly used in the management of acute coronary syndromes

A
  1. ischaemic risk = GRACE score

2. bleeding risk = CRUSADE score

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27
Q

What are the ECG criteria to diagnose a ST elevation MI?

A
  1. LBBB

2. at least 1mm elevation in leads II and III

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28
Q

What is an ejection systolic murmur, heard loudest in the aortic area, radiating to the carotids?

A

aortic stenosis

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29
Q

What is a mid-diastolic rumbling murmur, heard best with the bell of the stethoscope at the apex with the patient in the left lateral position?

A

Mitral stenosis

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30
Q

What is a pansystolic murmur, best heard at the apex of the heart, radiating to the axilla?

A

Mitral regurgitation

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31
Q

What is an early diastolic murmur heard best at the 4th ICS with the patient sat forward in expiration?

A

aortic regurgitation

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32
Q

Why is it important to get the flu vaccination when you have asthma?

A

Influenza (flu) can be more serious for people with asthma, even if their asthma is mild or their symptoms are well-controlled by medication. This is because people with asthma have swollen and sensitive airways, and influenza can cause further inflammation of the airways and lungs. Influenza infection in the lungs can trigger asthma attacks and a worsening of asthma symptoms. It also can lead to pneumonia and other acute respiratory diseases.

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33
Q

Define the peak expiratory flow rate (PEFR).

A

maximal rate that a person can exhale during a short maximal expiratory effort after a full inspiration.

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34
Q

What are the 3 important questions to ask in an asthma review?

A
  1. in the last month/week have you had difficulty sleeping due to your asthma?
  2. Have you had your usual asthma symptoms during the day?
  3. Has your asthma interfered with your usual daily activities?
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35
Q

What conditions can a wheeze be heard in? (hint there’s 6)

A 
asthma
COPD
cardiac failure
pulmonary disease
foreign body aspiration
eosinophilic lung disease
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36
Q

What are various triggers of asthma?

A

cold, pollen, exercise, dust, stress, cigarettes, pollution, anxiety, animals, alcohol, chest infections, flu

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37
Q

What parts of a clinical history support asthma as an appropriate diagnosis?

A
  1. episodic symptoms
  2. wheeze on auscultation
  3. evidence of diurnal variability
  4. atopic history
  5. absence of symptoms, signs, clinical history to siggest an alternative diagnosis
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38
Q

What are the features of moderate acute asthma?

A

increasing symptoms
PEF 50-75% of predicted
no features of acute severe asthma

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39
Q

What are the features of acute severe asthma?

A

Any one of:

  1. PEF 33-50% predicted
  2. RR greater than 25
  3. HR more than 110/min
  4. Inability to complete sentences in one breath
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40
Q

What are the features of life-threatening asthma?

A

A pt with symptoms of severe plus any one of:

  1. PEF less than 33%
  2. SpO2 less than 92%
  3. PaO2 less than 8kPa
  4. Normal PaCO2
  5. Silent chest
  6. Cyanosis
  7. Poor respiratory effort
  8. Arrhythmia
  9. exhaustion
  10. Hypotension
  11. Altered conscious level
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41
Q

What is involved in the initial assessment of asthma? (HINT 5 things)

A 
Clinical features assessed
PEV or FEV1
Pulse oximetry
ABGs
CXR
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42
Q

What treatments are involved in acute asthma?

A

B2 agonsts, steroids and oxygen initially

2nd line = nebulised ipratropium bromide and consider IV magnesium sulphate

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43
Q

What are 2 common side effects of salbutamol?

A

Tachycardia and tremor

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44
Q

When should a follow up be arranged following a severe asthma exacerbation?

A

2 working days

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45
Q

When is jaundice clinically apparent?

A

when bilirubin concentration exceeds 50 micromoles per litre

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46
Q

How much bile is produced each day? When is it released from the gallbladder?

A

500 – 1000 ml/day.

Released in response to hormonal (CCK-PZ) and vagal response to food.

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47
Q

What is added to conjugate bilirubin? Making it water soluble

A

Glucoronic acid

- this process is controlled by the enzyme glucuronyl transferase

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48
Q

What type of hyperbilirubinaemia gives pale stools and dark urine?

A

conjugated aka obstructive or hepatocellular jaundice

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49
Q

What are the (i) common and (ii) uncommon causes of OBSTRUCTIVE jaundice?

A

(i) gallstones = biliary colic, cholecystitis/cholangitis
carcinoma of the head of the pancreas
(ii) sclerosing cholangitis, cholangiocarcinoma

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50
Q

What are the (i) common and (ii) uncommon causes of HEPATOCELLULAR jaundice?

A

(i) alcohol hepatitis or cirrhosis, viral hepatitis, drug induced eg paracetamol OD, NAFLD
(ii) autoimmune liver disease, haemochromatosis, Wilson’s disease

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51
Q

What type of pain is biliary colic? If it is associated with jaundice and fever what does it suggest?

A

RUQ pain

- indicates cholangitis aka sepsis in the biliary ducts

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52
Q

What type of pain arises in pancreatitis? What is is usually caused by?

A

severe epigastric pain, radiating to the back

- usually caused by alcohol excess or a stone blocking the CBD

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53
Q

What are the important LFTs and what are they indicative of?

A
  1. clotting factors (INR and PT)
  2. Albumin - monitors degree of liver damage
  3. Liver enzymes = bilirubin, transaminases (ALT, AST), ALP
    note: if rise in ALT, AST is greater than rise in ALP then HEOATOCELLULAR
    but if rise in ALT, AST is less than the rise in ALP then OBSTRUCTIVE cause
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54
Q

What is delirium tremens?

A

Acute confusional state from immediate/abrupt alcohol withdrawal
If left untreated, it can result in seizures, and even death

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55
Q

What is the treatment for acute alcohol withdrawal?

A
  1. Benzodiazepine or carbamazepine
    - alternative = clomethiazole
    To treat delirium tremens use oral lorazepam
    (2nd line = parenteral lorazepam or haloperidol)
    dont use phenytoin to treat alcohol withdrawal seizures
    lastly, thiamine is used for suspected/at risk individuals for Wernicke’s encephalopathy
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56
Q

What two things does cirrhosis typically consist of?

A
  1. fibrosis of the liver

2. nodule formation

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57
Q

What is fulimant hepatitis?

