Medicine 1 Flashcards

Question

T2DM - insulin therapy

Answer 1

Continue metformin Tx to prevent excess weight gain. Immediate acting insulin injected once/twice daily according to need. Biphasic preparations can be used if the Pt’s HbA1c is particularly high.

Answer 2

Structured education programme => DAFNE – dose-adjustment for normal eating. Screen for complications (less common in early-onset disease) Monitor CV risk Lifestyle advice: - Diet – carbohydrate counting is the most important advice, as per DAFNE education. - Advice for how to adjust diet/insulin for exercise and consuming alcohol. Insulin regimen Annual review

Answer 3

1. all patients with T1DM that present below the age of 40 2. all patients with T2DM that fail to respond to full medical Tx / are unsuitable for medical Tx

Answer 4

basal bolus regimens are recommended: - Twice daily long-acting insulin – e.g. Detemir - Rapid acting insulin with each meal – e.g. Novorapid. If this is not possible, twice-daily mixed insulin regimens can be tried. If the patient cannot achieve HbA1c <8.5%, insulin pumps can be considered by a specialist team.

Answer 5

The body’s natural response to illness results in higher blood glucose levels due to the release of stress hormones and release of glucose from your body’s stores. 1. DO NOT STOP INSULIN – seek advice from diabetes team on how to adjust insulin dose. 2. Monitor Blood glucose more frequently. => Every 3-4 hours, including overnight. 3. Consider blood/urine ketone monitoring: => If raised, contact GP/diabetic service immediately. 4. Maintain normal meal pattern where possible. => Replace meals with sugary drinks if appetite reduced. 5. Drink at least 3L of fluid per day: => Seek advice if unable to do so => IV fluids may be needed 6. Once better, continue to control blood glucose carefully until it returns to normal.

Answer 6

Patients are only required to inform the DVLA if: 1. They have had 2 episodes of severe hypoglycaemia within the last 12 months. 2. They have reduced awareness of hypoglycaemic episodes 3. They are on insulin therapy: => If on insulin, they must test their blood glucose every 2 hours on long journeys and also carry appropriate glucose stores in case of hypoglycaemic events.

Answer 7

1. Assess Cardiovascular Risk => BMI, BP, Smoking Status, Blood lipid levels, Consider ECG 2. Assess for microvascular complications: - Hx – erectile dysfunction, neuropathic pain - Foot examination (incl. neurovascular status) - Fundoscopy – retinal involvement - Urine dip, first pass urine and plasma creatinine – renal involvement 3. Assess Diabetic Control: - Self-monitoring results? - HbA1c (should be checked 6-monthly) 4. Assess for concordance to diet/lifestyle advice 5. Assess for adverse events: - Hospitalisations - Sx of hypoglycaemic episodes - Medication side effects - Injection site reactions 6. Is the patient driving? => If so, do they know the DVLA advice. 7. Assess for depression and anxiety

Answer 8

1. Decrease hepatic glucose production 2. Increase peripheral insulin sensitivity

Answer 9

- eGFR <30 for standard release, <45 for modified release. - Alcohol addiction - People at risk of lactic acidosis (e.g. DKA) - People at risk of tissue hypoxia (e.g. cardiac/respiratory failure).

Answer 10

GI effects – N&V, abdo pain, loss of appetite Lactic acidosis – rare but serious; occurs due to drug accumulation; insidious onset with non-specific symptoms; more common when combined with alcohol. Vitamin B12 deficiency

Answer 11

Increase insulin secretion (thus only work if some residual function of pancreatic beta-cells). Can get different lengths of drug action: - SA – tolbutamide - Medium acting – gliclazide - LA – Glibenclamide (rarely used if there is a risk of hypoglycaemia).

Answer 12

The elderly – risk of hypoglycaemic events The obese – will encourage weight gain

Answer 13

Inhibit sodium-glucose transport protein 2; thereby preventing renal glucose resorption. NOT effective in kidney disease Help weight loss & reduce risk of major adverse CV events

Answer 14

PPAR-gamma activators; increase peripheral insulin sensitivity.

Answer 15

Weight gain (redistribution of ectopically stored lipid) Fluid retention – contraindicated in CCF Liver dysfunction – monitor LFTs Association with bladder cancers – assess risk factors

Answer 16

work by increasing post-prandial insulin release.

Answer 17

E.g. enaxatide; liraglutide Cause significant weight loss NICE recommend that if triple therapy is ineffective, then the gliptin/pioglitazone can be replaced by GLP-1 mimetics if: - The patient has BMI >35 - The patient has BMI <35 and weight loss would benefit other comorbidities/insulin therapy would have negative occupational impacts.

Answer 18

e.g. Humalog, Novarapid Aim to mimic the body’s insulin secretion in response to food. Injected with food Onset of action = 15 mins

Answer 19

e.g. Actrapid, Humalin S (also short-acting) Generally injected 30 mins before food. Onset of action = 30-60 mins Duration of action = up to 8 hours

Answer 20

e.g. Humalin I, Insulatard Mimic basal insulin secretion Onset of action = 1-2 hours Maximal effects between 4-12h Duration of action up to 16-35 hours

Answer 21

e.g. Lantus, Levemir, Tresiba, Detemir Mimic basal insulin secretion Used once/twice per day Achieve a steady-state level after 2-4 days.

Answer 22

- Weight gain (avoided by DAFNE) - Insulin resistance can develop - At the injection site – pain, redness/swelling, abscess, lipohypertrophy (can result in erratic insulin absorption).

Answer 23

Hyperglycaemia leads to formation of advanced glycation end products (AGE) on arterial endothelial cells and activation of inflammatory pathways This exacerbates the process of atheroma formation, leading to artery occlusion and subsequent macrovascular complications.

Answer 24

occur via AGE-activated biochemical pathways resulting in cellular damage caused by abnormal extracellular protein matrix accumulation and reactive oxygen species production. => Microvascular complications are specific to diabetes.

Answer 25

Coronary Artery Disease (=> 4x increased risk of MI) Cerebrovascular Disease (=> 2x increased risk of Stroke) Peripheral Vascular Disease

Answer 26

Diabetic Eye Disease Nephropathy Neuropathies

Answer 27

MACROVASCULAR Good glycaemic control only has modest effects on CV risk – need to work on other factors such as smoking/alcohol, BP, cholesterol, diet, exercise, etc. MICROVASCULAR Regular screening Good glycaemic control

Answer 28

= development of new vessels on the optic disc/retina as a response to significant retinal ischaemia (VEGF => new vessels). The vessels are fragile and likely to bleed; giving rise to pre-retinal or vitreous haemorrhage. If untreated, the blood vessels will cause fibrosis and a tractional retinal detachment Tx: - Pan-retinal photocoagulation (aim = to reduce the ischaemic drive and VEGF production). - Vitrectomy can be used to remove persistent vitreous haemorrhage.

Answer 29

Usually asymptomatic ALWAYS occurs at some severity after 8-10 years of DM Features on fundoscopy: - Microaneurysms - Exudates - Haemorrhages – dot, blot, flame - Cotton wool spots (>5 of these indicated pre-proliferative retinopathy). Can progress to PDR Mx = good glycaemic control

Answer 30

A specific type of retinopathy that affects the macula. Typically presents with blurring of vision Three subtypes – focal, diffuse, ischaemic Mx = focal laser to stop focal leaks, but may require more complex Tx

Answer 31

PDR / NPDR Maculopathy Cataracts Glaucoma

Answer 32

Symmetrical Polyneuropathy Acute Painful Neuropathy Mononeuropathy Diabetic Amyotrophy Autonomic Neuropathy

Answer 33

“Glove and stocking” sensory loss => Vibration, deep pain and temperature lost first Loss of proprioception Interosseus wasting of small muscles of the feet results in a characteristic foot shape, and abnormal pressure areas lead to ulcers. Unrecognised trauma with poor wound healing may lead to ulcers => Can lead to Charcot's foot

Answer 34

Painful burning pains in the feet, shins and anterior thighs; Typically worse at night Associated with poor glycaemic control Usually remits after 3-12 months of good glycaemic control. More chronic forms can be resistant to all forms of therapy.

Answer 35

Cranial Nerve lesions can occur in patients with diabetes – mainly CN III, IV and VI (ocular palsies). Isolated peripheral nerve lesions can also occur Any nerve compression syndrome is more common in DM (e.g. carpal tunnel) Foot drop may occur due to lesions of the sciatic nerve. When more than one nerve is affected, this is known as mononeuritis multiplex.

Answer 36

Amyotrophy = progressive wasting of muscle fibres. In DM, it presents as painful wasting of the quadriceps Course is variable, often with gradual but incomplete improvement.

Answer 37

Sympathetic dysfunction leads to: - Postural hypotension - Ejaculatory failure - Reduced sweating - Horner’s syndrome Parasympathetic dysfunction leads to: - Erectile dysfunction - Constipation - Urinary retention - Holmes-Adie Pupil

Answer 38

Usually manifests 15-25 years after diagnosis The single most important intervention is BP control Test every patient every 6 months for microalbuminuria (i.e. negative urine dip but early morning albumin:creatinine ratio >3) Every patient with microalbuminuria should be started on an ACEI, regardless of BP.

Answer 39

= a medical emergency, in which hyperglycaemia is associated with metabolic acidosis due to greatly raised ketone levels.

Answer 40

SYMPTOMS - N&V - Generalised abdominal pain - Confusion / drowsiness - Blurred vision - Polyuria - Coma (severe cases) SIGNS: - Smell of ketones on the breath - Signs of dehydration - ABG/VBG will show an acidosis (or compensated acidosis) due to bicarbonate consumption by acidic ketone bodies. Lactate levels will also be raised.

Answer 41

all 3 required: 1. Blood glucose >11 mmol/L (or previously known diabetes). 2. Capillary ketones >3 mmol/L (or Ketones >2+ in urine). 3. Venous pH <7.35 (or venous bicarbonate <15 mmol/L)

Answer 42

U&Es Blood glucose Venous blood gas => Metabolic acidosis with raised anion gap ECG/ CXR / cultures / pregnancy test based on clinical suspicion to identify cause

Answer 43

Severity is determined by pH rather than blood glucose: - Mild = pH >7.3 - Moderate = pH 7.1-7.3 - Severe = pH <7.1

Answer 44

ABCDE 1L 0.9% sodium chloride over 1 hour if SBP >90 => 500 ml bolus over 10 mins if <90, reassess & repeat if poor response Start IV insulin infusion: => 50 units human soluble Actrapid Insulin added to 50ml 0.9& sodium chloride (giving a 1 unit / mL solution) => Start syringe driver at a fixed rate of 0.1 units/kg/hour (can use estimated weight). Treat any precipitating factors of the DKA (e.g. infection). Urgent critical care review if: => severe DKA / drowsy / pregnant / sats <94% / on 40% oxygen / persistent hypotension after 2L sodium chloride.

Answer 45

Continue fixed-rate insulin at 0.1 units/kg/hour, and continue normal long-acting insulin. Continue IV 0.9% sodium chloride - First bag = 1L over 1 hour - Second bag = 1L over 2 hours - Consider KCl from second bag onwards - Third bag = 1L over 2 hours - Fourth bag = 1L over 4 hours. When glucose is <14 mmol/L, add 10% glucose at 125 mL/hour => Adjust to keep blood glucose between 8-14 mmol/L Potassium: - If plasma K+ <5.4, add 40 mmol KCl per litre NaCl - Consider after the first litre of fluid has run through Clinically reassess the patient hourly for the first 4-6 hours Regular lab monitoring of glucose, ketones, potassium and bicarb required.

Answer 46

Transfer to s.c. insulin once the patient is able to eat and drink normally and venous pH >7.3 Stop the IV insulin infusion 1 hour after the next s.c. injection of insulin Refer all patients to the diabetes team prior to discharge.

Answer 47

= a severe hyperglycaemia leading to diuresis (leading to a hyperosmolar state) in the absence of severe ketosis and acidosis. Even a small amount of insulin is sufficient to prevent ketosis. The patients will be more severely dehydrated than DKA patients, but there will be no raised ketones. Mortality is 10x more likely in HHS than DKA

Answer 48

- Dehydration - Stupor/coma/seizures - Evidence of an underlying illness

Answer 49

Marked hyperglycaemia (often >30 mmol/L) Hypovolaemia No significant ketonaemia/ketonuria No significant Acidosis (pH >7.3, bicarb >15mmol/L) Confirm by calculating osmolality => Normal Osmolality = 280-295 mmol/kg; HHS = >320 mmol/kg

Answer 50

Fluid replacement alone will cause the glucose levels to fall. Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as water moves out of the intravascular space, with a resulting decline in intravascular volume

Answer 51

A-E assessment Aggressive IV fluids: => 1L 0.9% NaCl over 1 hour => Aim for positive balance of 3-6L over 12 hours. Low-dose fixed IV insulin infusion: => If there are some ketones – treat as per DKA => If no ketones – fluid replacement alone should cause a fall in glucose. => Start insulin once fall in glucose is <5 mmol/L/hour = 0.05 units/kg/hour Consider potassium replacement Give prophylactic LMWH (due to very high risk of thrombosis) Regular monitoring of vitals, fluid balance, glucose, osmolality, U&Es hourly for 1st 6 hours. Transfer to s.c. insulin once eating and drinking normally and biochemistry has normalised => Stop IV infusion 1 hour after starting s.c. insulin Refer to diabetes team

Answer 52

Defined as plasma glucose <3mmol/L, but individual thresholds for symptoms are variable.

Answer 53

AUTONOMIC Sweating Anxiety Hunger Tremor Palpitation NEUROGLYCOPAENIC Confusion Drowsiness / Coma Seizures

Answer 54

Excess insulin – either exogenous or insulinoma Depletion of hepatic glycogen – malnutrition, fasting, exercise, alcohol; also liver failure. (Pituitary insufficiency, adrenal insufficiency, non-pancreatic neoplasms)

Answer 55

Promptly consume 10-20g of fast-acting form of carbohydrate (preferably liquid form). Recheck blood glucose after 10-15 minutes. - Should reverse in 10 mins - Improvements in signs and symptoms may lag behind improvement in blood glucose. If inadequate response, repeat as above and recheck again. When symptoms improve, the patient should eat some long-acting carbohydrate.

Answer 56

Administer IM glucagon immediately: - If <8 years = 500 micrograms - If >8 years = 1mg If glucagon is not available, the patient has consumed alcohol, or the person does not respond to glucagon within 10 minutes – call 999 for emergency hospital transfer => Glucagon is NOT effective if alcohol has been consumed If the patient responds to glucagon, advise intake of long-acting carbohydrates when able. Vomiting is common in recovery, which can precipitate further episodes of hypoglycaemia. Within hospital: - 100ml of 20% glucose can be used as an alternative to glucagon (can be repeated 3 times). - If IV access is not available, administer IM glucagon whilst gaining access.