A

acute hepatitis with liver failure and encephalopathy within 28 days of jaundice
- poor prognosis, often needs transplantation

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58
Q

What are the symptoms associated with the two areas cirrhosis damages (i) loss of function (ii) portal hypertension?

A

(i) jaundice, coagulopathy, decreased drug metabolism, decreased hormone metabolism and increased sepsis
(ii) varices, piles, ascites, encepphalopathy, renal failure

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59
Q

What are the causes of cirrhosis?

A

hazardous alcohol, chronic hep B and C, autoimmune liver disease, haemachromatosis, Wilsons disease, chronic obstruction

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60
Q

What are the typical stigmata of cirrhosis?

A

palmar erythema, leuconychia, spider naevi, caput medusae

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61
Q

What are the two things bile consists of? Where are these two things derived from?

A

Bile pigments - from haemoglobin breakdown

Bile salts - from cholesterol

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62
Q

What are the causes of haemolytic jaundice?

A

Due to increased RBC breakdown:

  1. RBC abnormality eg sickle cell disease
  2. Incompatible blood transfusion
  3. Drug reaction
  4. Hypersplenism
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63
Q

What type of bilirubin is in abundance in haemolytic jaundice? Explain

A

Liver function is normal but glucuronyl transferase is saturated. The liver compensates by increasing conjugated bilirubin output, therefore, dark stools
- the excess of unconjugated in plasma results in little to no colour in urine

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64
Q

What are the causes of hepatocellular jaundice?

A
  • congenital “neonatal” jaundice
  • acquired (as a result of liver damage) = infection, cirrhosis 2o to alcohol, cirrhosis 2o to steatohepatitis, damage by toxins/drugs
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65
Q

Why can neonatal jaundice be fatal?

A

In babies, unconjugated bilirubin can penetrate the BBB. It is toxic to neural tissue and can cause short and long term neurological dysfunction

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66
Q

What are the common causes of obstructive jaundice?

A
  1. obstruction of duct by stone
  2. obstruction of duct by tumour
  3. intra-hepatic cholestasis
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67
Q

What are the imaging techniques used to diagnose jaundice?

A

USS is first line

  • if duct dilatation then CT
  • if ducts normal on USS then must be pre-hep or hepatocellular
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68
Q

What are the 4 categories of causes of ‘hepatitis’?

A
  1. Hereditary = haemochromatosis, Wilson’s
  2. Drug induced = medications, paracetamol OD, alcohol
  3. Infection
  4. Autoimmune
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69
Q

What are the (i) infective (ii) lifestyle (iii) drug (iv) extrahepatic (v) autoimmune and (vi) hereditary causes of liver disease?

A

(i) INFECTIVE = EBV, CMV, Hep A, B or C
(ii) LIFESTYLE = alcohol excess, obesity, diabetes mellitus
(iii) DRUGS = methotrexate, flucloxacillin, anti-epileptics, rifampicin, paracetamol OD
(iv) EXTRAHEPATIC = cancer of pancreas, gallstones
(v) AUTOIMMUNE = PSC, PBC, autoimmune hepatiis
(vi) HEREDITARY = haemchromatosis, Wilson’s, alpha-1-antitrypsin deficiency

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70
Q

What are risk factors for poor pancreas health?(HINT there’s 5)

A
  1. alcohol consumption
  2. high fat diet
  3. overweight
  4. tobacco products
  5. Genetics (eg cystic fibrosis)
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71
Q

What pathological process happens in acute pancreatits? (HINT autodigestion). What do patients experience symptom wise?

A

The enzymes used to breakdown food are activated early and begin to digest pancreatic tissue
V. painful, radiating to the back. Also experience nausea and vomiting

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72
Q

What are the causes of acute pancreatitis? What test(s) confirm its diagnosis?

A

CAUSES: 40% heavy alcohol use
40 % gallstones
20 % other = abdominal trauma, medications, infections, tumours, genetic/anatomical variants, high triglyceride or calcium levels
Diagnosis by raised blood amylase and lipase, plus CT to confirm

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73
Q

What are the causes of chronic pancreatitis?

A

Common = lifestyle factors in predisposed patients aka long standing heavy alcohol use or long term heavy smoking
Less common = medications, increased triglycerides, autoimmune conditions, inherited/genetic conditions (CF, hereditary pancreatitis)

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74
Q

What are the symptoms which result from chronic pancreatitis?

A

Affects nutrient absorption so can cause weak bones or vision loss

  • some patients have persistent pain and can struggle to gain or maintain weight
  • the pain in chronic is the same as acute
  • risk of developing diabetes
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75
Q

What are the symptoms of a migraine?

A

Paroxysmal headaches that are usually severe and unilateral (occassionally bilateral)
- photophobia, vomiting, phonophobia, pulsating, visual disturbances (flickering lights, spots or zig zag lines, fortification spectra, blind spots), paraesthesia, unilateral numbness, hemiplegia

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76
Q

What medication is used to treat migraines? What can be used as prophylaxis?

A

Triptans (oral) used acutely

- prophylaxis = propranolol, or topiramate (2nd line)

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77
Q

What are the symptoms of a tension type headache?

A

bilateral/generalised mild-moderate headache

  • often described as pressing/tightening/band like/vice like pain
  • occur at/shortly after waking
  • multiple (more than 10) previous episodes
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78
Q

What is used to treat tension type headaches? What can be done as prophylaxis?

A

Analgesia - NSAID, aspirin, paracetamol

- 10 sessions of acupuncture over 5 to 8 weeks

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79
Q

What are the symptoms of a cluster headache?

A

Severe unilateral pain often starting in sleep and waking the patient

  • frequent recurrence in short periods followed by months of remission
  • ipsilateral lacrimation
  • rhinorrhoea/nasal blockage, often ipsilateral
  • ipsilateral conjunctival redness
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80
Q

How are cluster headaches treated?

A

Oxygen and/or subcutaneous or nasal triptan

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81
Q

What are the symptoms of a sub arachnoid haemorrhage?

A

sudden onset severe headache without any alteration in consciousness/neurological signs
- vomiting/seizure/confusion/neck stiffness can be present but not commonly

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82
Q

What are the tell tale symptoms of meningitis?

A

photophobia, neck stiffness, fever, drowsiness

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83
Q

What are the symptoms of temporal arteritis (GCA)?

A

Temporal headache, myalgia, fever, maybe malaise

- jaw claudication, diplopia, scalp tenderness and occasionally blindness

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84
Q

What class of drugs are used to treat temporal arteritis?

A

corticosteroids - high dose as soon as possible

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85
Q

What are the symptoms of a sinus headache/sinusitis?

A 
Nasal congestion/rhinitis
Frontal/maxillary headache
May have fever/flu symptoms
Fullness/headache worse when bending forward
May feel unsteady
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86
Q

What are the symptoms of a brain tumour?

A

Papilloedema, new seizure, cancer diagnosis (esp lung and breast), abnormal neurological signs, change in consciousness/confusion/lack of coordination

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87
Q

What are the symptoms of trigeminal neuralgia?

A

Sudden onset but severe stabbing pain lasting a few seconds to 2 minutes

  • often described as ‘electric shock like’ in one or more branches of the trigeminal nerve
  • triggered by vibration/skin contact/wind/oral intake/brushing teeth
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88
Q

What percentage of migraine sufferers experience aura?

A

20-30%

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89
Q

What are some triggers for migraines?

A 
flickering lights on tv screen
jet lag
relaxing after stress
cheese
menstruation
contraceptive pills
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90
Q

When are the 2 times that triptans are contraindicated?

A

A history of TIA or IHD

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91
Q

What can woman who suffer from menstrual migraines take?

A

Transdermal oestrogen patches

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92
Q

What is the criteria for considering prophylactic migraine treatment? (hint there’s 4)

A
  1. QoL/business duties/school attendance severely affected
  2. 2 or more attacks a month
  3. Attacks dont respond to acute drug treatment
  4. Frequent, v.long or uncomfortable auras occur
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93
Q

What are the differential diagnoses for meningitis?

A
  • encephalitis
  • no infectious causes (blood, trauma, drugs) of meningeal irritation
  • subdural empyema
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94
Q

What does a rapid onset of meningitis suggest?

A

that it is bacterial

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95
Q

What are some risk factors for developing meningitis? (HINT there’s 4)

A
  1. extremes of age
  2. living in close proximity
  3. vaccination history (absence of)
  4. immunosuppression/deficiency
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96
Q

What investigations are performed in suspected meningitis?

A
  1. CSF
  2. blood culture
  3. serology for viruses
  4. throat swab (n. meningitides, strep. pneumoniae)
  5. urine pneumococcal antigen
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97
Q

What are the 2 tests performed to diagnose encephalitis?

A
  1. CT or MRI - oedema of temporal lobes

2. EEG - characteristic slow waves

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98
Q

What is the treatment for meningitis?

A

If suspected bacterial = IV ceftriaxone (If GP setting use IM benzylpenicillin)
- if listeria is suspected ADD ampicillin
If h. influenzae or n. meningitis are the cause then household contacts offered antimicrobials (rifampicin) as prophylaxis

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99
Q

What does pronator drift suggest?

A

subtle pyramidal tract dysfunction

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100
Q

What are the presentations of brain cancer?

A
  1. symptoms due to raised ICP
    - headache, vomit. blurred vision, decreasing conscious level
    - bradycardia. hypertension, papilloedema
  2. symptoms of neurological deficit due to compression/damage
  3. symptoms of cortical/meningeal irritation
  4. hormonal effects
  5. systemic effects/generally unwell
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101
Q

What is the typical presentation in a frontal lobe lesion?

A

weakness
dysphagia
personality changes
dementia

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102
Q

What is the typical presentation in a parietal lobe lesion?

A

sensory symptoms
dressing ataxia
visual field

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103
Q

What is the typical presentation in a temporal lobe lesion?

A

dysphagia

visual field defects

104
Q

What is the typical presentation in a occipital lobe lesion?

A

visual fields

105
Q

What is the typical presentation in a posterior fossa lesion?

A 
dysmetria
in-coordination
gait ataxia
cranial nerve palsies
tremors 
nystagmus
106
Q

What is the most common primary brain tumour?

A

glioblastoma multiforme (GBM)

107
Q

What is the most common benign brain tumour?

A

meningioma

108
Q

Describe a vestibular schwannoma.

A

Benign lesion usually affects 5th, 7th or lower cranial nerves
- ipsilateral hearing problems and tinnitus

109
Q

What is normal ICP? When is it pathological? What can happen when standing?

A

less than 15 mmHg
pathological when greater than 20 mmHg
It can be negative when standing

110
Q

What are the symptoms of raised ICP?

A
  • nausea and vomiting
  • headache
  • visual problems
  • decreasing consciousness
  • respiratory depression
  • HT and bradycardia
111
Q

How do you manage a sustained acute rise in ICP? (there’s 6 steps)

A
  1. heavy sedation and paralysis
  2. CSF drainage
  3. osmotic therapy (mannitol)
  4. hyperventilation
  5. barbituate therapy
  6. decompressive craniotomy
112
Q

What are the general signs of an extradural haematoma?

A

Usually bleed of middle meningeal artery

  • pt regains consciousness after brief loss at time of injury
  • conscious level then slowly starts to decline. The initial ‘lucid interval’ can cause delayed/missed diagnoses
113
Q

What are the general signs of a subdural haematoma?

A

Venous in origin, elderly and alcoholics at increased risk

  • develops v slowly so latent period can be weeks to months
  • headache, drowsy and confused at later stages
  • fluctuating conscious levels are common
114
Q

What is an important side effect of sumatriptan?

A

can cause drowsiness

115
Q

Name the 1 anabolic and 4 catabolic hormones.

A 
catabolic = insulin
anabolic = glucagon, catecholamine, cortisol, growth hormone
116
Q

Not all hyperglycaemia is diabetes, what is the definition of diabetes mellitus?

A

the level of hyperglycaemia sufficient to cause diabetic microvascular complications (retina, kidney, nerve)

117
Q

What do lesser degrees of hyperglycaemia cause a risk of?

A

Increased chance of developing into T2DM

  • increased risk of macrovascular disease
  • in pregnancy it causes gestational diabetes
118
Q

What HbA1c levels indicate (i) diabetes (ii) non-diabetic hyperglycaemia?

A

(i) more than 48mmol/mol

(ii) 42-47 mmol/mol

119
Q

What ethnicities are more at risk of developing T2DM?