Answer 57

Symptoms tend to be variable but recurring: - Wheeze - SoB - “Tight” chest feeling - Cough (classically nocturnal) Symptoms tend to be worse at night or early in the morning

Answer 58

- Viral infections - Cigarette smoke - Cold weather - Emotion - Excercise - Atmospheric pollution - Pets / pollen / other allergens - Occupational pollutants – e.g. flour/chemicals

Answer 59

HPC Known precipitants Diurnal variation Acid reflux symptoms (known association) Hx of atopy Hx of these episodes (incl. whether they required hospital admission/ITU) DHx NSAIDs Beta-blockers FHx Atopy, asthma SHx Smoking Days off work/school Occupation (identify occupational pollutants) Pets

Answer 60

Asthma is a CLINICAL DIAGNOSIS – if there are suggestive symptoms, then a structured clinical assessment is needed to see if: * Episodes are recurrent * Sx are variable * PMHx/FHx of atopy * Recorded observation of expiratory wheeze * Variable PEF or FEV1 * Absence of symptoms of an alternative diagnosis If these give a high probability of asthma, diagnose as suspected asthma and initiate treatment. DIAGNOSIS IS CONFIRMED AFTER AN OBJECTIVE IMPROVEMENT AFTER Tx

Answer 61

If response to treatment is poor, refer for spirometry to test for airway obstruction with bronchodilator reversibility => FEV1/FVC <70% with bronchodilator reversibility is diagnostic

Answer 62

= Type I hypersensitivity reaction Most frequently occurs in atopic individuals who show positive skin prick tests to common allergens, implying a definite extrinsic cause.

Answer 63

= Due to non-immune mechanisms Occurs in middle-aged individuals, when no causative agent can be identified. Generally more severe, and associated with quicker deterioration of lung function.

Answer 64

Acute episodes of bronchospasm that are triggered by recognised triggers. Triggers activate mast cells, which lead to two phases of airway narrowing Early phase – bronchospasm due to spasmogen production (histamine, PG D2, leukotrienes) causing smooth muscle contraction in the airways. Late phase – due to chemotaxins causing an inflammatory response, causing narrowing of the airways). There will also be airway hyper-reactivity in the late phase, which can lead to further acute deterioration.

Answer 65

no daytime Sx, no night-time waking, no need for rescue medication, no limitations on activity

Answer 66

1. Short acting beta2-agonist inhaler => For all in whom asthma is suspected 2. Add inhaled low-dose ICS (e.g. beclomethasone, budesonide or fluticasone) => For all patients with CONFIRMED asthma => Remember steroids take 2-3 days to take effect. 3. Trial of LABA (e.g. Salmeterol) - ALWAYS use LABA in combination with a steroid - If no response from LABA, stop it and increase dose of ICS. - If some response but more control required, continue LABA but increase ICS. - Consider use of LTRA (e.g. montelukast), theophylline or a LAMA. 4. Increase dose of ICS (up to highest dose) - Refer to specialist 5. Specialist management - Can include oral steroids, oral beta2-agonists, biologics (e.g. omalizumab). If salbutamol inhaler is used more than 2 times a week, this indicates that their current control is inadequate, and the care needs to move up a step.

Answer 67

ALWAYS use LABA in combination with a steroid

Answer 68

Increasing symptoms PEF 50-75% NO features of acute severe asthma

Answer 69

Requires any one of: * PEF 33-50% predicted best * RR >25/min * HR >110 * Inability to complete sentences in one breath

Answer 70

Any one of: * PEF <33% predicted * SpO2 <92% * PO2 <8kPa * Normal or RAISED PaCO2 (4.6-6) * Silent chest * Cyanosis * Poor respiratory effort * Arrhythmia * Exhaustion * Altered consciousness * Hypotension

Answer 71

If a patient has ANY life-threatening feature, an ABG is the only immediate investigation required whilst treatment is initiated. Certain blood gas features are markers of a life-threatening attack: => Normal PaCO2 (should normally be low due to hyperventilation). => RAISED PaCO2 indicates near-fatal asthma. => Severe hypoxia <8 kPa => A low pH

Answer 72

1. O2 to maintain sats at 94-98% (unless COPD) – usually 15L/min non-rebreather mask 2. Salbutamol 5mg via O2 driven NEB => Add ipratropium to nebuliser if required 3. PO Prednisolone 50mg => Or IV hydrocortisone 100mg If life-threatening features present: - Discuss with senior and ICU - Add IV magnesium sulphate 2g - Keep giving nebulised salbutamol 5mg every 15-30 mins - Senior clinicians may consider IV aminophylline or IPPV

Answer 73

If the patient is stable and improving: - Continue prednisolone dose daily for at least 5 days. - Continue nebulised salbutamol 4 hourly until discharge. - Chart PEF before and after nebulisers, at least 4 times daily while in hospital. Prior to discharge: - Check inhaler technique - Agree on written asthma action plan - Ensure GP follow-up within 2 working days.

Answer 74

= A disease of progressive airflow obstruction that is not fully reversible. Associated with an abnormal inflammatory response of the lungs to noxious stimuli (predominantly [90%] cigarette smoke). Encompasses a spectrum of illnesses: 1. chronic bronchitis – increased mucous, airway obstruction and intercurrent infections 2. emphysema – destruction of alveoli.

Answer 75

= Dilation of any part of the respiratory acinus (the air spaces distal to the terminal bronchioles), with destructive changes in the alveolar walls. Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs, leading to air entrapment in the lungs and inadequate ventilation

Answer 76

Changes are limited to the central part of the lobule, directly around the terminal bronchiole. Normal alveoli elsewhere Most common form – associated with smoking.

Answer 77

Leads to destruction and distension of the whole lobule. Can happen in smokers, but more common in alpha1-antitrypsin deficiency

Answer 78

= Daily cough with sputum for at least 3 months per year Primary abnormality seen is abnormal amounts of mucous, which causes plugging of the airway lumen. Hypersecretion is associated with hypertrophy and hyperplasia of the bronchial mucous-secreting glands.

Answer 79

Cigarette smoke exposure!!! Occupational toxins – e.g. coal dust Alpha1-antitrypsin deficiency Recurrent chest infections in childhood Low socio-economic status Asthma/atopy

Answer 80

- Productive morning cough, following many years of “smokers cough” - Increased frequency of LRTIs - Slowly progressive dyspnoea - Exacerbated in acute infective episodes - Wheezing - Respiratory failure - Chronic right heart failure (occurs late).

Answer 81

MILD – widespread wheeze SEVERE: - Tachypnoea, possibly cyanosis and/or flapping tremor - Hyperinflation, intercostal recession on inspiration, signs of respiratory distress. - Raised JVP if right heart failure - Poor chest expansion - Hyper-resonant throughout, loss of cardiac/hepatic dullness - Decreased breath sounds, prolonged expiratory phase, polyphonic wheeze.

Answer 82

Clubbing is NEVER present in pure COPD

Answer 83

Patients remain sensitive to CO2, thus keep a low CO2 and near-normal O2. Tachypnoeic, tachycardic, using accessory muscles to increase ventilation. Breathless but not cyanosed. Very thin – large amounts of calories used to breathe. Can progress to type 1 respiratory failure. More emphysematous.

Answer 84

Patients are insensitive to CO2. Severe chronic bronchitis/COPD. Not particularly breathless but are cyanosed and oedematous (cor pulmonale). Blood gas will show type 2 respiratory failure (low oxygen, retaining CO2. Oxygen should be given with care to these patients.

Answer 85

There is no single diagnostic test for COPD – diagnosis can be clinical if there are typical Sx, in a person >35 in the presence of a risk factor. Everyone suspected of COPD should then undergo post-bronchodilator spirometry, CXR, FBC.

Answer 86

Hyperinflation (>7 anterior and >11 posterior ribs) Flattened hemidiaphragm

Answer 87

Can show - Secondary polycythaemia - Anaemia of chronic disease

Answer 88

Stage 1 – FEV1 >80% predicted (clinical diagnosis); mild. Stage 2 – FEV1 50-79% predicted; moderate. Stage 3 – FEV1 30-49% predicted; severe. Stage 4 – FEV1 <30% predicted; very severe.

Answer 89

- Normal in mild disease - Developing to type 1/2 respiratory failure as disease progresses.

Answer 90

Patient Education: => How to recognise an exacerbation early => Action plan/rescue medication (in patients with frequent exacerbations). Lifestyle advice: => Diet, exercise, SMOKING CESSATION Pneumococcal and Flu vaccination Medical Mx

Answer 91

Short-acting bronchodilators (SABA or SAMA) are 1st line Further medications are added if ongoing symptoms are limiting QoL or persistent exacerbations. => If no features of asthma/steroid responsiveness: - Add a long-acting beta-agonist (LABA) and muscarinic agonist (LAMA) - Add inhaled corticosteroids if still symptomatic - Remove ICS after 3 months if no improvement. => If features of asthma/steroid-responsiveness* are present => LABA + ICS.

Answer 92

Previous diagnosis of asthma/atopy, Blood eosinophilia, Substantial variation in FEV1 over time or diurnally.

Answer 93

Pulmonary rehabilitation Oral aminophylline/theophylline Mucolytics – e.g. carbocysteine Roflumilast – PDE4 inhibitor Nutritional supplements – consider for those with low BMI Long-term oxygen therapy => Remember to warn patient not to smoke. Surgery

Answer 94

Dyspnoea and wheeze become worse Increased production / change in colour or smell of sputum.

Answer 95

- Severe breathlessness - Rapid symptom onset - Acute confusion - Cyanosis - Low O2 sats (<90%) - Worsening peripheral oedema

Answer 96

Increase dose/frequency of SABA (using a spacer if they don’t already use one) Prescribe 30mg prednisolone for 7-14 days for breathlessness interfering with regular activities. Prescribe oral ABX on local ABX prescribing guidelines. Safety net and follow-up in 6 weeks to optimise medical Tx.

Answer 97

O2 should be titrated according to the patient’s alert card If unknown patient, titrate saturations to 88-92% using a venturi system. => Start on a 28% mask at 4L/min Mx as per outpatient regime, with targeted oxygen therapy and regular monitoring.

Answer 98

= signs of infection of the pulmonary parenchyma, PLUS new shadowing on CXR (separates it from bronchitis).

Answer 99

1. Clinical lower respiratory tract infection AND 2. New pneumonic changes on CXR AND 3. Onset of symptoms in the community OR within 48 hours of hospital admission.

Answer 100

Acute systemic illness – fever/ rigors / vomiting Cough => Initially short, dry and painful => Progresses to productive with mucopurulent sputum. Dyspnoea Pleuritic chest pain => May be referred to shoulder to anterior abdominal wall. Elderly populations may report very few Sx but be very unwell.

Answer 101

Inspection => Tachypnoea Palpation => Decreased chest expansion on affected side Percussion => Dullness over affected area Auscultation => Coarse crackles and pleural rub over affected area => Bronchial breathing => Increased vocal resonance => “99” heard better due to consolidation.

Answer 102

CONVENTIONAL S. pneumoniae H. influenzae ATYPICAL Mycoplasma pneumoniae Chlamydia pneumoniae Legionella pneumophila

Answer 103

STANDARD: Observations (including O2 sats) Bloods – FBC, U&E, CRP, LFTs => Consider ABG => May need blood cultures. Confirm diagnosis – CXR Sputum sample for MC&S (plus mycoplasma PCR if suspected) Throat swab in viral transport medium if severe / suspected viral pneumonia. EXTRA: Urine for legionella/pneumococcal antigen if moderate/severe => Empirical Tx will not cover legionella Serum mycoplasma IgM if suspected.

Answer 104

Criteria for severe CAP = CURB65: Confusion – mini-mental test score of 8 or less (new*) Urea >7 mmol/L (new*) Respiratory Rate >30 breaths per minute Blood Pressure – systolic BP <90 mmHg or diastolic BP <60 mmHg 65 or more years old One point for each new finding. Score 0-1 = low severity Score 2 = moderate Score 3 or more

Answer 105

Low-severity CAP (score 0 or 1): - Outpatient care - PO Amoxicillin - Alternatives available in penicillin allergy/atypical organism Moderate severity CAP (score 2): - PO amoxicillin + clarithromycin - Usually admit the patient. Severe CAP (score > 2): - Can be >20% mortality - Requires admission to at least Level 1 unit or even HDU/ICU. - IV co-amoxiclav + clarithromycin. => Penicillin allergy/MRSA suspicion – vancomycin and levofloxacin. - Treatment for at least 10 days.

Answer 106

Aspiration of gastric contents leading to chemical inflammation and infection. This does not always show on CXR – suspect it e.g. in someone who has a low GCS and evidence of vomiting (so at risk of aspirating). If suspected can add metronidazole for HAP or CAP – this is to cover anaerobic bacteria.

Answer 107

1. Clinical lower respiratory tract infection AND 2. New pneumonic changes on CXR AND 3. onset of symptoms > 48 hours after admission OR admission in the last 7 days

Answer 108

Enteric gram-negative bacilli – ~60% HAP cases. => Enterobacteriaceae (e.g. Klebsiella) => Pseudomonas spp. Strep. pneumoniae H. influenzae Staph. aureus

Answer 109

Assess MRSA risk factors Assess HAP severity – no evidence-based guidelines => clinical decision Mild HAP – oral doxycycline. Severe HAP – IV Tazocin. THESE PATIENTS SHOULD BE DISCUSSED WITH MICROBIOLOGY

Answer 110

Follow-up CXR at 6 weeks => to ensure resolution of consolidation => to assess for persistent abnormalities of the lung parenchyma. Non-resolution => ?endobronchial obstruction as cause of pneumonia (e.g. lung cancer)

Answer 111

Sepsis Lung abscess Empyema – pus-filled collection in the pleural space. => Often develops from a parapneumonic effusion Lung abscess/empyema can be suspected if there is a persistent swinging pyrexia and rising CRP despite treatment.

Answer 112

Primary infection centres around the bronchi, spreading to involve adjacent alveoli which become consolidated. Initial consolidation is patchy (involves lobules), but if left untreated can involve whole lobes.

Answer 113

Organisms gain entry to distal air spaces rather than colonising bronchi, thus there is rapid spread of infection through alveolar air spaces. Macroscopically, the whole lobe becomes consolidated and airless.

Answer 114

SPONTANEOUS PTX => Primary => Secondary TRAUMATIC PTX => Penetrating trauma, rib fractures IATROGENIC PTX => Lung biopsy, endoscopy, subclavian cannulation, positive pressure ventilation.

Answer 115

Lung parenchyma otherwise normal; Often occurs in tall, thin young men.

Answer 116

Underlying lung disease/abnormality – e.g. COPD, asthmatic, malignancy, CF.

Answer 117

May be asymptomatic if small / primary (low index of suspicion required). Sudden onset of unilateral pleuritic pain Progressive dyspnoea

Answer 118

May be few physical signs Reduced expansion on affected side Increased resonance to percussion on affected side Decreased breath sounds and reduced vocal resonance on affected side If TENSION PTX: - Tracheal deviation away from affected side; - Cyanosis - Severe tachypnoea - Tachycardia - Hypotension

Answer 119

= Medical Emergency Air in the pleural space leading to cardiac compromise. Arises due to a one-way valve system, allowing air entry into the pleural space during inspiration but no air exit during expiration. This results in very high intrapleural pressure, deflating the lung and decreasing venous return to the heart (leads to circulatory collapse).