A

Black africans and carribeans are 3x more likely

- south asians are 6x more likely

120
Q

What drugs are used to treat T2DM?

A

1st line = metformin (biguanide)
2nd line = add one of
- sulfonylurea (glicazide, glipizide, glibenclamide)
- DPP-4 inhibitor (sitagliptin, vildagliptin, linagliptin, alogliptin)
- SGL2 antags (dapagliflozin, canagliflozin, empagliflozin)
3rd line = triple therapy with combos of above + pioglitazone
4th line = GLP1 agonists (incretins = exenatide, liraglutide) with metformin + sulfonylurea

121
Q

What is the salvage therapy used for diabetic eye disease?

A

vitrectomy

122
Q

What are the complications of diabetes in pregnancy?

A

1st trimester = congenital anomalies

2nd and 3rd trimester = accelerated growth (IUGR)

123
Q

What is diabetic cheiroarthropathy?

A

thickened skin and limited joint mobility of the hands and fingers leading to finger contractures

124
Q

What is the association between depression and diabetes?

A

Depression is increased 2-3x risk for people with diabetes

125
Q

What are the clinical features of DKA?

A
  • hyperventilation
  • vomiting
  • dehydration
  • hypotension with warm peripheries
  • decreased conscious level (CV shock)
126
Q

With DKA/HHS, what 5 steps are used to treat urgently?

A
  1. Hypovolaemic shock = FLUID RESTRICTION
  2. Aspiration Pneumonitis = AIRWAY PROTECTION IF COMATOSE (GCS less than 9)
  3. Cerebral Oedema (F) = CAREFUL IV FLUIDS
  4. Fatal arrhythmia = MONITOR/REPLACE K+
  5. Pulmonary embolism = PROPHYLACTIC LMWH
127
Q

What are the symptoms of severe hypoglycaemia?

A
  1. Adrenergic symptoms = sweating, trembling, hunger

2. Neuroglycopenia = paraesthesiae, blurred vision, confusion

128
Q

When is severe hypoglycaemia more likely?

A
  • alcohol excess
  • v young or v old
  • long duration DM
  • recent severe hypo
  • pregnant
  • autonomic neuropathy
  • renal/hepatic impairment
129
Q

What is a side effect of irbesartan (angiotensin 2 receptor antagonist)?

A

Hyperkalaemia

130
Q

If APTT corrects when mixed with plasma, what does this mean?

A

The individual has a coagulation factor deficiency

131
Q

What clotting factors affect APTT?

A

Factors VIII, IX, XI, XII and Von willebrand factor

132
Q

What type of deficiency is (i) haemophilia A (ii) haemophilia B?

A

(i) Factor VIII deficiency

(ii) Factor IX deficiency

133
Q

What factors make up the (i) extrinsic (ii) intrinsic coagulation pathway?

A

(i) VII

(ii) XI and XII

134
Q

What are causes of a prolonged prothrombin time (PT)?

A

warfarin

factor II, V, VII (most common) and X

135
Q

What are causes of a prolonged APTT?

A

heparin

Factor VIII, IX, XI, XII and von willebrands disease

136
Q

What should you think of if both APTT and PT are prolonged?

A 
with low fibrinogen:
- vit K deficiency
- DIC
With normal fibrinogen:
- heparin toxicity
- rarely; factor V or X deficiencies
137
Q

What is the diagnostic triad of bleeding disorders?

A
  1. personal history of bleeding
  2. family history of bleeding
  3. supportive lab tests = platelets (FBC, PFA), tests of coagulation (PT, APTT, TT, Clauss, 50/50 mix), tests of clot stability (euglobin clot lysis, factor XIII assay, PAI-D)
138
Q

What is the 50/50 tests? What does it distinguish?

A

If a patient had a prolonged APTT or PT, redo the test with a 50/50 mix of normal plasma

  • if it CORRECTS = factor deficiency
  • if it FAILS to correct = factor inhibitor
139
Q

How is haemophilia A treated?

A

Factor VIII (half life is 8hrs so taken 1-3x daily)
OR
Desmopressin (DDAVP) which releases stored factor VIII

140
Q

How is haemophilia B treated?

A

Factor IX (half life 18-24hrs so taken 1x daily)

141
Q

How do you treat mixed haemophilia A and B?

A

Tranexamic acid (an anti-fibrinolytic)

142
Q

What are the 3 types of Von Willebrand’s disease?

A

TYPE 1 = decreased amount of normal vW protein
TYPE 2 = abnormal vW protein
TYPE 3 = little or no vW protein

143
Q

How is Von Willebrands tested for? How are type 1 and type 2 differentiated?

A

Tested for by Factor VIII, vW antigen and vW activity

- if the ratio of vWF activity: vWF antigen is MORE than 0.6 it is type 1 and if it is LESS than 0.6 it is type 2

144
Q

What is used to treat the 3 types of Von Willebrand’s disease?

A 
1 = DDAVP + tranexamic acid
2 = vWF concentrate (avoid DDAVP in 2b)
3 = vW factor
145
Q

How is venous thromboembolism prevented?

A
  • anti embolism stockings or intermittent pneumatic compression sleeves
  • LMWH (SC), low dose UFH (IV), direct anti-xa and anti-thrombin drugs (oral) (DOACs)
146
Q

How are venous thromboembolisms managed?

A

Wells score
Don’t investigate first (1hr for PE, 4hr for DVT)
Use heparin (LMWH)
Start oral warfarin (takes 48-72 hrs to take effect, then discontinue heparin)

147
Q

What is homan’s sign?

A

A tender calf which is worse with ankle dorsiflexion

148
Q

What do you do in a suspected VTE if the wells score is low?

A

D-dimer

- if positive then further imaging is required; doppler of leg or CTPA

149
Q

What is a massive PE? How does it present and how is it treated?

A

Large clot lodges in R side of heart or in both pulmonary arteries (saddle embolus)

  • presents with syncope and other PE symptoms
  • presence of arterial hypotension or cardiogenic shock/cardiac arrest
  • medical emergency that requires urgent thrombolysis
150
Q

When are anti-embolus stockings contraindicated?

A

In pts with intermitted claudication

- they can exacerbate pre existing PAD

151
Q

What electrolyte levels should be closely monitored when patients are on LMWH (enoxaparin) for more than 7 days?