Answer 120

Diagnosis is clinical (there is no time for imaging).

Answer 121

1. Call for help immediately. 2. A-E 3. Oxygen therapy 4. Needle decompression with a cannula => 2nd intercostal space, midclavicular line with a 14g (orange) cannula. => After decompression, patient will require rapid insertion of a chest drain.

Answer 122

Basic Hx and Examination ABG – if signs of respiratory distress / chronic lung disease Erect CXR = diagnostic => you should not be able to see the edge of the lung; if you can, there is likely to be a PTX.

Answer 123

Estimating the size of a pneumothorax is important for management. Estimation of size from a CXR is imperfect but most practical. => General rule is that a 2cm interpleural distance at the level of the hilum equates to a pneumothorax of 50% of the volume of the lung. => <2cm is a small pneumothorax and patient may not need treatment.

Answer 124

Rim of air <2cm and patient is not SoB/hypoxic: => Discharge, with interval CXR at 2 weeks => Safety net – return to hospital if become SoB => Advise to avoid strenuous exercise and quit smoking. Rim of air >2cm => Attempt aspiration => If successful (<1cm residual rim of air), discharge as above. => If unsuccessful, will require chest drain.

Answer 125

Rim of air <1cm => Give oxygen and admit for 24h observation Rim of air 1-2cm => Attempt aspiration => Chest drain if <1cm residual rim of air. Rim of air >2cm => Will require chest drain.

Answer 126

After PTX, air travel should be avoided for 6 weeks, and scuba-diving should be permanently avoided. If there is recurrent PTX (>2 occasions) or PTX that does not resolve within 5 days of a chest drain, then surgery may be indicated.

Answer 127

= a build-up of excess fluid (normal = 15 mL) found between the layers of the pleura (i.e. outside the lungs and therefore different to pulmonary oedema).

Answer 128

Haemothorax = accumulation of blood, due to trauma. Empyema/pyothorax = accumulation of pus, due to infection. Chylothorax = accumulation of lymph, due to thoracic duct leakage. Fluid effusion = fluid accumulation, can be transudative or exudative

Answer 129

= Protein concentration <30 g/L Occur due to increased hydrostatic pressure or decreased oncotic pressure. CAUSES: * Organ failure – Cardiac, Liver, Renal * Peritoneal Dialysis * Hypothyroidism * Ovarian tumours More often bilateral

Answer 130

= Protein concentration >30 g/L Causes: * Infections – bacterial pneumonia, TB * Neoplasm – lung primary/secondary, mesothelioma. * Pulmonary Embolism * Autoimmune disease – RA/SLE * Abdominal disease – pancreatitis, subphrenic abscess. More often unilateral

Answer 131

Decreased chest expansion Tracheal deviation away (if large) Dull percussion – due to underlying fluid Decreased breath sounds Can be bronchial breathing above effusion due to compression of lung Reduced vocal resonance Examination should also focus on features of possible cause – e.g. signs of liver/kidney disease, malignancy. Cardiac failure, RA/SLE, etc.

Answer 132

caused by bacterial invasion of the pleural space either from an adjacent pneumonia or from direct inoculation (e.g. poor aseptic technique in a chest drain).

Answer 133

Clinically presents as fever plus signs of pleural effusion Aspirated fluid is yellow and turbid, with pH <7.2, low glucose, high LDH Require IV ABX and chest drain

Answer 134

CXR => On Erect PA/AP, >300mL fluid is typically needed before effusion becomes evident. USS => Can detect smaller amounts of fluid than CXR => Recommended to guide aspiration Aspiration: => Fluid sent for MC&S, clinical chemistry (protein, LDH, glucose) and cytology => Also run through blood gas machine to determine pH.

Answer 135

Transudate vs Exudate is determined by protein level, but if protein level is borderline (25-35 g/L), one positive element of LIGHT'S CRITERIA will suggest an exudate: * Pleural fluid protein/serum protein >0.5. * Pleural fluid LDH/serum LDH >0.6. * Pleural fluid LDH more than two-thirds the upper limit of normal serum LDH.

Answer 136

If aspirated fluid is turbid/purulent (or if pH <7.2 this also suggests empyema): => Place chest drain => Consider IV ABX Drainage should also take place if symptomatic Manage the underlying cause of effusion

Answer 137

1. Intra- and extracellular buffers (rapid) 2. Ventilation (rapid) 3. Renal regulation of H+ and HCO3 (slower)

Answer 138

1. How is the patient? 2. Assess oxygenation - On air – PaO2 should be >10kPa = On Oxygen – PaO2 should be ~10kPa less than the % inspired concentration. 3. Determine the pH - <7.35 is acidaemic - >7.45 is alkalaemic 4. Determine the respiratory component - If acidaemic, is the PaCO2 >6? Respiratory acidosis - If alkalaemic, is the PaCO2 <4.7? Respiratory alkalosis 5. Determine the metabolic component - If acidaemic, is the HCO3- <22? Metabolic acidosis - If alkalaemic, is the HCO3- >26? Metabolic alkalosis 6. Is there any evidence of compensation? 7. Base excess - Negative in metabolic acidosis - Positive in metabolic alkalosis

Answer 139

* Central – e.g. drugs, stroke, infection * Airway obstruction * Parenchymal emphysema * Neuromuscular * Obesity

Answer 140

= Decrease in gaseous exchange leading to retention of CO₂ COMPENSATION: High pCO₂ leads to renal retention of bicarbonate to buffer excess H⁺ Compensation by the kidneys results in an increase in secretion of H⁺ over 3-5 days leading to increase in plasma bicarbonate level

Answer 141

Hyperventilation => excess exhalation of CO₂, resulting in low pCO₂ and thereby increased pH

Answer 142

* Anxiety, Pain * Hypoxia => Altitude, pneumonia, aspiration, severe anaemia * Drugs – progesterone, salicylates * Sepsis

Answer 143

Results from the body producing too much acid or the kidneys failing to excrete enough H⁺. COMPENSATION: Initially this creates a decrease in bicarbonate as carbonic acid is produced to buffer the H⁺ The lungs compensate by hyperventilation and blowing of the CO₂

Answer 144

The anion gap can be used to differentiate causes: Normal Gap = bicarbonate is being lost: - GI loss (e.g. diarrhoea) - Renal disease allowing loss. High anion gap = increased production of acids - Lactic acidocis - DKA - Drugs (e.g. NSAIDs)

Answer 145

Results from increased bicarbonate due to either decreased H⁺ concentration or a direct increase in bicarbonate. Bicarbonate shift can occur from retention, an intracellular shift in H⁺ or by ingestion of large amounts of alkali (e.g. antacids). COMPENSATION: The lungs compensate by slower breathing to retain more CO₂

Answer 146

Excess base – e.g. Ingestion Loss of acid (Vomiting, NG suction) Burns Hyperaldosteronism Hypokalaemia

Answer 147

PaO2 low (<8 kPa) PaCO2 normal or low T1RF occurs with diseases of the lung parenchyma => e.g. Pulmonary oedema, pneumonia, PE, COPD, ARDS => An asthma attack is initially type 1, with type 2 indicating a peri-arrest state

Answer 148

PaO2 low (<8 kPa) PaCO2 high (>6 kPa) INSUFFICIENT VENTILATION to excrete the volume of CO2 being produced by tissues => Severe pulmonary disease – asthma, COPD, pulmonary fibrosis, OSA => Reduced respiratory drive – CNS pathology, sedation => Thoracic wall disease – rib fractures (pain), kyphoscoliosis, flail chest => Neuromuscular disease – diaphragm paralysis, MG, Guillain-Barre, poliomyelitis

Answer 149

- Headache - Tachycardia - Bounding pulse - CO2 retention flap - Papilloedema Features of acidosis: - Kussmaul respiration – “air hunger”, giving deep and laboured breathing. - CV dysfunction – acidosis is negatively ionotropic - K+ abnormalities - Cerebral dysfunction – confusion or coma.

Answer 150

- Treat the underlying cause - Give high-flow oxygen via a face mask. - Consider assisted ventilation if PaO2 remains <8kPa (e.g. CPAP)

Answer 151

Respiratory centre may be reliant on hypoxic drive – oxygen therapy should be given with care (starting at 24% O2) and rechecking ABG after 20 mins.

Answer 152

= generic term used to describe a number of conditions that affect the lung parenchyma.

Answer 153

EXOGENOUS STIMULI - Occupational / environmental – asbestosis, silicosis, coal dust inhalation - Drugs - Hypersensitivity reactions – e.g. EAA, Bird Fancier’s Lung - Infections – TB/fungal/viral infections ENDOGENOUS STIMULI: - Sarcoidosis - RA - CTDs – SLE, systemic sclerosis, Sjogren’s IDIOPATHIC - Idiopathic Pulmonary Fibrosis = most common cause of interstitial lung disease

Answer 154

nitrofurantoin, amiodarone, sulfasalazine, methotrexate, some anti-cancer chemotherapy drugs

Answer 155

SYMPTOMS: - dyspnoea on exertion - non-productive cough. O/E: - Inspection – may be signs of respiratory distress - Palpation – reduced expansion - Percussion – normal (unless secondary pathology). - Auscultation – bilateral, fine end-inspiratory crackles; sometimes expiratory wheeze. May also be signs of decompensation – i.e. signs of pulmonary HTN and right heart failure.

Answer 156

= most common cause of ILD Aetiology unknown Along with the dry cough and dyspnoea, patients will report malaise and weight loss, with arthralgia. Hx should attempt to exclude occupational exposures and connective tissue diseases. O/E – fine end-inspiratory crackles and also can be cyanosis and clubbing. Complications: - T2RF - Pulmonary HTN - Increased risk of lung cancer

Answer 157

BLOODS – FBC, ANA/RF if suspecting CTDs CXR => reduced lung volume, bilateral reticulo-nodular shadowing. HIGH-RESOLUTION CT – more sensitive, essential for diagnosis => “honeycombing” seen on CT SPIROMETRY – restrictive deficit, reduced gas exchange (DLCO)

Answer 158

Bronchoalveolar lavage – may indicate disease activity in IFF/EAA Lung biopsy (via bronchoscopy or surgical) – only if diagnosis is uncertain.

Answer 159

typically poor prognosis and limited Tx options

Answer 160

Lifestyle: - Smoking cessation - Healthy diet and regular exercise Pneumococcal and Flu vaccines Many cases will be unresponsive to Tx There are some monoclonal antibodies used in IPF if the patient meets the criteria: => Pirfenidone, Nintedanib 20% respond to long courses of prednisolone, tapered down. Some patients will be suitable for lung transplantation

Answer 161

1. Oxygen: High flow nasal oxygen, NIV rarely indicated as usually T1RF 2. Exclude treatable pathology 3. Empirical antibiotics 4. Enoxaparin if suspect PE 5. High dose steroids 6. Careful consideration of ICU vs palliation

Answer 162

Epigastric/upper abdo pain Occurs following a meal Central, no radiation Worse with bending/lying down and when drinking hot liquids/alcohol Improves with sitting upright and antacids.

Answer 163

- Dyspepsia - Acid reflux - Waterbrash - Bad breath - Bloating and belching - Nausea and/or vomiting - Odynophagia and/or dysphagia There may be atypical chest pain due to distal oesophageal muscle spasm and a nocturnal cough/wheeze (giving asthma type symptoms).

Answer 164

- Hiatus Hernia - Raised IAP (pregnancy / obesity) - Large meals, eaten late at night - Smoking - High caffeine intake - (High fatty food intake) - Drugs => Anticholinergics, nitrates, TCAs, CCBs

Answer 165

- Oesophageal ulcers – bleeding, pain, odynophagia. - Oesophageal strictures – dysphagia, odynophagia. => Caused by repeated ulcers/inflammation - Barrett’s Oesophagus - Oesophageal Cancer

Answer 166

Diagnosis is usually based on symptoms and treated empirically If there are any RED FLAG SYMPTOMS (ALARM55) – patient should be referred for endoscopy Also refer if: - Unsure of GORD diagnosis - Symptoms are persistent, severe or unusual - Not controlled by medication - May benefit from surgery

Answer 167

1. Lifestyle changes 2. Medical Management - 1st line = Antacids (e.g. magnesiums or aluminium hydroxide) +/- alginates (e.g. Gaviscon) - 2nd line = H2RAs (e.g. Ranitidine) / PPIs for 4-8 weeks. - If symptoms return after the initial course, then test for H. Pylori in primary care. => Need 2 weeks PPI-free before testing.

Answer 168

- Weight loss and smoking cessation - Eat small and regular meals; >3h before bed. - Avoid hot drinks/alcohol. - Avoid drugs that exacerbate the condition/damage the mucosa (e.g. NSAIDs)

Answer 169

In patients with long-standing reflux, the normal stratified squamous epithelium of the oesophagus undergoes metaplasia to glandular columnar epithelium. Continued inflammation can lead to dysplasia and malignant changes (risk approx. 0.5% per patient per year). The process of metaplasia is asymptomatic, but the patient will have Sx of GORD

Answer 170

OGD – if present, it will be visible and biopsies can be taken Normal oesophageal squamous mucosa => metaplastic columnar mucosa

Answer 171

Regular endoscopic surveillance with biopsies to look for dysplasia/carcinoma in situ (which can be treated with endoscopic resection. The risk of malignant change is ~0.5% per year.

Answer 172

Occur in older patients (>55) Mainly on the lesser curve of the stomach Pain is worse on eating Pain relieved by antacids May present with small bleed (iron deficiency anaemia) or major haemorrhage (haematemesis)

Answer 173

4x more common than gastric ulcers 90% located within 2cm of the pylorus. Pain is at night and before meals. Relieved by eating food/drinking milk. May present with bleeding or perforation

Answer 174

H. pylori infection Zollinger-Ellison Syndrome => Excessive acid secretion due to non-insulin secreting islet cell tumour of the pancreas, secreting gastrin-like hormone. => Often leads to extensive ulceration. Drugs: - Long-term NSAIDs - Long-term / high-dose Corticosteroids Increased ICP (Cushing ulcers) Post severe burns (Curling ulcer) Hepatic/renal failure Smoking, alcohol, caffeine

Answer 175

Nearly 75% of patients are asymptomatic. Symptoms can be: - Burning epigastric pain - Pain related to food intake. => Typically relieved by eating in duodenal ulcers, worse on eating in gastric ulcers. - Feeling of fullness, bloating or belching. - Appetite changes - Unexplained weight loss - Haematemesis/melaena - Nausea - Severe abdominal pain (?perforation)

Answer 176

Urgent OGD (2WW) if fit the ALARM-55 criteria. => Multiple biopsies taken from rim/ base for (histology & H/pylori) as well as brushings (cytology). No investigation required if <55 and no ALARM55 criteria: - Lifestyle measures - PPIs/H2RAs If symptoms persist on Tx, investigate for H. pylori If previous peptic ulcer, assume H. pylori and eradicate with “triple therapy”.