A

Potassium levels

- pts with diabetes, chronic renal impairment and on meds that can increase K are at risk of hyperkalaemia

152
Q

What are the 3 most common causes of hyperthyroidism?

A
  1. Grave’s disease (autoimmune)
    2 Toxic multinodular goitre
  2. solitary toxic adenoma
    - another cause is drugs (interferon + amiodarone)
153
Q

What are some of the symptoms of hyperthyroid (thyroroxicosis)

A

Increased pulse and BP, risk of AF

  • warm, moist hands
  • exophthalmos, lid lag, goitre
  • agitation, tremor, oncholysis, acropachy
  • conjunctival oedema, opthalmoplegia, pretibial myxoedema
  • prox myopathy, hyperreflexia, frequent bowel actions
154
Q

What are the risks associated with thyroid eye disease?

A
  • intraocular pressure
  • optic nerve damage exposure
  • corneal ulceration
155
Q

What are the treatments used in thyroid eye disease?

A
  • steroids
  • immunosuppression
  • surgical decompression
  • radiotherapy
156
Q

What are the treatment options for thyrotoxicosis?

A
  1. Beta adrenergic blockers
  2. Antithyroid drugs = Carbimaxole, Propylthiouracil
    - usually pts receive carbimazole or propylthiouracil for 6-24 months
  3. Radioactive iodine (cancer risk)
  4. Surgery (sub-total/near-total thyroidectomy)
    - complications = parathyroid damage, vocal cord paralysis, bleeding, keloid scars
157
Q

What are the side effects of antithyroid drugs?

A

Most important (severe) are agranulocytosis or leucopenia

  • rash, itching, arthralgia
  • nausea and vomiting
158
Q

What symptoms are only found in Graves disease?

A
  • opthalmoplegia
  • exopthalmos
  • pretibial myxoedema
  • thyroid acropachy
159
Q

What is neonatal hyperthyroidism?

A

Thyroid stimulating antibodies (in Graves) can cross the placenta and stimulate the thyroid gland of the foetus

160
Q

When is RAI-131 contraindicated?

A

In pregnancy or women who are breastfeeding

161
Q

What is the most common cause of hypothyroidism in the UK? Who does it tend to affect?

A

Hashimotos (chronic autoimmune thyroiditis)

- Women over 40

162
Q

What is secondary hypothyroidism?

A

Due to TSH deficiency due to pituitary or hypothalamic disease
- TFTs show low T4 and low TSH

163
Q

What are the features of hypothyroidism?

A
  • weight gain, lethargy, cold intolerance
  • cool dry skin, dry brittle hair, nail changes
  • constipation, heavy periods, muscle cramps
164
Q

How is hypothyroid treated?

A

Thyroxine (t4)

usually 100-125 micrograms a day

165
Q

What are the side effects of over-replacement of thyroxine?

A

AF and osteoporosis

166
Q

What are the 6 red flags for thyroid malignancy? What investigations are performed?

A
  1. growing mass
  2. dysphagia
  3. neck pain
  4. hoarseness
  5. Hx of neck radiation
  6. FHx of thyroid cancer
    - USS followed by FNA of lump
167
Q

What are the types of thyroid malignancy? How are they treated?

A 
Papillary carcinoma (70%)
Follicular carcinoma (20%)
- anaplastic carcinoma, lymphoma, medullary cell carcinoma
treatment = surgery - post op RAI treatment - thyroid hormone suppression
168
Q

Describe medullary cell carcinoma.

A

Can be inherited

- associated with phaeochromocytoma (adrenal tumour) and hyperparathyroidism

169
Q

What is Sheehan’s syndrome?

A

Affects woman who lose a life-threatening amount of blood in childbirth OR who have a severe low BP during or after childbirth, depriving the body of O2 this can damage the pituitary gland
- causing hypopituitarism, and in turn secondary hypothyroidism

170
Q

What is the pathological process that leads to Type II respiratory failure in COPD? What physiological compensatory mechanisms occur in the body to reduce the level of acidaemia?

A

In COPD the elastic recoil of the lungs is lost. This causes gas trapping and reduced excretion of CO2. In the blood, the CO2 combines with water to form carbonic acid. In an acute setting, the increased acid levels in the blood would lower the pH levels and the patient would become unwell very quickly. However when CO2 retention is progressive, as is often the case in chronic COPD, the body can compensate for this by utilising the bicarbonate buffer system of the blood. The kidneys are stimulated to reabsorb more bicarbonate, which acts as a base and neutralises the carbonic acid, thus restoring the pH back to the normal range.

171
Q

How is hypertension diagnosed?

A

Readings from both arms must be taken and there must be less than a 20 mmHg difference in each arm
Clinic BP is 140/90 or higher than take a second measurement, if substantially different then take a third. Record the lower of the last 2 measurements as clinic BP
- offer ABPM to confirm diagnosis, if patient cannot tolerate this, HBPM is a suitable alternative to confirm diagnosis

172
Q

How is ambulatory blood pressure monitoring performed? How is home BP monitoring performed?

A 
ABPM = 2 measurements per hour taken during persons normal waking hours. Use ave value of at least 14 measurements to confirm HT diagnosis
HBPM = for each reading, 2 consecutive readings are taken, at least 1 min apart, with the person seated. Recording done twice daily (morning + evening), do for a min of 4 days, ideally 7. Discard day 1 measurements and take an average of the rest
173
Q

What are the stages of hypertension?

A 
STAGE 1 (mild) = systolic 140-159 diastolic 90-99
STAGE 2 (moderate) = systolic 160-179 diastolic 100-109
STAGE 3 (severe) = systolic greater than 180, diastolic greater than 110
174
Q

What scoring system is used to assess CVD risk in HT?

A

QRISK score

175
Q

What are the 3 things involved in the short term control of blood pressure?

A
  1. CNS response
  2. Baroreceptors
  3. Chemoreceptors
176
Q

What are the clinical uses of (i) adrenaline (ii) noradrenaline?

A

(i) anaphylactic shock, cardiogenic shock and cardiac arrest

(ii) severe hypotension and septic shock

177
Q

What are the clinical uses of (i) dopamine (ii) dobutamine?

A

(i) acute HF and cardiogenic shock

(ii) acute HF, cardiogenic shock, refractory HF

178
Q

How is BP controlled long term?