Answer 177

Generally now only reserved for disease complications: => Haemorrhage, perforation, strictures, malignant changes Sometimes in patients who cannot tolerate medical therapy

Answer 178

Infection will cause: 1. Gastritis (mainly in the gastric antrum) 2. Increased acid secretion (due to neutralisation of acid) and abnormal mucous production, leading to epithelial damage. H. pylori is also associated with duodenal ulcers.

Answer 179

13C Urea Breath Test Stool antigen test Serum test (if its performance has been locally validated) OGD – biopsies can be added to a urea solution with phenol red dye, and if H. pylori is present there will be a colour change to the urease.

Answer 180

- Patient ingests 13C-labelled Urea. - If H. pylori is present, the urease enzyme will metabolise this to 13CO2 which can be detected on the breath. - This will become negative when H. pylori is eradicated (unlike stool/serum tests) !!! The patient should not take ABX for 4 weeks or PPI for 2 weeks before testing, as these can cause a false negative !!!

Answer 181

H. pylori eradication involves triple therapy: => PPI + 2 antibiotics for 7 days. Omeprazole + clarithromycin + amoxicillin (metronidazole in penicillin allergy)

Answer 182

= a relapsing functional bowel disorder, with no discernible structural or biochemical cause. It is shown to have a negative impact on quality of life, but it is not associated with the development of serious pathology. The mechanisms may be differences in the “brain-gut axis”, leading to increased visceral perception and decreased visceral pain threshold.

Answer 183

Stress and other psychological factors Dietary triggers (alcohol, caffeine, spicy foods) Enteric infection

Answer 184

Diagnosis of IBS is made POSITIVELY on symptom-based diagnostic criteria Consider the diagnosis if any of the following symptoms for AT LEAST 6 months: - Abdominal pain, or - Bloating, or - Change in bowel habit. Make a diagnosis of IBS if a person has abdominal pain which is either: - Related to defecation, and/or - Associated with altered stool frequency (increased or decreased), and/or - Associated with altered stool form or appearance (hard, lumpy, loose, or watery) AND at least 2 from the following: - Altered passage of stool (straining, urgency, tenesmus) - Abdominal bloating/ distension/ hardness - Symptoms aggravated by eating - Passage of rectal mucus - Associated gynaecological, urinary symptoms, or back pain.

Answer 185

History to ensure there are no Red Flag symptoms. => E.g. unintentional weight loss, PR bleeding, FHx bowel/ovarian cancer, change in bowel habit >60, incontinence, having to frequently open bowels at night. Examination: - For signs of anaemia / masses Bloods: - CRP/ESR + faecal calprotectin to exclude IBD - TTG/ anti-endomysial antibodies to exlcude coeliac disease - FBC – any anaemia ? In cases that meet the criteria for IBS, no further investigations are required.

Answer 186

Form a therapeutic alliance and self-help materials Lifestyle: - Regular exercise - Regular mealtimes, lots of water, limit tea/coffee, limit high insoluble fibre intake. - Relaxation techniques. Further dietary advice may be given by a dietician if initial measures are unsuccessful (i.e. low FODMAP diet). Peppermint oil

Answer 187

1st Line Medical Mx: => Antispasmodics (e.g. mebeverine) as 1st line medical Mx => Laxatives can be given for constipation - But AVOID lactulose (bloating) => Loperamide is 1st choice anti-motolity agent for diarrhoea. Further Medical Mx: => 2nd Line = Low dose TCAs once nightly. => 3rd Line = SSRIs, if TCAs are unsuccessful

Answer 188

defined as symptoms persisting after 12 months of antidepressant medications. At this stage, referral for CBT may be made

Answer 189

1. Destruction of Liver Cells 2. Associated chronic inflammation, stimulating fibrosis 3. Regeneration of hepatocytes to form nodules. => nodules lack normal vascular and bile drainage connections

Answer 190

Nodules <3mm occurs as a result of alcoholic liver disease or biliary tract disease.

Answer 191

Nodules >3mm occurs due to previous hepatitis

Answer 192

COMMON * Alcoholic Liver Disease * Cryptogenic Liver Disease (no cause found on investigation) * Non-alcoholic Fatty Liver Disease (NAFLD) * Chronic viral hepatitis LESS COMMON * Autoimmune hepatitis * Primary biliary cirrhosis * Primary sclerosing cholangitis * Budd-Chiari Syndrome * Cystic fibrosis RARER * Haemochromatosis * Wilson’s disease * Alpha-1 antitrypsin deficiency

Answer 193

= Autoimmune destruction of the intra-hepatic bile canaliculi Occurs mainly in 40-60 year old females (90%) Related to IBD Often presents with jaundice, pruritis, skin xanthomas It is a slowly progressive condition Replacement of fat-soluble vitamins is important in Mx.

Answer 194

Raised anti-mitochondrial antibodies (AMA) is considered diagnostic.

Answer 195

= Autoimmune inflammation and fibrosis around the bile ducts in the liver. This leads to secondary cirrhosis, due to chronic biliary obstruction. 70% associated with IBD Cholangiocarcinoma can develop No effective Tx other than transplantation

Answer 196

= Rare inborn error of copper metabolism, leading to deposition of copper in many organs. Classically the liver, basal ganglia and cornea (Kayser-Fleischer rings) It is treatable, so any person with hepatic/neurological problems should be screened.

Answer 197

Ix: - Serum caeruloplasmin (reduced), urinary copper (increased) - Liver biopsy shows increased copper Tx = chelating agents (e.g. D-penicillamine or trientene).

Answer 198

= Inherited condition characterised by excess iron deposition in various organs, leading to fibrosis and organ failure. Classic triad (only present in gross overload): - Bronze skin discoloration - Hepatomegaly - DM Hypogonadism is a common presenting feature (impotence, testicular atrophy) due to pituitary iron deposition).

Answer 199

Ix: - Serum iron/ferritin (both raised) - Total iron binding capacity decreased - Genetic testing - Liver biopsy Tx: => Venesection (1 unit per week initially until iron levels are normal, then 2-4 times per year; usually lifelong).

Answer 200

Fatigue Weight loss/anorexia - Early satiety with hepatomegaly - BUT Patient may often note “central weight gain” of ascites. Jaundice Leg swelling => Due to decreased oncotic pressure and increased intra-abdominal pressure) Bleeding/bruising => Due to decreased synthetic function) Itching => Due to bile salt accumulation in peripheral nerves => Tx = cholestyramine

Answer 201

Nails => Leukonychia due to low albumin => Clubbing Hands: => Palmar erythema => Dupytren’s Contracture => Liver flap Skin: => Pigmentation / jaundice => Spider naevi => Striae Feminisation: => Gynaecomastia, testicular atrophy and loss of body hair Signs of portal HTN: => Caput medusae => Hepatosplenomegaly => Ascites Signs of hepatocellular failure: => Bruising => Prolonged clotting

Answer 202

Secondary hyperaldosteronism (due to activation of RAAS because hypoalbuminaemia leads to a lower circulating volume)

Answer 203

- Alcohol binge - Variceal bleed - Hepatotoxic drugs - Portal/hepatic vein thrombosis

Answer 204

Gives prognosis for patients with chronic liver disease Uses variables: A - albumin B - bilirubin C - clotting (INR / PTT) D - distention (ascites) E - encephalopathy

Answer 205

Liver function – albumin & INR are the best indicators Liver damage – LFTs Complications: => U&Es (hepatorenal syndrome) / ABG (hepatopulmonary syndrome). LIVER SCREEN to find cause: - Viral serology - Serum autoantibodies/Ig - AFP - Iron studies (hereditary haemochromatosis) - Serum copper/caeruloplasmin (Wilson’s disease) - Alpha1-antitrypsin level IMAGING: - USS & duplex of liver and abdomen. - Endoscopy – detection and Tx of any varices; should be undertaken in anyone with suspected cirrhosis. - MRI if indicated Further Ix: - Ascitic Tap - Liver biopsy (gold-standard, but not always required)

Answer 206

should be undertaken in anyone with suspected cirrhosis. for detection and Tx of any varices (as 90% of cirrhosis patients develop these)

Answer 207

Tx depends on the patient, and cause, severity, and complications May include: * Avoidance of alcohol * Laxatives to maintain bowel movements, ideally >2 per day * Good nutrition and advice from a specialist dietician * Avoidance of drugs that cause hepatic impairment The ONLY definitive treatment is liver transplant (if suitable, depending on cause). => However, there is a shortage of donated livers available.

Answer 208

= fluid in the peritoneal cavity, which can accumulate slowly or rapidly. Mild abdo pain is common => If severe pain, consider spontaneous bacterial peritonitis. Mx = - Initially bed rest, fluid restriction, low-salt diet and spironolactone - Ideally the patient should lose 0.5-1kg in 24 hours. - Furosemide can be added if the response is poor - Therapeutic paracenteses and albumin infusion reserved for large volume ascites.

Answer 209

suspected if ascites with fever, pain, deterioration => Ceftriaxone IV until sensitivities are known (diagnostic tap) => Long-term norfloxacin (as recurrence is high).

Answer 210

Caused by nitrogenous waste build-up in the circulation. Leads to cerebral oedema when astrocytes attempt to clear it. Severity: - Grade I – altered mood/behaviour, sleep disturbances - Grade II – increasing drowsiness and confusion - Grade III – stupor, incoherence, restlessness - Grade IV – Coma

Answer 211

ICU admission with 20 degree head tilt Oral lactulose, with regular enemas to clear the bowel of nitrogen-forming organisms If there is evidence of cerebral oedema, IV mannitol and hyperventilation may be used.

Answer 212

Cardia of the stomach => gastric/oesophageal varices Anus => rectal varices Retroperitoneal organs => stromal varices Paraumbilical veins of anterior abdominal wall => caput medusae. When portal blood flow is obstructed, blood from the portal territory is able to use these collateral routes to return to the heart (as the portal system has no valves, so blood can flow in a reverse direction).

Answer 213

= pressure in the portal vein >10mmHg (normal = 5-10 mmHg)

Answer 214

PRE / POST-HEPATIC Portal vein thrombosis (Budd-chiari syndrome) HEPATIC Cirrhosis Hepatitis Idiopathic non-cirrhotic portal HTN Schistosomiasis Congenital hepatic fibrosis

Answer 215

= obstruction of hepatic veins, most commonly due to thrombosis or obstruction due to external mass

Answer 216

Variceal Bleeding Haemorrhoids/caput medusae Ascites Splenomegaly Porto-systemic encephalopathy (toxins bypass liver).

Answer 217

(also “crescendo angina”) = Angina occurring at rest, or sudden increased frequency/severity of existing angina. Pathologically caused by fissuring of atheromatous plaques, this there is a risk of subsequent total vessel occlusion and progression to MI.

Answer 218

Infarct of one segment of the ventricular wall Nearly always due to thrombus formation on an atheromatous plaque, giving prolonged ischaemia. The area of regional infarction depends on the artery occluded.

Answer 219

If there is lysis of the thrombus, or a strong collateral supply, the infarct is limited to the subendocardial zone (the most distal point from the blood supply).

Answer 220

Caused by general hypoperfusion of all coronary arteries, usually due to hypotensive episode in arteries already affected by high-grade atherosclerosis.

Answer 221

The diagnosis of MI requires elevations in serum cardiac troponin levels (i.e. cardiac myocyte death) Additional categorisation based on ECG: => ST elevation / new LBBB = STEMI => No ST elevation/LBBB = NSTEMI

Answer 222

STEMI generally correlates with a full-thickness MI NSTEMI is often a partial-thickness lesion.

Answer 223

Supplies RA, RV, posterior septum Gives posterior/inferior MI => Leads II, III, aVF Also supplies the AVN in 80% and SAN in 60%

Answer 224

Splits into the circumflex and left anterior descending artery. Gives a massive antero-lateral MI. => Leads I, aVL, and V1-V6

Answer 225

Mainly supplies LA and LV Gives lateral MI => Leads I, aVL, V5 & V6

Answer 226

Mainly supplies the LV and anterior septum Gives antero-septal MI => Leads V1-V4

Answer 227

I aVL V5 V6

Answer 228

II III aVF

Answer 229

V1 V2 V3 V4

Answer 230

The end result is replacement of the necrotic area with collagenous scar, which occurs in a predictable time-course - 12-24 hours – infarct pale and blotchy, with intercellular oedema - 24-72 hours – infarcted area excites acute inflammatory response, with dead area soft and yellow with neutrophilic infiltration. - 10 days to several months – collagen deposition, infarct replaced by collagenous scar

Answer 231

Severe crushing, gripping or heavy chest pain lasting longer than 20 minutes. - Not relieved by 3x GTN sprays at 5 minute intervals. Radiates to the left arm, neck or jaw. Associated with dyspnoea, nausea, fatigue, sweatiness and palpitations, with distress and a feeling of “impending doom”.

Answer 232

MI without chest pain More common in the elderly and diabetics

Answer 233

Sympathetic activation – tachycardia, HTN, pallor, sweatiness. Vagal stimulation – bradycardia, vomiting. Myocardial impairment – hypotension, narrow pulse pressure, raised JVP, basal crepitations, 3rd heart sound. Tissue damage – low-grade pyrexia

Answer 234

Pericardial rub = an extra heart sound due to friction => Resembles the sound of squeaky leather and often is described as grating, scratching, or rasping. => Best heard between the apex and sternum but may be widespread Peripheral oedema Pan-systolic murmur due to papillary muscle rupture/ventriculo-septal defect

Answer 235

ECG = essential in all patients presenting with chest pain. => Repeated every 15 minutes whilst in pain, or continuous monitoring in ACS (due to high chance of arrythmias developing). Bloods: - FBC, U&E - Glucose, lipids - Cardiac Enzymes to confirm MI CXR: - Consider for evidence of cardiomegaly/ pulmonary oedema (heart failure), widened mediastinum (aortic dissection) If Dx still in doubt => Transthoracic Echocardiography may confirm, or help detect alternative diagnoses.

Answer 236

Troponins are 1st Line: - Rise 4-8 hours following onset of symptoms - Peak at 24 hours - Detectable for 10 days (Also raised in critically unwell patients with non-cardiac causes)

Answer 237

a. At onset of pain – the ECG shows a normal sinus complex b. Within 1 hour – noticeable ST segment elevation has developed c. Following treatment – subsequently, T-wave inversion may develop d. 24h later – ST segment has returned to baseline, T-wave inversion persists e. Days/Months later – deep Q-wave indicating tissue death => A deep Q wave will remain on the ECG (i.e. if only pathological Q-waves are present, this could be from a previous MI).

Answer 238

can be assumed as a STEMI, as further interpretation of the ECG is not possible.

Answer 239

In unstable angina: There may be ischaemic ST depression in the leads affected, There will be NO troponin rise (i.e. no infarction).

Answer 240

INFORMANT INvestigations => ECG, Troponin, U&Es, glucose, Hb, ?angiography => If there is ST elevation on ECG, immediate referral to cardiology for PCI is required. Fondaparinux => 2.5 mg SC OD for 2-8 days (until no chest pain for >24 hours) Oxygen => Prescribe, but only indicated if SpO2 <94% Reassurance Morphine => 5-10mg by slow IV injection initially => Usually need to co-prescribe metoclopramide 10mg IV (unless contraindicated). Aspirin => 300 mg PO; such or chew for faster absorption Nitrate => Sublingual GTN (e.g. 400 mucrogram spray) => Consider IV infusion if pain continues Ticagrelor => First dose = 180mg PO => Continues for 12 months at 90 mg bd

Answer 241

Percutaneous Coronary Intervention (PCI) is gold-standard, if available in a timely fashion. => Door to balloon within 90 minutes. PCI is contraindicated if there are significant co-morbidities Thrombolysis is indicated in STEMI when PCI is contra-indicated

Answer 242

High risk – if GRACE mortality >3% in 6m, or raised troponins, persistent pain, ST depression, or diabetes. => Organise semi-elective PCI as an inpatient Low Risk – i.e. resolved unstable angina or GRACE <3% => Potentially can be discharged with long-term medication and outpatient follow up.

Answer 243

48 hour bed rest with continuous ECG monitoring Daily U&Es and cardiac enzymes for 2-3 days Thromboprophylaxis => Fondaparinux s.c. 2.5mg o.d. for max 8 days (until chest pain free for 24h) DUAL ANTIPLATELET THERAPY => Aspirin 75mg o.d. continued for life => Ticagrelor OR clopidogrel for ONE YEAR Bisoprolol for life, titrated to maximum tolerated dose. ACEI titrated to maximum tolerated dose Atorvastatin 80mg o.n. GTN Spray for angina Sx Address modifiable risk factors

Answer 244

IMMEDIATE Arrythmias - VT, VF, AF, bradycardia/block (if AVN/SAN affected) SHORT-TERM Pulmonary Oedema Cardiogenic Shock Thromboembolism Ventriculo-septal defect Ruptured chordae tendinae Rupture of ventricular wall LONG-TERM Heart failure Dressler’s Syndrome Ventricular aneurysm formation

Answer 245

= Immune-mediated pericarditis; associated with high ESR and sometimes anti-myocardial antibodies. Develops in a very small number of cases, 2-10 months after an MI. Pericarditis gives sharp chest pain (different to that of MI), exacerbated by movement and lying down, relieved by sitting forwards. O/E – classic pericardial friction rub at lower left sternal edge, with the patient leaning forwards. Tx = high-dose aspirin/NSAIDs It is important to recognise that pericarditis (non-immune mediated) can occur at any time following MI, and this is more common than Dressler’s syndrome. => Tx = opioids for pain.

Answer 246

Gradual Distension of the infarcted part of the ventricular wall, which has been replaced by collagen scar. Aneurysmal rupture will lead to cardiac tamponade and death.

Answer 247

Usually occurs 2-10 days after the infarct, due to re-organisation and softening of the wall. Leads to haemopericardium, cardiac tamponade and rapid death.

Answer 248

Common Causes 1. IHD (most common) 2. Dilated cardiomyopathy 3. HTN Rarer Causes * Other cardiomyopathies * Valvular Disease * Congenital heart disease * Cor pulmonale * Alcohol / drugs * AF / heart block * Anaemia

Answer 249

The left side of the heart must work harder to pump the same amount of blood. Poor output of the impaired left ventricle leads to an increase in left atrial and pulmonary venous pressure. => causes pulmonary oedema, as the increased pulmonary venous pressure prevents the reuptake of fluid at the level of the capillaries.

Answer 250

RV output fails. Predominantly due to lung disease (cor pulmonale) and pulmonary valvular stenosis. This typically leads to peripheral oedema.

Answer 251

LVF and RVF may be present at the same time, due to either: i. Disease (e.g. IHD) affecting both sides of the heart ii. LVF leading to pulmonary congestion which can then lead to RVF = “congestive heart failure”

Answer 252

Symptoms: - Fatigue - Exertional dyspnoea, Paroxysmal nocturnal dyspnoea, Orthopnoea Signs are often very few until late stages (unless failure is acute): - Pulmonary oedema/congestion - 3rd heart sound, plus “Gallop rhythm” if tachycardic. - Cardiomegaly, laterally displaced apex beat.

Answer 253

Symptoms: - Fatigue - Breathlessness - Anorexia/nausea (due to hepatomegaly) - Swollen Ankles Signs tend to be more prominent than symptoms: - Jugular venous distension - Hepatomegaly - Cardiomegaly - Peripheral oedema - Pleural effusions - Ascites

Answer 254

A syndrome of life-threatening weight loss due to a combination of: 1. Hepatomegaly (nausea and anorexia) 2. Increased metabolic demands

Answer 255

- Reduced CO leads to activation of the SNS and RAAS. - RAAS activation leads to vasoconstriction (increasing afterload) and sodium/water retention (increasing preload) thus further increasing BP and cardiac work. - SNS activation initially maintains cardiac output by increasing contractility, yet prolonged stimulation leads to myocyte apoptosis and necrosis.

Answer 256

Atrial Natriuretic Peptide (ANP) is released in response to atrial stretch, and acts to antagonise the fluid-conserving effects of aldosterone.

Answer 257

Class I Disease present, but no limitation of physical activity. Class II Dyspnoea present on ordinary activities Class III Marked limitation of activity (breathlessness with minimal exercise) Class IV Dyspnoea present at rest, any activity causes discomfort.

Answer 258

Bloods: - FBC, LFT, U&Es, TFTs - Cardiac enzymes in acute failure B-type natriuretic peptide (BNP) => Normal level will exclude heart failure, so a good screen for breathlessness in GP CXR: => Cardiomegaly and pulmonary oedema. ECG: => For signs of ischaemia, hypertension or arrythmias. Echo = gold standard for diagnosis. => EF <45% is diagnostic

Answer 259

Upon confirmed diagnosis of LV dysfunction: 1. Lifestyle advice 2. ACEi and beta-blocker are 1st line => Proven mortality benefit in heart failure! 3. Add diuretic if symptomatic oedema 4. Aldosterone antagonists (e.g. spironolactone) / ARB / hydrasalazine plus nitrate = 2nd line. 5. Cardiac resynchronisation therapy / digoxin / ivabradine = 3rd line

Answer 260

Patient education Weight control Dietary modification (fluid and salt restriction in severe heart failure) Smoking cessation Physical Activity: => Bedrest is important following an exacerbation => Low level endurance exercise is recommended in all patients with compensated heart-failure. Vaccination – against pneumococcal disease and flu. Sex – patients should not take Viagra.

Answer 261

Work to reverse the neurohormonal adaptation in CHF. Low dose used and titrated upwards.

Answer 262

Used to block the SNS activity causing maladaptation. Also anti-arrhythmic effects. By reducing sympathetic drive, the symptoms initially become worse! => WARN THE PATIENT!!! => Low dose and then titrate up.

Answer 263

Mainly used for symptomatic relief of oedema, but also venodilate. Thiazides (Bendroflumethiazide) are used in mild failure or in elderly patients, where massive diuresis may be intolerable. Loop diuretics (furosemide) are used especially in pulmonary oedema. Both types can cause hypokalaemia (thus can be useful to counteract the hyperkalaemia from ACEi) Spironolactone = potassium-sparing diuretic => Used at low (non-diuretic) dose of 25mg to reverse the neurohormonal adaptation

Answer 264

Used in refractory heart failure. Positive ionotrope and negative chronotrope => increases force of contraction but decreased heart rate. Impairs AVN conduction and also increases vagal activity. Contra-indicated in heart block and bradycardia. DOSING: - Dosage is according to eGFR (drug is 2/3rds renally cleared). - Dosage titrated to make sure HR does not fall below 60 bpm. NARROW THERAPEUTIC WINDOW => toxicity suggested by anorexia, nausea, visual disturbances, diarrhoea.

Answer 265

Always monitor renal function in patients being treated for heart failure: - Digoxin is renally cleared - Thiazides are ineffective in renal failure - ACEis are used with caution in renal failure - Diuretics and ACEis can lead to hyperkalaemia.

Answer 266

Sit the patient up and give high flow oxygen IV Furosemide 40-80mg GTN spray 2 puffs SL (unless SBP <90) Continue with necessary history and investigations If SBP >100 – start IV infusion of nitrate => Consider NIV (e.g. CPAP) if not improving If SBP <100 – treat as cardiogenic shock, alert ICU => May require invasive ventilation

Answer 267

episodic pain that takes place when there is increased myocardial demand (usually upon exercise), in the presence of impaired perfusion by blood.

Answer 268

REDUCED PERFUSION – atheroma, embolus, thrombosis, spasm or inflammation of coronary arteries, generalised hypotension. REDUCED BLOOD OXYGENATION – anaemia, carboxyhaemoglobinaemia INCREASED TISSUE DEMANDS – increased CO2, cardiac hypertrophy.

Answer 269

Non-specific thickening and hardening of the walls of arteries, causing a loss of contractility and elasticity and decreased blood flow. Often due to prolonged HTN in smaller arteries

Answer 270

Damage to the endothelium due to a variety of RFs => allows entry of LDLs into the intima. The lipid is taken up by macrophages in the intima, and accumulates excessively as it is able to bypass normal receptor mediated uptake, forming a “fatty streak” As the macrophages take up more and more lipid, they release free lipid into the intima. The macrophages also stimulate cytokines, which lead to collagen deposition by inflammatory cells and the intimal lipid plaque becomes fibrotic. At this stage it appears raised and yellow, and leads to pressure atrophy of the media an disruption of the elastic lamina. Increased secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white. Advanced plaques also show free lipid as well as lipid in macrophages The endothelium is fragile and often ulcerates, allowing platelet aggregation.

Answer 271

Ischaemic pain of the myocardium => Varying from a mild ache to a severe pain that provokes sweating and fear Pain provoked by exercise => Especially after meals, in the cold, and if the patient is angry/excited. Pain fades quickly with rest / GTN In some, the pain occurs predictably at certain levels of exertion. May be some associated SoB

Answer 272

Usually no abnormal findings O/E Occasionally a 4th heart sound BP should always be taken

Answer 273

1. Decubitus angina 2. Variant / Prinzmetal’s Angina

Answer 274

angina precipitated by lying down (as there is increased venous return to the heart) => Associated with LVF

Answer 275

occurs without provocation at rest, as a result of coronary artery spasm => There is ST elevation during the episode, so consider if ST elevation but no troponin rise.

Answer 276

Clinical assessment alone can be sufficient to confirm stable angina. Exclude other causes => FBC, glucose, lipids, TFTs Resting 12-lead ECG – usually normal, may be signs of previous infarction => Consider aortic stenosis if LVH / LBBB Consider stress 12-lead ECG Then use clinical assessment and ECG findings to estimate the likelihood of coronary artery disease using the NICE tool.

Answer 277

if resting ECG is normal, use Bruce protocol on treadmill, with ST depression >1mm indicating ischaemia. => If positive within 6 minutes then angiography indicated (only 70% sensitive).

Answer 278

Education & lifestyle advice: - Explain diagnosis - Inform that the disease has a good prognosis - Healthy balanced diet, weight loss if necessary - Reduce alcohol, smoking cessation Treat underlying problems and co-morbidities Symptomatic Tx: - SL GTN Spray = 1st line for relief - Add beta-blocker OR RL CCB to reduce symptoms - 2nd line = combination therapy (beta-blocker and NON-RATE LIMITING CCB) or Nicorandil Secondary Prevention: - Consider Statin (if QRISK high) - Consider low-dose aspirin (75mg o.d.) Refer to cardiology if any doubt over the diagnosis, atypical features or refractory symptoms.

Answer 279

Patients should be advised to: 1. Sit down, rest and spray once beneath the tongue 2. Wait for 5 mins 3. Spray again if there is still pain 4. If there is still pain at 10 minutes, call 999 and unlock the door They can also be used prior to performing activities that will provoke angina.

Answer 280

Nitrates cause marked venorelaxation, thus REDUCES pre-load and afterload, and INCREASES coronary artery dilation. => decreases the oxygen requirement of the myocardium, and coronary vasodilation leads to increased oxygen delivery. (Nitrates also relieve the coronary artery spasm of Prinzmetal angina. )

Answer 281

beta1 selective blockers are used to reduce cardiac rate and force (this reduces myocardial oxygen consumption), with as little broncho-constrictive effect as possible. They also have anti-arrhythmic effects (class II)

Answer 282

Both types work to prevent smooth muscle contraction, reducing afterload and causing coronary vasodilatation. The rate-limiting agents also act on cardiac calcium channels in the AVN to control the heart rate, exhibiting class IV anti-arrhythmic effects CCBs are 1st line in Prinzmetal angina

Answer 283

Flushing and headache (as with all vasodilators) Ankle swelling Constipation

Answer 284

Mitral = Patient on their left hand side Aortic = Patient leaning forward, breath held in expiration Pulmonary = Breath held in inspiration Tricuspid = Breath held in inspiration

Answer 285

Post-inflammatory scarring (history of rheumatic fever in >50%)

Answer 286

- The LA is unable to empty, leading to pulmonary HTN. - The LA becomes dilated and hypertrophied - Pulmonary HTN leads to RHF - AF commonly develops due to muscular hypertrophy.

Answer 287

Dyspnoea & haemoptysis – pulmonary HTN Fatigue, weakness, abdominal / LL oedema – RHF Palpitations – secondary AF

Answer 288

Inspection: * Malar flush – due to vascular stasis * Small volume regular pulse (or irregularly irregular in AF) * Raised JVP Palpation: * Left parasternal heave, due to RV hypertrophy (aka right ventricular heave). Auscultation: * “Rumbling” mid-diastolic murmur, loudest at the apex, just prior to systole. * Also a loud S1, and “opening snap”

Answer 289

Treat AF appropriately Diuretics – reduces pre-load & pulmonary venous congestion Surgical Mx => If medical measures fail (symptoms still limiting activity) - Balloon valvuloplasty if valve pliable / non-calcified - Open valvotomy.

Answer 290

Post-inflammatory scarring – commonly rheumatic Post-infarction papillary muscle dysfunction LV dilation – i.e. in LVF, hypertrophic cardiomyopathy Mitral prolapse

Answer 291

Inspection: * Signs of LHF/RHF develop in later disease * AF can also develop (but less common than in mitral stenosis) Palpation: * Laterally displaced apex beat * Systolic thrill Auscultation: * Pansystolic murmur at the apex, radiating to the axilla. * Soft S1 * Prominent third heart sound (due to sudden rush of blood into dilated LV in diastole if decompensated).

Answer 292

Treat AF Treat Heart failure Surgery if Sx are deteriorating to prevent irreversible LV impairment => Generally considered at NYHA grade 2

Answer 293

Calcification of congenital bicuspid valve Post-inflammatory scarring – rheumatic fever Senile calcific degeneration – no known cause

Answer 294

Progressive outflow obstruction leads to LV hypertrophy, which may lead to angina. There is a risk of sudden cardiac death due to arrythmias Without surgical intervention prognosis is poor with death in 2-3 years.

Answer 295

Exercise induced syncope Angina Dyspnoea

Answer 296

Inspection: * Small pulse volume, slow rising carotid pulse * Narrow pulse pressure (e.g. 110/95) as stroke volume small * Signs of LVF then CCF Palpation: * Normal apex beat * May be systolic thrill in aortic area Auscultation: * Ejection systolic murmur with a crescendo-decrescendo characteristic. * Best heard in the aortic valve area * Can radiate to carotids * S2 is soft

Answer 297

Prompt valve replacement if symptomatic Percutaneous valvuloplasty if unfit for surgery.