A
  1. Renin angiotensin aldosterone system

2. Vascular remodelling and contractility

179
Q

What does primary hyperaldosteronism cause? What 2 things can cause it? What do patients present with?

A

Causes raised BP

  1. Unilateral aldosterone producing adenoma aka Conns syndrome (50-60%)
  2. Bilateral adrenal hyperplasia (40-50%)
    - pts present with: hypokalaemia, muscle weakness, cramping, palpitations
180
Q

What do people with Addison’s disease present with?

A
  • lethargy, weight loss, fainting, hyperpigmented skin creases, postural hypotension, dehydrated
  • hyponatraemic, hyperkalaemic and acidotic
181
Q

What are the investigations and treatment in Addison’s disease?

A 
Investigations = short synACTHen test
treatment = replace glucocorticoid, mineralocorticoid and sex steroid production
182
Q

What are the organ damages that hypertension can cause?

A 
EYES = hypertensive retinopathy
BRAIN = hypertensive cerebrovascular disease
HEART = IHD with or without HF, LVH
KIDNEYS = hypertensive nephropathy
183
Q

List diseases/conditions/drugs that can cause secondary hypertension.

A
  • renovascular disease
  • primary renal disease
  • oral contraceptives, NSAIDs, stimulants (caffiene + methylphenidate), calcineurin inhibitors, antidepressants
  • phaeochromocytoma
  • primary aldosteronism
  • cushing’s syndrome
  • sleep apnea syndrome
  • coarctation of the aorta
  • hypothyroid and primary hyperparathyroidism
184
Q

What is the treatment strategy for patients with hypertension and UNDER 55?

A

1st line = ACEI or ARB if ACEI not tolerated

  • then add calcium channel blocker
  • if still hypertensive add thiazide type diuretic eg indapamide, chlortalidone
  • then add further diuretics or alpha blocker or beta blocker
185
Q

What is the treatment strategy for patients with hypertension and OVER 55 or African/Caribbean?

A

Start with calcium channel blocker

  • then add ACEI or ARB
  • followed by C+A+D
  • then add further diuretics or alpha blocker or beta blocker
186
Q

What are the healthy lifestyle interventions recommended to reduce BP?

A 
healthy diet
decrease salt intake
decrease coffee intake
quit smoking
decrease alcohol intake
regular exercise
relaxation therapies (not available on NHS)
187
Q

What is the most important//main side effect for the following drugs; (i) ACEI (ii) beta blockers (iii) ca channel blocker (iv) thiazide diuretics (v) loop diuretics (vi) aldosterone antagonists?

A

(i) tickly cough
(ii) bradycardia
(iii) ankle oedema
(iv) hyponatraemia + increased K
(v) gout attack
(vi) hyperkalaemia

188
Q

What drugs can be used in pregnancy to treat HT?

A

labetolol, nifedipine, methyldopa

189
Q

What are the symptoms which differentiate between right and left heart failure?

A 
Right = ankle oedema, hepatomegaly and elevated JVP
Left = bibasal crepitations
190
Q

What are the 4 gradings of murmurs?

A
  1. only heard on listening for some time
  2. faint murmur heard immediately on auscultation
  3. loud murmur with no palpable thrill
  4. loud murmur with a palpable thrill
191
Q

What are the 4 New York Heart association levels for staging heart failure?

A 
1 = no symptoms and no limitations in ordinary physical activity
2 = mild symptoms and slight limitation during ordinary activity
3 = marked limitation in activity due to symptoms, even during less than ordinary activity
4 = severe limitations, symptoms at rest
192
Q

What are the investigations involved in diagnosing heart failure?

A
  • bloods: FBC, haematinics, U+E, TFT, Glucose
  • brain natriuretic peptide (BNP): normal levels rule out HF, high levels = worse outcomes
  • CXR
  • Echocardiography: info relating to EF of LV (normal = 60%, abnormal less than 45%)
  • ECG
193
Q

How is HF treated with (i) preserved LV function (EF greater than 45%) and (ii) impaired systolic function (EF less than 45%)?

A

(i) diuretics followed by treatment of comorbidities eg HTN, DM
(ii) DIuretics
ACEI and b blockers first line
- aldosterone receptor antags (elperenone + spironolactone) used in severe LV dysfunciton (NYHA II, EF less than 35%)
- devices (CRT/ICD)

194
Q

What can cause (i) increased (ii) decreased contractility?

A

(i) catecholamines and calcium

ii) acidosis and some negatively inotropic drugs (anaesthetic agents

195
Q

What are the 2 most common causes of heart failure in the UK?

A

CHD and hypertension

196
Q

What are the 4 causes of mitral regurgitation?

A
  1. Rheumatic heart disease
  2. IHD
  3. Valvular vegetations (endocarditis)
  4. Physiological MR due to dilated LA
197
Q

When should you not cardiovert someone? Why is this the case?

A

Who has been in AF for more than 48 hours unless it is going to be lifesaving as the risk of clots increases after 48 hrs, therefore if normal sinus rhythm is restored by cardioversion clots could dislodge and cause an embolic stroke

198
Q

What criteria is used for diagnosis of infective endocarditis?

A

Modified Duke Criteria

199
Q

What does adrenaline do to the frank starling curve

A

pushes it to the left

200
Q

What scoring system is used for AF stroke risk? What does it comprise of?

A 
CHADS-2
CHF history
HT history
Age more than 75
DM history
Stroke or TIA history (2 points)

Moderate risk = 1-2
high risk = greater than 3

201
Q

Name examples of loop diuretics? (there’s 4)

A

Bumetanide
Furosemide
Tosemide
Ethacrynic acid

202
Q

What kind of drug is rivaroxaban?

A

A direct factor Xa inhibitor

203
Q

What are the 3 hallmark COPD symptoms?

A

SoB
chronic cough
sputum production

204
Q

What is COPD characterised by?

A

Airflow obstruction that’s usually progressive, NOT fully reversible and doesn’t change markedly over several months
- it is predominantly caused by smoking

205
Q

What are the 3 pathological changes which occur in COPD? What symptoms do these give?

A
  1. Goblet cell hyperplasia = cough and sputum
  2. Airway narrowing = breathless and wheeze
  3. Alveolar destruction = breathlessness
206
Q

What are the symptoms of COPD?

A

Smoker/ex-smoker over 35

  • exertional breathlessness
  • chronic cough
  • regular sputum production
  • winter exacerbations
  • wheeze
207
Q

What are the physical signs of COPD?