Answer 298

- Post-inflammatory scarring - Infective endocarditis - Age-related calcification - Dilation of the aortic root

Answer 299

Usually asymptomatic until acute left ventricular failure. Symptoms may include angina (due to low diastolic BP) and dyspnoea.

Answer 300

Inspection: * Bounding/collapsing pulse * Wide pulse pressure (e.g. 140/40) * Signs of LVF Auscultation: * Early diastolic murmur with a “decrescendo” quality. Specific Signs in severe disease: * Quinke’s sign – capillary pulsation in nail beds * De Musset’s sign – head nodding with each heartbeat * Duroziez’s sign – murmur on the femoral arteries if pressure applied distally. * Pistol shot femorals – sharp bang in time with the heartbeat if femorals auscultated.

Answer 301

Aim to replace valve before there is significant LV dysfunction (indicated if there are increasing Sx, cardiomegaly, ECG deterioration).

Answer 302

STENOSIS - Symptoms of RHF - Signs of pre-systolic liver thrill and mid-diastolic murmur. REGURGITATION - Symptoms of RHF - Signs of systolic liver thrill and pan-systolic murmur. - Classic in cor pulmonale.

Answer 303

STENOSIS - Symptoms of RHF - Signs of RV heave and ejection systolic murmur REGURGITATION: - Usually asymptomatic, with a diastolic murmur. - Can occur secondary to pulmonary HTN

Answer 304

Aortic Stenosis Mitral Regurgitation Pulmonary Stenosis Tricuspid Regurgitation VSD/ASD

Answer 305

Aortic Regurgitation Mitral Stenosis Pulmonary regurgitation

Answer 306

= continuous throughout systole and diastole Patent Ductus Arteriosus

Answer 307

occurs when there is a right to left shunt across a structural heart lesion, bypassing the lungs. Occurs due to VSD, ASD or PDA => Can develop after 1-2 years with large defects or in adulthood with small defects.

Answer 308

Initially left-to-right shunt as pressure is higher in LV => blood still travels to the lungs Over time the extra blood flowing into the right side of the heart and the lungs increases the pressure in the pulmonary vessels. => PULMONARY HTN. When the pulmonary pressure exceeds the systemic pressure, the shunt switches to right-to-left. This causes deoxygenated blood to bypass the lungs and enter the body => CYANOSIS

Answer 309

RV heave Clubbing Cyanosis Loud S2 (due to forceful shutting of the pulmonary valve) A murmur depending on where the shunt is: - Atrial septal defect: mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border - Ventricular septal defect: pan-systolic murmur loudest at the left lower sternal border - Patent ductus arteriosus: continuous crescendo-decrescendo "machinery" murmur

Answer 310

Ideally the underlying defect should be managed optimally or corrected surgically Once significant pulmonary HTN has developed, the structural defects are considered irreversible and the only Tx is heart and lung transplant.

Answer 311

INFECTIVE ENDOCARDITIS until proved otherwise

Answer 312

= an infection of the endocardial surface of the heart. Patients with a structural abnormality of the heart (e.g. valve disease, valve replacements, congenital cardiac defects) => insidious onset, caused by normal GI/skin commensals Patients with structurally normal heart valves (often IVDU) => Acute, fulminating presentation; Pathogenic organisms that directly invade the valve

Answer 313

Staphylococcus viridans = most common Staph aureus / Strep epidermis both also seen

Answer 314

- Previous IE - Acquired valvular heart disease - Valve replacement - Structural congenital heart disease (excl. ASD or fully-repaired VSD/PDA)

Answer 315

Classical presentation = acute febrile illness plus a new murmur. However, may present as insidious illness (malaise, lethargy, anorexia, arthralgia) and thus high index of suspicion is required. Other Presentations may be distal infarctions or AKI due to immune complex deposition.

Answer 316

Fever + changing / new heart murmur Microscopic haematuria Splenomegaly Osler’s Nodes Roth's Spots Janeway Lesions Clubbing Splinter haemorrhages Petechial rash Digital infarcts

Answer 317

Bloods: => FBC, CRP/ESR, U&E => Cultures – 3 sets at different sites Urinalysis: => Look for proteinuria and microscopic haematuria ECG: => At regular intervals – can get MI due to emboli or conduction defects. CXR: => To look for evidence of heart failure or abscess / emboli Transthoracic Echocardiography: => Should be done in all patients with ?IE => Negative echo does not rule out endocarditis.

Answer 318

MAJOR Positive culture (typical organism in 2 cultures) Endocardial involvement on echo (vegetations, abscess, new regurgitation) MINOR Predisposition Fever >38o Vascular / immunological signs Culture / echo positivity not sufficient for “major” criteria -- Diagnosis can be made if there are 2 major or 1 major and 3 minor criteria.

Answer 319

Bacterial proliferation in the valve leads to necrosis of the valve tissue, with rapid perforation of the valves. Leads to acute cardiac failure.

Answer 320

As the infective organisms are poorly virulent, there is very gradual onset and destruction of the valves Stimulation of thrombus formation leads to systemic embolization, and the persistent low grade inflammation leads to immunological phenomena

Answer 321

Systemic Emboli (or pulmonary abscess in right-sided disease) Valvular incompetence and CCF Glomerulonephritis

Answer 322

If suspected, consult a microbiologist early. EMPIRICAL Tx: - Amoxicillin and gentamicin IV for 4 weeks - Different regimen if prosthetic valve endocarditis or penicillin allergic. Subsequent therapy is dependent on the organisms and sensitivities

Answer 323

ABX prophylaxis is no longer recommended for people undergoing dental procedures (no evidence of any benefit) Patients at risk of infective endocarditis should be: => Advised to maintain good oral hygiene; => Told how to recognise signs of infective endocarditis, and advised when to seek expert advice.

Answer 324

=> cardiac contusion can give ECG changes similar to MI Management is conservative.

Answer 325

Cardiac Tamponade is suggested by Beck’s triad: 1. Hypotension 2. Raised JVP 3. Muffled heart sounds

Answer 326

Complex investigation and management (often surgical) will be required. CXR is vital due to risk of damage within the thoracic cavity, and should be upright if possible Can cause cardiac tamponade

Answer 327

Ix: - CXR may show cardiomegaly with or without an epicardial fat pad sign suggesting a pericardial effusion. - Echo = 1st line for diagnosis (diagnosis and approach planning for pericardiocentesis) - CT provides valuable information about the possible nature of pericardial effusions based on the attenuation measurements Tx: - Time is bought with pericardiocentesis, prior to sternotomy and repair.

Answer 328

= Most common myocardial tumour Benign, usually sporadic Signs: - Mimic either IE or mitral stenosis Ix: - Confirmed on echocardiogram Tx: - Excision

Answer 329

Pericardial Inflammation can result in constriction of the whole pericardium. Causes - TB, RA, Pericardial trauma / radiotherapy Clinical signs: - Pulmonary and systemic congestion (as it affects all 4 heart chambers) Tx: - Excision of whole pericardium

Answer 330

Work: - May return to office work after two months - Certain occupations (e.g. pilots, divers) should not return to work - Heavy manual labourers should seek lighter work Travel: - Avoid air travel for 2 months Sex: - Avoid intercourse for 1 month Driving: - The DVLA do not need to be notified - If successfully treated with PCI, driving can continue after 1 week - Otherwise driving may recommence after 4 weeks

Answer 331

The DVLA do not need to be notified. Driving can continue unless angina occurs at rest / whilst driving / with emotion. Recommence when adequate symptom control gained.

Answer 332

Notify the DVLA if >6cm Annual review to permit licensing, will be disqualified if >6.5cm

Answer 333

In general, all CV diagnoses lead to revocation of licenses for 6 weeks => 3 months post-CABG Re-licensing can then be permitted if exercise / other functional requirements are met

Answer 334

Occurs due to an increase in fluid in the alveolar wall (pulmonary interstitium), which then affects the interstitial spaces.

Answer 335

Dyspnoea Paroxysmal nocturnal dyspnoea Orthopnoea: - Due to increased venous return on lying down - Can be measured objectively by number of pillows required to sleep Cough: => Producing frothy, blood-stained sputum

Answer 336

Severe dyspnoea Productive cough Anxiety and sweating Cheyne-stokes respiration in LVF: => Cycling apnoea / hyperventilation due to impaired response of respiratory centre to CO2

Answer 337

Tachypnoea Tachycardia, with gallop rhythm Raised JVP Peripheral shutdown Auscultation: - Widespread course crackles / reduced breath sounds - Wheeze can also be associated with pulmonary oedema and is referred to as 'cardiac asthma'.

Answer 338

ABG: - Initially T1RF due to hyperventilation - Later T2RF due to impaired gas exchange. Bloods: - FBC, U&E, glucose, D-dimer, CRP CXR: - Diffuse haziness (“bat wings”) - Kerley B lines - Upper zone vessel enlargement - Cardiomegaly (HF) - Pleural effusions ECG: - Tachycardia - Arrythmia - Signs of cardiac cause Echo: - To demonstrate a cardiac cause

Answer 339

MOST COMMON = LVF Increased capillary pressure: - Cardiogenic – LVF, valve disease, arrythmias, VSD, cardiomyopathies, negatively inotropic drugs. - Pulmonary venous obstruction - Iatrogenic fluid overload Increased capillary permeability: - ARDS - Infection – pneumonia/ sepsis - DIC - Inhaled toxins Reduced plasma oncotic failure: - Renal / Liver failure – hypoalbuminaemia Lymphatic Obstruction: - Tumour / parasitic infection Others: - Neurogenic – raised ICP / head injury - PE - Altitude

Answer 340

Pulmonary HTN secondary to prolonged pulmonary oedema leads to irreversible structural changes to pulmonary arteries. This in turn puts more pressure on the right ventricle of the heart, which eventually leads to RV hypertrophy and RHF => “cor pulmonale”

Answer 341

= a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs Due to the pulmonary response to either direct (inhalation) or indirect (blood-borne) insults, leading to non-cardiogenic pulmonary oedema

Answer 342

DIRECT Aspiration of gastric contents Smoke / toxin inhalation Pneumonia Near-drowning INDIRECT Sepsis Multiple trauma Pancreatitis Transfusion reactions Anaphylaxis Drug reactions

Answer 343

Neutrophil infiltration of pulmonary capillaries leading to increased capillary permeability and protein-rich pulmonary oedema. There is also damage to type 2 pneumocytes, leading to surfactant depletion and alveolar collapse due to lack of lung compliance.

Answer 344

SOB, tachypnoea, cyanosis Hypoxaemia Absence of signs of raised right atrial pressure Diffuse bilateral infiltrates on CXR Impaired lung compliance.

Answer 345

These patients will often be admitted to ICU for respiratory / circulatory support. Sit the patient up with 100% oxygen Non-invasive positive pressure ventilation (e.g. CPAP) used initially => BUT most will require mechanical ventilation IV nitrates titrated upwards until clinical improvement seen (or drop in SBP) IV furosemide (40-80mg) IV morphine + anti-emetic Aminophylline if bronchospasm also present The patient will then be kept on bed rest with continuous monitoring, and investigation / Tx for underlying cause.

Answer 346

Factor VIII deficiency X-linked recessive inheritance (but a high rate of new mutations)

Answer 347

Factor IX deficiency (Also known as Christmas disease) X-linked recessive inheritance

Answer 348

Major bleeds following minor trauma Recurrent haemarthroses leading to crippling arthropathies Compartment syndrome / nerve palsies can develop due to pressure effects. Women can be CARRIERS and have a milder version of the disease.

Answer 349

- FBC - Clotting screen – raised APTT - Fibrinogen activity Upon contacting haematology: => vWF => Intrinsic factor assays: - Low factor VIII or IX (depending on type)

Answer 350

Avoid NSAIDs and IM injections Minor bleeding: - Compression & elevation - Desmopressin (recombinant ADH) – raises factor VIII levels and may be sufficient Major bleeding (e.g. haemarthrosis): - Recombinant factor VIII / IX to raised factor levels to 50% of normal Life-threatening bleeds: - Raise levels to 100% of normal

Answer 351

= the absence or abnormal function of vWF: TYPE 1 – most common and least severe; due to reduced levels of vWF; => bleeding is mostly only a problem if after surgery/ injury/ dental surgery TYPE 2 – vWF does not work properly TYPE 3 – most severe and rarest; very low or no vWF; => Bleeding from the mouth, nose and gut is common => Also joint and muscle bleeds after an injury.

Answer 352

This gives symptoms of platelet type disorder: => Mucocutaneous bleeding - Epistaxis / menorrhagia / petechial rash Haemarthroses are rare

Answer 353

autosomal recessive or autosomal dominant => Recessive – type 3 / complete absence of detectable vWF (20%) => Dominant – type 1 or 2; less severe depletion of vWF (80%)

Answer 354

Expert Mx is required: - Transexamic acid for mild bleeding - Desmopressin / recombinant factor VIII for more severe bleeds (vWF has a secondary role of binding factor VIII to prevent destruction, so low factor VIII levels co-exist).

Answer 355

- Haemophilia - Liver disease - DIC - Vitamin K deficiency - Anticoagulant drugs

Answer 356

Site of bleed: => Muscle / joint bleeds – coagulation issue => Purpura / epistaxis / menorrhagia / GI haemorrhage – platelet issue => Recurrent bleeds at one site – local endothelial abnormality Duration of Hx / FHx => Congenital vs. acquired Seriousness? => Spontaneous bleeds indicate a more serious issue than post-traumatic bleeds Surgical Hx => Bleeding that starts immediately after => suggests platelet issue => Bleeding that starts several hours later => suggests coagulation issue PMHx: => Renal / liver failure ? DHx: => Anticoagulants => Steroids / NSAIDs

Answer 357

Skin: => Any bruises / purpura / telangiectasia? Joints: => Any evidence of haemarthrosis? Abdomen: => Splenomegaly? => Evidence of hepatic dysfunction?

Answer 358

= the process of stabilisation of the soft haemostatic plug through a complex interaction between platelet membrane, enzymes and coagulation factors

Answer 359

I = Fibrinogen Ia = Fibrin

Answer 360

II = prothrombin IIa = thrombin

Answer 361

Clotting factors are primarily synthesised in the liver, and many act as serine proteases to activate other factors. INTRINSIC or EXTRINSIC pathway can be activated, but both activate a final common pathway that leads to production of fibrin and thus a thrombus can be formed. At the same time, thrombin, in the presence of calcium ions, activates factor VIII which stabilises the fibrin clot by cross-linking fibrin molecules.

Answer 362

Found in leafy green vegetables, dairy products and soya beans. Intestinal flora can also synthesise many forms of vitamin

Answer 363

VitK is a co-factor necessary for the production of some clotting factors. => Factor II, VII, IX and X Deficiency of VitK thus leads to clotting factor deficiencies, leading to an increased PT and haemorrhage. Deficiencies arise from: - Malabsorptive conditions (VitK = fat soluble vitamin) - Cholestatic jaundice (no bile salts) - ABX (gut flora disturbances).

Answer 364

Anti-thrombin III – serine protease inhibitor (potentiated by heparin) Activated protein C – also generated by vitamin K, and activated by thrombin. => APC acts with the co-factor protein S to induce fibrinolysis => It destroys factor V and VIII, reducing further thrombin generation and inhibits stabilisation of the fibrin clot.

Answer 365

Plasminogen is converted to plasmin by tissue plasminogen activator (t-PA), produced by the endothelium. Many mediators, including thrombin and APC, stimulate the release of t-PA. Plasmin is a serine protease that breaks down fibrinogen and fibrin into fibrin degradation products (FDPs) – e.g. D-dimer => D-dimer presence in the plasma thus indicates that the coagulation mechanism has been activated.

Answer 366

FBC and Blood Film – platelet number and morphology Platelet function tests – e.g. PFA/closure time, platelet aggregometry. Complex platelet test by specialist Von Willebrand factor assays

Answer 367

CLOTTING SCREEN => PT (extrinsic) => APTT (intrinsic). => INR => APTT ratio => derived fibrinogen

Answer 368

Tests the extrinsic pathway, by addition of a tissue factor substitute to the patient’s plasma. Prolonged in: - Liver disease - Patients on warfarin

Answer 369

Addition of a surface activator to the plasma Tests the intrinsic (contact) pathway Used for monitoring of unfractionated heparin (not required for LMWH)

Answer 370

Ratio of patient’s PT to a normal control whilst using an international reference preparation (standardises laboratories worldwide) 0.9 – 1.1 = normal range Used for warfarin dosing

Answer 371

Addition of thrombin to the patient’s plasma Prolonged with: - Fibrinogen deficiency / abnormal function - Inhibitors such as heparin

Answer 372

= Characterised by vascular contraction, platelet adhesion and formation of a soft haemostatic plug.

Answer 373

when the endothelium is in continuity it secretes mediators such as prostacyclin (PGI2) and nitric oxide that prevent platelet adhesion.

Answer 374

Vasoconstriction => slows blood flow, enhances platelet adhesion and activation. Exposed collagen and vWF => triggers platelet adhesion Platelet adhesion leads to degranulation of the platelets, releasing ADP ADP stimulates further platelet aggregation at the site Platelets also synthesise the prostaglandin thromboxane A2 (TXA2), which causes both vasoconstriction and further aggregation. Receptors on the platelet surface then activate the coagulation cascade, which generates fibrin to form a fibrin/platelet thrombus (= soft haemostatic plug). This process is short-lived and the weak plug is easily sheared off.

Answer 375

Low-dose (75mg) aspirin irreversibly inhibits COX enzyme, preventing conversion of arachidonic acid to endoperoxides such as PGI2 and TXA2. After administration of aspirin, the nuclei of endothelial cells are quickly able to secrete mRNA for PGI2 production. The anucleate platelets cannot form TXA2, so levels decrease until new platelets are formed (in approximately 7 days). Low-doses of aspirin every 24-48 hours thus decrease synthesis of TXA2, without massively affecting PGI2 production.

Answer 376

can be used as an alternative or an adjunct to aspirin It works as an ADP receptor antagonist, thus preventing glycoprotein expression and platelet aggregation.

Answer 377

REDUCED PRODUCTION Aplastic Anaemia Marrow Infiltration Marrow Suppression EXCESS DESTRUCTION Immune thrombocytopaenic purpura (ITP) Other autoimmune causes – SLE, CLL, viruses Thrombotic thrombocytopaenic purpura (TTP) Haemolytic uraemic syndrome (HUS) Sequestration – hypersplenism

Answer 378

Bruising / purpura of the skin Epistaxis / menorrhagia Major haemorrhage is very rare Physical examination is generally normal.

Answer 379

= isolated thrombocytopaenia without an isolated cause. Presentation: - In children, ITP is usually acute and self-limiting – following a virus or immunisation. - In adults, the presentation is usually less acute, classically in women with other autoimmune disorders.

Answer 380

FBC – only thrombocytopaenia seen Clotting screen – to r/o other clotting disorders Bone marrow examination: - Not usually performed in children - Normal / increased megakaryocyte numbers found, otherwise normal Platelet autoantibodies => Positive in 70% of patients, but does not confirm diagnosis.

Answer 381

Children are not usually treated. => If clinically necessary, they may be treated with prednisolone or IVIG Chronic thrombocytopaenia is rate, and requires specialist management. In adults: => corticosteroid are 1st line => IVIG can be used if a rapid rise in platelets is required => Splenectomy may be 2nd line Platelet transfusions are reserved for severe haemorrhage.

Answer 382

Growth Hormone (GH) Prolactin Adrenocorticotropic Hormone (ACTH) Thyroid-stimulating Hormone (TSH) Gonadotrophin Luteinizing Hormone (LH) Follicle Stimulating Hormone (FSH)

Answer 383

stores and secretes hormones that were produced in the hypothalamus (connected by the pituitary stalk) Anti-diuretic Hormone (ADH) Oxytocin

Answer 384

Benign tumour of the glandular tissue (BUT can be life-threatening due to mass effects or secretory actions) Size: - >1cm = macroadenoma - <1cm = microadenoma Tumours are classified as “functioning” or “non-functioning” (silent) on the basis of whether they are secretory or not.

Answer 385

Bitemporal Hemianopia – due to compression of the optic chiasm Ocular Palsies – due to compression of CN III, IV or VI Hypopituitarism – destroys the normal functioning tissue Signs of raised ICP Hypothalamic compression symptoms – altered appetite, thirst, sleep/wake cycle

Answer 386

Acromegaly – excessive GH production Hyperprolactinaemia – excessive prolactin production Cushing’s Syndrome – excessive ACTH production Functioning Adenomas can also cause any of the mass effects. Many tumours can secrete multiple hormones, however tumours producing TSH / LH / FSH are very rare.

Answer 387

Prolactin stimulates milk production in the breast, and also inhibits GnRH and gonadotropin production. Clinical Features: - Gynaecomastia - Galactorrhoea in females (spontaneous and expressible) - Oligo/amenorrhoea - Decreased libido - Subfertility - Arrested puberty in younger patients In the long-term, osteoporosis may develop due to androgen/oestrogen deficiency.

Answer 388

- Pituitary Adenoma - Breast stimulation / stress - Drug induced - Idiopathic

Answer 389

pituitary MRI

Answer 390

Dopamine Agonists are 1st line (dopamine inhibits prolactin release) => Lifelong Ropinirole / bromocriptine => These reduce tumour bulk without the surgical risks => Sx usually recur on stopping medication Surgery is 2nd line if medical Tx ineffective

Answer 391

GH stimulates skeletal and soft tissue growth Excess GH can cause: => Gigantism in children (if prior to epiphyseal plate closure) => Acromegaly in adults

Answer 392

Acromegaly is almost exclusively due to pituitary tumours Rarer causes – paraneoplastic release of GH from non-pituitary tumours.

Answer 393

Raised IGF-1 level - Used as this level correlates with GH levels over the past 24 hours (GH levels themselves are too variable) - Mainly used for monitoring rather than diagnosis Glucose tolerance test: - Normally will suppress GH secretion - In acromegaly, concentrations are >2mcg/mL at 2 hours.

Answer 394

Change in appearance Increased hand/foot size Tiredness Excessive sweating Poor libido Symptoms of diabetes Headaches Visual Deterioration Symptoms of hypopituitarism

Answer 395

Protruding mandible Prominent supraorbital ridge Interdental separation Large tongues Spade-like hands/feet Tight rings Visual field defects HTN

Answer 396

Somatostatin analogues may be used to shrink the tumour => Short-term prior to surgery => Long-term if surgical removal not possible. Surgical Mx = via transphenoidal approach

Answer 397

- Exogenous administration of steroids (most common) - Cushing’s disease = Increased ACTH from the pituitary - Ectopic ACTH (non-pituitary ACTH-secreting tumour – classically small cell lung cancer) - Excess adrenal cortisol production

Answer 398

Cushing's syndrome = umbrella term describing the symptoms of increased circulating glucocorticoid. Cushing’s disease = specifically due to increased ACTH from the pituitary

Answer 399

SYMPTOMS Central weight gain Change of appearance Depression Insomnia Poor libido Thin skin/easy bruising Excess hair growth / acne Diabetes symptoms SIGNS Moon face Frontal balding Striae HTN Pathological Fractures “Buffalo hump” Proximal myopathy (There may also be hypokalaemia due to the mineralocorticoid activity of cortisol)

Answer 400

1. Overnight dexamethasone suppression test => Normal = negative feedback leads to cortisol level <50 mmol/L => Cushing’s = failure to suppress cortisol secretion 2. If abnormal, localisation tests are required: => Plasma ACTH – if undetected, adrenal cause is likely => adrenal CT => If ACTH is detectable, pituitary vs. ectopic sources must be separated. 3. High-dose dexamethasone suppression test: - Complete / partial suppression indicates Cushing’s disease (the pituitary retains some feedback control) => MRI pituitary - No suppression indicates an ectopic source => CXR/find primary tumour

Answer 401

= Defective production of all pituitary hormones PRESENTATION - Fatigue, myalgia, hypotension – GH/ ACTH deficiency - Diabetes insipidus – ADH deficiency - Hypothyroidism – TSH deficiency Can have pituitary or hypothalamic causes DIAGNOSIS - Pituitary hormones = low - Effector gland hormones = low - Low response to stimulation tests - Imaging to localise pathology

Answer 402

Pituitary causes: - Obliteration of the pituitary by primary/metastatic tumour - Surgical removal / irradiation of pituitary - Ischaemic necrosis due to hypotensive shock Hypothalamic causes: - Destruction of hypothalamus by primary tumour/ infection/ sarcoid/ infection.

Answer 403

Occur mainly as a result of damage to the hypothalamus (e.g. tumour invasion or infarction). Failure of ADH production leads to Cranial diabetes insipidus (as opposed to nephrogenic DI) Excessive ADH production leads to SIADH

Answer 404

Failure of ADH production leads to cranial diabetes insipidus => Presents with polyuria and polydipsia, hypernatraemia Ix: - Low urine osmolality - High serum osmolality - Water deprivation test Mx = treat underlying cause; desmopressin (synthetic ADH) can be used in cranial DI.

Answer 405

Post-operative from major surgery Infection, particularly atypical pneumonia and lung abscesses Head injury Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,) Malignancy, particularly small cell lung cancer Meningitis Excess pituitary secretion

Answer 406

Excessive ADH production results in excessive water reabsorption in the collecting ducts. This water dilutes the sodium in the blood so you end up hyponatraemia The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”. The urine becomes more concentrated as less water is excreted by the kidneys therefore patients with SIADH have a “high urine osmolality” and “high urine sodium”.

Answer 407

- Assess Fluid status – euvolaemia - U&Es – hyponatraemia - Urine sodium and osmolality will be high

Answer 408

Treat cause; Fluid restriction (0.5 – 1 L); Correct sodium SLOWLY (~10 mmol/day) Potentially ADH receptor blockers or Demeclocycline (a tetracycline antibiotic that inhibits ADH)

Answer 409

= painless enlargement of thyroid gland. It can be defined by certain characteristics: 1. Diffuse vs. nodular – pattern of swelling 2. Simple vs. toxic – actively secreting thyroid hormone 3. Benign vs. malignant

Answer 410

Physiological - Puberty - Pregnancy Autoimmune - Grave’s disease - Hashimoto’s disease Thyroiditis - Subacute (De-Quervain’s) thyroiditis - Riedel’s thyroiditis Endemic - Iodine deficiency Drugs - Anti-thyroid drugs - Lithium - Iodine excess - Amiodarone

Answer 411

Multinodular - Toxic multinodular goitre - Subacute thyroiditis Solitary Nodule: - Follicular adenoma - Benign nodule - Thyroid malignancy - Lymphoma - Metastasis - OR one prominent nodule from a multinodular goitre Infiltration (rare): - TB - Sarcoid

Answer 412

FBC – assess for related anaemia ESR – may indicate thyroiditis / autoimmune disease TFTs Thyroid autoantibodies CT neck and thorax – if pressure Sx USS – to distinguish between solid and cystic masses (not required in all cases) Fine needle aspiration for cytology (FNAC) – if concern regarding malignancy.

Answer 413

Mx depends on whether the patient is hyperthyroid or hypothyroid. In a euthyroid patient, Tx is not required for a non-malignant nodule unless it is causing pressure Sx.

Answer 414

COMMON Grave’s Disease Toxic multinodular Goitre LESS COMMON Solitary Toxic Adenoma Thyroiditis Drug-induced - Amiodarone; Excess levothyroxine Exercise Iodine intake Hashitoxicosis (the hyperthyroid phase of Hashimoto’s disease) RARE Secondary causes: - TSH secreting pituitary adenoma - Resistance to thyroid hormone

Answer 415

IgG autoantibodies stimulate thyroid follicular cells, out of the normal pituitary feedback mechanism => HYPERTHYROIDISM

Answer 416

Both causes of hyperthyroidism hyperactive nodule(s) develop, outside of TSH control

Answer 417

Anxiety / irritability Heat intolerance Increased appetite Palpitations Weight loss Tremor Diarrhoea Fatigue / weakness Can rarely present with thyroid crisis/thyroid "storm"

Answer 418

Lid retraction / lid lag Goitre Systolic HTN Tachycardia / AF Tremor Hyperreflexia Warm peripheries Proximal Weakness Pre-tibial myxoedema Grave’s Ophthalmopathy* Acropachy*

Answer 419

Lagophthalmos – inability to close eyes completely Exophthalmos / proptosis – bulging eyes Ophthalmoplegia – especially affecting upwards and lateral gaze Periorbital oedema !! Graves’ Ophthalmopathy is much more common in smokers.

Answer 420

Generally occurs in periods of stress (infection, surgery, childbirth) in people with untreated/uncontrolled hyperthyroidism. - Hyperpyrexia - Severe tachycardia - Profuse sweating - Confusion / psychosis - If untreated, coma and death Treat with: - Propylthiouracil, propranolol, sodium iodide, high dose steroids - Supportive measures

Answer 421

TSH – fully suppressed (unless in rare cases of pituitary adenoma) Free T3/4 – elevated => Typically both elevated, in rare cases there can be T3-toxicosis with T4 within reference range. TSH receptor antibody (TRAb) – sensitive and specific for Grave’s disease Thyroid Peroxidase (TPO) is not elevated in all Grave’s patients, so no longer routinely used. Technetium uptake scan – if TRAb not present => Diffuse pattern of uptake in Grave’s disease => One or more “hot” nodules in toxic multinodular goitre => Reduced/absent uptake in thyroiditis Radioiodine scans can be used, but are less common CT/MRI Orbit – to assess extent of eye disease in Grave’s

Answer 422

Non-selective beta-blocker – e.g. propranolol => 20-40 mg t.d.s for rapid relief of symptoms => May be the only Tx required for cases of thyroiditis Refer to specialist endocrinologist => Options include antithyroid drugs, radioactive iodine therapy, surgical management.