A

tar-staining, central cyanosis, tachypnoea, chest hyperexpansion (barrel shaped), reduced lateral and increased vertical chest expansion, paradoxical lower chest motion, decreased breath sounds, wheeze, palpable liver edge

208
Q

How are airflow obstruction and restriction differentiated?

A 
Obstruction = FEV1/FVC less than 0.7
Restriction = FEV1/FVC greater than 0.7
209
Q

What are the 4 GOLD stages of COPD severity?

A 
STAGE 1 (mild) = FEV1 greater than 80% predicted
STAGE 2 (moderate) = FEV1 50-79% predicted
STAGE 3 (severe) = FEV1 30-49% predicted
STAGE 4 (v. severe) = FEV1 less than or equal to 30% predicted
210
Q

What are the differences in type 1 and type 2 respiratory failure?

A

Type 1 = PaO2 is low but CO2 and HCO3 are normal

Type 2 = PaO2 is low but PaCO2 and HCO3 are raised

211
Q

What is cor pulmonale?

A

Hypoxia - pulmonary arterial vasocontsriction - increased pulmonary arterial pressure - RV hypertrophy - causing RVF

212
Q

What is the treatment for COPD?

A
  1. Stop smoking advice/help
  2. SABA
  3. if still breathless add LABA/antimuscarinic
  4. If FEV1/FVC less than 50% or frequent exacerbations, add ICS
  5. If still breathless add antimuscarinic/LABA
  6. If still breathless consider pulmonary rehab, increased dose bronchodilators, theophylline
213
Q

What are the complications which can occur in COPD?

A
  • pneumonia
  • pneumothorax
  • RVF
  • peripheral neuropathy
  • cachexia
  • exacerbations
214
Q

What are the side effects of B2 agonists?

A
  • tachycardia
  • arrhythmias
  • MI
  • tremor
  • paradoxical bronchospasm
  • hypokalaemia
215
Q

What are the signs and symptoms of hypercapnia?

A

dilated pupils, bounding pulse, hand flap, myoclonus, confusion, drowsy, coma

216
Q

What are the signs on a CXR of pts with COPD?

A
  • flattened diaphragm
  • smaller heart size
  • hyperinflated lung
  • horizontal ribs
217
Q

What is evident on an ECG to suggest p-pulmonale?

A

Peaked P waves (more than 2.5mm in lead II)

RA enlargement

218
Q

What is target oxygen saturations in patients with COPD?

A

88 to 92%

219
Q

What are the 5 most common infective causes of COPD exacerbations?

A
  1. Strep pneumoniae
  2. Viruses
  3. Moraxella catarrhalis
  4. H. influenzae
  5. Pseudomonas aeruginosa
220
Q

When is long term O2 therapy indicated in COPD patients?

A

With a PaO2 less than 7.3 kPa on air

221
Q

What are the general signs of anaemia?

A
  • fatigue
  • weakness
  • pale/yellowish skin
  • irregular heartbeats
  • SOB
  • dizzy/light-headed
  • chest pain
  • cold hands + feet
  • headache
222
Q

What type of anaemia does acute blood loss cause?

A

Normocytic normochromic

- note that initially the Hb concentration does not alter

223
Q

List examples of hypochromic microcytic anaemias.

A
  1. iron deficiency anaemia: inadequate diet, malabsorption (coeliac), blood loss GI tract (NSAIDs)
  2. Thalassaemia: beta major and minor, alpha thalassaemia (3 deletions = Hb H, 4 deletion = Bart hydrops fetalis)
224
Q

How is iron deficiency anaemia diagnosed? What are problems faced with measuring ferritin? What alternatives is there?

A
  • low Hb, MCH and MCV
  • ferritin = acute phase reactant protein and so can be falsely high in infections and patients with long term inflammatory conditions (rheumatoid disorders, severe skin diseases)
  • other ways to measure iron = serum iron, transferrin saturation, zinc protoporphyrin
  • gold standard = give iron and watch for effect
225
Q

What are specific iron deficiency signs and symptoms?

A
  • headache (especially on activity)
  • craving to eat non food items (called ‘pica’)
  • sore or smooth tongue
  • brittle nails or hair loss
  • spoon shaped nails (koilonychia)
226
Q

What are the types of macrocytic anaemias?

A

folate and B12 deficiencies

227
Q

Name some acquired B12 deficiencies.

A
  1. Nutritional = vegan, poor diet, pregnancy
  2. Malabsorption = gastric (surgery, pernicious anaemia), intestine (ileal resection, fish tapeworm)
    note you get malabsorption of B12 (not deficiency) in Crohns, coeliac, CF
228
Q

Name some acquired folate deficiencies.

A
  1. Nutritional = poor diet, goats milk
  2. Intestinal = coeliac, jejunal resection
  3. Excessive requirement = pregnancy, prematurity
  4. Increased turnover = chronic haemolysis, severe skin disease
  5. Drugs = methotrexate, anticonvulsants
  6. Excess loss = dialysis
  7. Miscellaneous = alcohol (though beer is a good source of folate)
229
Q

What are the signs and symptoms specific to (i) B12 and (ii) folate deficiencies?

A

(i) insidious onset, mild jaundice and anaemia, glossitis, angular chelitis, neuropathy (peripheral, SADC, optic, dementia)
(ii) as for B12 but more often a sensory peripheral neuropathy only
- deficiency in pre conception is associated with an increased incidence of neural tube defects in babies

230
Q

Describe hereditary spherocytosis. What symptoms does it cause? How is it diagnosed and how is it treated?

A

Inherited abnormality of red cell membrane proteins. Autosomal dominant

  • neonatal jaundice, chronic haemolysis, jaundice, gallstones
  • diagnosed by FHx, FBC, reticulocyte count, blood film. And if still uncertain do EMA-binding test
  • treat by giving folic acid regularly, often pts require a splenectomy
231
Q

What is Glucose-6-Phosphate deficiency? What symptoms occur? What do pts have to avoid?

A

X-linked. Pts feel well between attacks. Usually a FHX or a Hx of neonatal jaundice

  • sudden onset of feeling unwell and lacking energy, becoming pale and yellow, having backache, passing dark coloured urine
  • AVOID beans (broad and fava), a number of drugs and moth balls
232
Q

What is sickle cell disease? How is it managed? What complications can occur?

A

Autoinfarction of the spleen with increased infection risk

  • management = keep warm and hydrated, keep regular hours, eat well, take penicillin and folic acid
  • long term management = hydroxyurea and stem cell transplant
  • complications include stroke, increased risk of infection, acute chest syndrome and pulmonary hypertension
233
Q

What is beta thalassaemia MAJOR? How is it managed?

A

Inherit 2 abnormal beta genes. Severe anaemia from 4-6 months of age
- management = long term transfusions and iron chelation (desferrioxamine or desferasirox) or stem cell transplantation

234
Q

What is autoimmune haemolytic anaemia? What are the two types and causes of each?

A

2 types: warm and cold
- DAT is +ve in warm and for complement in cold
WARM: idiopathic
- 2ndary causes = rheumatoid disease (SLE), lymphoma, chronic lymphatic leukaemia, drugs eg cephalosporins, ovarian teratoma
COLD: idiopathic
- 2ndary causes = EBV infections, mycoplasma pneumonia, ulcerative colitis

235
Q

What is the main cause of death in beta thalassaemia major?

A

cardiac iron overload

236
Q

What are the components of the CURB-65 score?

A 
Confusion
Urea greater than 7mmol/l
RR 30 breaths/min or more
BP systolic less than 90 mmHg or diastolic less than 60 mmHg
Aged 65 or older 
0-1 = low severity
2= moderate
3-5 = high severity
237
Q

What are the types of URTI?

A
  • common cold ‘coryza’
  • sinusitis
  • pharyngitis
  • laryngitis

ALL are mainly viral

238
Q

What are types of LRTI?

A

acute bronchitis - mainly viral

  • pneumonia
  • exacerbations of COPD
  • exacerbations of bronchiectasis
  • lung abscess
  • empyema
239
Q

What are the 4 main subcategories of pneumonia?

A
  1. Community acquired = gram +ve, mycoplasma, influenza
  2. Nosocomial (hospital acquired) = gram -ve bacteria, MRSA
  3. The immunosuppressed (organ transplant, chemo, risk for HIV) = unusual organisms, commensals, fungi
  4. Aspiration (swallowing problems, reduced consciousness) = chemical pneumonitis, anaerobic bacteria
240
Q

What are the common symptoms and signs of pneumonia?

A

Cough, fever, rigors, anorexia, chest pain (pleuritic, sudden onset), dyspnoea, abdominal pain
- the elderly suffer from mental dysfunction, falls and incontinence

  • dull to percuss, bronchial breathing, whispering pectoriloquy, aegophany, mental confusion
241
Q

What investigations are performed in suspected CAP?

A
  1. Gas exchange = SaO2, ABGs
  2. Fluid balance = U+Es
  3. Diagnosis = WCC, CRP, CXR
  4. Cause = sputum gram stain (culture, sensitivity), blood culture, urine pneumococcal and legionella antigen
242
Q

What treatment is given for CAP?

A
  1. Place of care
  2. Oxygen
  3. Fluids
  4. Antibiotics
    - low severity = amoxicillin oral
    - moderate = amoxicillin + clarithromycin oral
    - severe = co-amoxyclav + clarithromycin IV
243
Q

What are the complications associated with pneumonia?

A
  • simple para-pneumonic effusion
  • empyema
  • metastatic infection (joint, brain)
  • pulmonary VTE
  • antibiotic side effects
244
Q

How is pneumonia prevented?

A
  • smoking cessation
  • adult vaccination for influenza and pneumococcal
  • child vaccination
245
Q

What symptoms are common in legionella or mycoplasma?

A

Myalgia and arthralgia

246
Q

What is bacterial pneumonia characterised by?

A

Acute inflammation of the lung parenchyma

247
Q

What are (i) typical (ii) atypical causes of CAP?

A

(i) Strep. pneumoniae (80%, +ve)
H. influenzae (-ve)
Klebsiella pneumoniae (-ve)
Staph. aureus (+ve)
(ii) Mycoplasma pneumoniae (treat w macrolides)
Legionella pneumophilia (macrolides)
Chlamydia pneumoniae (macrolides, doxycycline)
Chlamydia psittaci (macrolides, doxycycline)
- common in contact w birds

248
Q

What are the (i) viral (ii) fungal causes of pneumonia?

A

(i) most common = influenza A+B
- adenovirus, para-influenza and RSV
- all diagnosed via PCR
(ii) Pneumocystitis jiroveci = most common type in UK
- common in immunocompromised including HIV, suppression, or those with COPD, CF

249
Q

What is hospital acquired pneumonia classified into? What are bacterial causes?

A

Onset occurs 48 hrs after admission

  • can have early (less than 5 days) or late (more than 5 days) onset
  • bacterial causes of late onset = E,coli, staph. aureus, pseudomonas sp, enterococcus sp
250
Q

Why is aspiration most likely in the right lower lobe?

A

As the right main bronchus is straighter than the left, and ends in the right lower lobe

251
Q

Who are high risk populations for TB? (there’s 3)

A
  • homeless
  • prisoners
  • drug users

it is a disease of low income countries

252
Q

What are the symptoms of TB?

A 
General = weight loss, night sweats, fever
Lung = cough +/- sputum, haemoptysis
Lymph = node enlargement
Pleura = pleuritic pain
Bone = bone pain
253
Q

What investigations are performed in suspected TB?

A
  • CXR
  • ESR/CRP
  • HIV testing
  • LFT
  • sample for microbiology = sputum smear and culture
254
Q

What will the CXR of a TB post primary disease pt show?

A
  • upper lobe consolidation
  • apical segment lower lobe
  • cavitation
  • volume loss
  • lymphadenopathy
  • pleural effusion
  • pneumothorax
255
Q

What treatments are given in TB? In the initial phase and continuation phase.

A

Initial phase (2 months) = isoniazid, rifampicin, pyrazinamide, ethambutol

Continuation phase (4 months) = rifampicin, isoniazid

256
Q

How long after pneumonia should patients start to feel well again?

A

AFTER:

  • 1 week = fever resolved
  • 4 weeks = chest pain + sputum reduced
  • 6 weeks = cough + breathlessness reduced
  • 3 months = fatigue still present
  • 6 months = most feel back to normal

MANCHESTER YEAR 3 (11 decks)

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