Answer 423

Patients with Grave’s disease are usually offered an intermediate course of antithyroid therapy (titration vs. block and replace) In other pathologies, antithyroid drugs control but do not cure the disease: => Patients are offered a choice of radio-active iodine (RAI) therapy or surgical management. - RAI generally first line - Drugs will always be used prior to RAI / surgery to render the patient euthyroid before definitive Tx. - Antithyroid drugs may be used long-term if these therapies are unsuitable.

Answer 424

Titration regimens – start at a high dose and titrate down until the patient is euthyroid. “Block and replace” – maintain a high dose, and thyroxine added in.

Answer 425

Carbimazole is 1st line Propylthiouracil is 2nd line => Due to risk of severe liver injury Both act as preferred substrate for thyroid peroxidase, the key enzyme in thyroid hormone synthesis. SEs: - Both can cause skin rashes or the more serious agranulocytosis/thrombocytopaenia. - Carbimazole can also cause cholestatic jaundice.

Answer 426

131I is used as first line in non-Grave’s pathology; or following failure of drug therapy in Grave’s. It is taken up by the thyroid cells, and induces DNA damage and cell death. Antithyroid drugs must be discontinued prior to therapy for at least 1 week to allow adequate uptake.

Answer 427

- Pregnancy - Active Grave’s ophthalmology (can cause worsening of eye symptoms) Patients should avoid prolonged contact with children for 3 weeks after treatment, and should not attempt to conceive for 6 months

Answer 428

Surgery is indicated if: - other measures have failed or are contraindicated, - There is suspicion of malignancy - To manage a large toxic goitre

Answer 429

COMMON Hashimoto’s Thyroiditis (goitre) Atrophic Thyroiditis (no goitre) Previous Tx for hyperthyroidism LESS COMMON Drugs (Amiodarone, iodine excess, lithium) Iodine Deficiency Thyroiditis Secondary causes (Hypothalamic/pituitary disorders) RARE Congenital agenesis Neoplastic infiltration

Answer 430

= most common cause of hypothyroidism in the UK T-cell destruction of the gland, plus B-cell secretion of inhibitory TSH-receptor antibodies. Often an initial hyperthyroid phase. There will be a goitre

Answer 431

Fatigue Depression / psychosis Cold intolerance Weight gain Constipation Menorrhagia Myxoedema coma (rare)

Answer 432

Hair loss Loss of outer third of eyebrow Anaemia Hoarse voice Goitre Bradycardia Dry skin Hyporeflexia

Answer 433

FBC – anaemia => Macrocytic due to co-morbid pernicious anaemia => Microcytic due to menorrhagia TFTs: => Raised TSH, reduced free T4 in primary causes => Low TSH in hypothalamic disease or “sick thyroid syndrome” (due to non-thyroidal illness) TPO autoantibodies => Raised in Hashimoto’s Cholesterol – can be raised in hepatic hypothyroidism

Answer 434

Levothyroxine => Low starting dose, titrated up to clinical effect => Reassess every 4-6 weeks, until TSH is in the lower half of the reference range in primary disease. => TSH is unreliable in secondary disease, titrate based on free T4 levels and clinical symptoms

Answer 435

Relatively uncommon May follow an URTI Presentation: - Initially fever and malaise, plus thyroid swelling and tenderness - Initially there are thyrotoxic features, as stored hormone is released. - After this, the patient develops hypothyroidism, which is usually transient but can occasionally be permanent There is classically low/absent uptake on technetium scanning Tx: - Propranolol in thyrotoxic phase - Simple analgesia - Occasionally prednisolone 30mg/day is used.

Answer 436

99% of the body’s calcium is in the bone – combined with phosphate as hydroxyapatite. 40% of plasma calcium is bound to albumin, and thus is inactive (Only free Ca2+ is biologically active) => Acidotic states increase ionised calcium, by decreasing albumin binding. => Alkalotic states decrease ionised calcium, by increasing albumin binding

Answer 437

40% of plasma calcium is bound to albumin Many labs will adjust for a low/high serum albumin to give a measure of the ionised calcium present ("adjusted calcium")

Answer 438

Plasma calcium normal range = 2.2 - 2.6 mmol/L Maintaining calcium at optimum range ensures normal excitability of nerve and muscle. Calcium is also required for clotting and complement cascades

Answer 439

There are 4 pea-sized parathyroid glands, lying just posteriorly to the thyroid. => These glands have calcium and vitamin D receptors. The chief cells of the parathyroid glands are responsible for secreting parathyroid hormone (PTH): => when plasma calcium levels are low. => in response to low vitamin D, or high phosphate levels.

Answer 440

PTH works to increase plasma calcium by: 1. Directly stimulating calcium reabsorption from bone, via increased osteoclast activity. 2. Directly increasing renal tubular calcium reabsorption. 3. Indirectly stimulating increased GI calcium absorption. => Via increased vitamin D activation in the kidney. PTH also has a secondary effect of increasing renal phosphate excretion

Answer 441

ENDOGENOUS - synthesised in the skin, forming D3 (cholecalciferol). => Action of UV light on the precursor to vitD (7-dehydrocholesterol) EXOGENOUS - ingested as D3/D2 => D3 – found in fish, liver, dairy products => D2 – found in plants/fungi (less potent than D3)

Answer 442

Calcitonin is secreted by the parafollicular/ “C” cells of the thyroid gland Secreted in response to increased plasma calcium levels. It acts to decrease plasma calcium levels, by antagonism of the effects of PTH on the bone. => Reducing osteoclast activity => Decreasing renal resorption of calcium and phosphate. HOWEVER the effects of calcitonin are controversial (evidence that there aren't many effects).

Answer 443

1. Excessive PTH secretion - Hyperparathyroidism - Ectopic PTH secretion (rare) 2. Malignant disease - Myeloma - Bone metastases - PTH-related protein secreting tumours (e.g. SCC of lung/other tissues) 3. Excess action of Vit D 4. Excessive calcium intake - “Milk-alkali syndrome” 5. Drugs 6. Hereditary - Familial hypocalciuric hypercalcaemia

Answer 444

Mild hypercalcaemia (<3.0 mmol/L) is usually asymptomatic. Symptoms in hypercalcaemia (>3.0 mmol/L): - BONES – bone pain, muscle weakness, chondrocalcinosis - STONES – renal colic (stones), polyuria, AKI/CKD - ABDOMINAL GROANS – abdominal pain, vomiting, constipation, pancreatitis, GI ulcers - PSYCH MOANS – depression, confusion, tiredness, hypotonicity. ECG will slow reduced QT interval, and this can lead to cardiac arrest.

Answer 445

80% due to parathyroid adenomas 20% due to diffuse hyperplasia of the glands PTH levels raised, calcium levels raised. Tx = Parathyroidectomy

Answer 446

Tx for primary and tertiary hyperPTH Indicated even in many asymptomatic cases, due to potential long-term adverse effects. Serum calcium should return to normal within 24h post-surgery There may be post-op hypocalcaemia (AdCal is usually given for 14 days post-op)

Answer 447

PHYSIOLOGICAL hypertrophy of all parathyroid glands in response to hypocalcaemia Seen in renal disease or VitD deficiency PTH levels raised, calcium levels are low/normal Tx = PTH will return to normal if the cause of hypocalcaemia can be corrected.

Answer 448

Occurs after long-standing secondary hyperparathyroidism Most commonly occurs in renal failure Plasma calcium is raised, PTH levels raised Phosphate is often grossly raised Tx = Parathyroidectomy usually necessary.

Answer 449

Primary can be separated from tertiary hyperparathyroidism fairly easily based on clinical presentation, and phosphate levels are also helpful => Phosphate low/normal in primary, grossly raised in tertiary.

Answer 450

- PTH – raised - Ca2+ – raised (if primary/tertiary) - PO43- - ALP – raised - 24h urinary calcium – raised - DEXA scan – vital to assess extent of osteoporosis - Tumour localisation: => Technetium scanning – show areas of increased uptake => USS (requires highly skilled operator)

Answer 451

= multiple endocrine neoplasia AUTOSOMAL DOMINANT INHERITANCE MEN 1 - Pancreatic endocrine tumours – gastrinoma / insulinoma - Pituitary adenoma - Parathyroid adenoma (causing hyperPTH) MEN2a: - Thyroid – medullary carcinoma - Adrenal – PCC - Parathyroid – hyperplasia (causing hyperPTH) MEN 2b: - Thyroid – medullary carcinoma - Adrenal – PCC - Mucosal neuromas - Marfanoid appearance.

Answer 452

If Ca2+ = >3.5 mmol/L and severe symptoms: 1. IV Fluids => 0.9% NaCl to increase calcium clearance. => Aim for 3-6L over the first 24 hours. (Diuretics no longer routinely used, but may be considered if there is a risk of fluid overload.) 2. Bisphosphonates: - Single dose of pamidronate - Lowers calcium over 2-3 days. 3. Calcitonin: - May be used to rapidly reduce levels in life-threatening hypercalcaemia (however effects are short-lived) 4. Dialysis: => May be required if there is renal impairment Further Mx is related to investigating and treating the cause of hypercalcaemia.

Answer 453

1. ARTIFACT of low serum albumin if not “corrected”. 2. With low PTH (hypoparathyroidism) - Idiopathic / primary hypoparathyroidism - H&N surgery / radiation - Infiltration – sarcoid / malignancy - Congenital absence of the gland (DiGeorge Syndrome) - Severe hypomagnesaemia (impairs PTH secretion) 3. With High PTH: - Vitamin D deficiency - Acute pancreatitis - Alkalosis - Acute hypophosphatemia – renal failure, rhabdomyloysis, tumour lysis - Drugs – bisphosphonates, calcitonin

Answer 454

Severe hypomagnesaemia impairs PTH secretion Always check serum magnesium levels Replacing magnesium is essential (calcium will not increase otherwise)

Answer 455

Signs of Peripheral irritability: - Tetany / cramps - Carpo-pedal spasm => Happens especially after occlusion of brachial artery (Trousseau’s sign) => Tapping over facial nerve causes twitches – Chvostek’s sign - Seizures - Depression / anxiety - Perioral paraesthesia - Cataracts

Answer 456

Serum calcium – low Serum PTH – high / low => Check parathyroid antibodies if low Serum vitamin D – r/o deficiency ECG – prolonged QT interval

Answer 457

Mild/moderate symptoms: => AdCal (calcium and vitamin D) Severe symptoms: => Calcium gluconate IV, 10ml of 10% bolus, then maintenance infusion. => Start AdCal without delay. => Find and treat the cause. If hypomagnesaemia, replace magnesium as calcium will not increase otherwise.

Answer 458

Small rod-shaped bacteria (bacilli) Have a waxy coating that makes gram staining ineffective. They are resistant to the acids used in the staining procedure (“acid-fastness”). => "ACID FAST BACILLI" They then stain red with Zeihl-Neelsen staining Infection affects predominantly the lungs, lymph nodes and gut.

Answer 459

- Non-UK born patients (areas where TB is endemic – e.g. South Asia, Africa) - Immunocompromise - Those with close contacts with TB. - People living in overcrowded conditions - Alcohol /drug abuse

Answer 460

strains that are resistant to more than one TB drug making them very difficult to treat. The most common drug resistance in the UK is isolated isoniazid, with resistance to Rifampicin being the marker for MDR-TB

Answer 461

= the syndrome produced by M. tuberculosis infection in those not previously affected There is a mild inflammatory response at the site of the infection: - Common sites of initial infection are sub-pleural in the mid zones of the lungs, in the pharynx or terminal ileum - Infection will then spread to hilar, cervical or mesenteric nodes respectively. 1-2 weeks after infection, with the onset of immune sensitivity, the tissue reaction at both sites of the primary complex changes to form characteristic caseating granulomas Viable bacteria may remain within the primary complex, giving latent TB.

Answer 462

= The combination of infective focus and lymph node involvement is known as the primary complex.

Answer 463

the infective focus of TB in the lung

Answer 464

Usually asymptomatic or have a single enlarged lymph node that may be palpable if cervical. There are several methods by which primary TB can become symptomatic: - The Ghon focus can erode through the visceral pleura to discharge organisms and cause TB pleurisy / pleural effusions - Enlarged hilar lymph nodes can cause bronchial obstruction and collapse - The hilar lymph nodes can also erode into the bronchus and rupture, causing TB bronchopneumonia - The enlarging nodes can erode into vessels, giving miliary dissemination to the lung or systemic dissemination. - Erythema nodosum is common in primary disease. Symptomatic presentation is more common in patients with incomplete immunity.

Answer 465

M. tuberculosis re-infection in tuberculin-sensitive individuals. => Infection can be from exogenous sources or more commonly from “reactivation” from a healed primary complex There is immediate granulomatous response to the disease, thus regional lymph involvement is not common The lesion may heal with fibrosis and calcification if the immune system is strong. => Will progressively enlarge in those with poor immune systems. => This has greater risks of eroding into vessels / airways

Answer 466

Secondary infection in the lung => classical apical lesion termed an Assman focus, with destruction of the lung parenchyma leading to cavitation.

Answer 467

Earliest symptoms are non-specific – malaise, night sweats, anorexia, weight loss. Specific symptoms can occur late: - Productive cough - +/- small amounts of haemoptysis - Pleural pain Can present with pneumonia or pleural effusion O/E: - May only be a fever and apical crepitations - May be clubbing in advanced disease

Answer 468

SPUTUM SAMPLES – at least 3, including one morning sample. => Microscopy for acid-fast bacilli, results within 24h => PCR – if rapid diagnostic results are required or suspected MDR-TB (however this will not differentiate between active and latent TB) => Culture = gold-standard diagnostic test; but takes 6 weeks. If sputum samples are negative, bronchoscopy with biopsy or bronchoalveolar lavage may be useful. CXR Investigate for extra-pulmonary disease as clinically indicated.

Answer 469

Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones Disseminated Miliary TB gives a picture of "millet seeds" uniformly distributed throughout the lung fields

Answer 470

- Mantoux test - Interferon-gamma Release Assay => also required to diagnose latent TB in immunocompromised individuals, as they can have false negatives in skin tests Positive results should lead to assessment for active TB (these tests cannot differentiate between active/latent TB) => If no evidence then treat for latent TB

Answer 471

TB antigen (does not contain live bacteria), injected intradermally on the arm; size of wheal reaction monitored: => A positive result indicates either previous vaccination, latent or active TB. Reactions >5mm Considered positive in immunosuppressed individuals, those with prior TB or recent contacts Reactions >10mm Considered positive in those with RFs Reactions >15mm Considered positive in any individual

Answer 472

Consider admission if severely unwell Assess risk factors for MDR TB (and assess with PCR if suspected) Normal ABX Regimen: R Rifampicin => 6 months I Isoniazid(+ prophylactic pyridoxine) => 6 months P Pyrazinamide => 2 months E Ethambutol => 2 months (If CNS involvement, the isoniazid and rifampicin are continued for 12 months) NOTIFIABLE DISEASE

Answer 473

- Previous TB treatment - From endemic areas - Contact with MDR-TB - Poor adherence to current Tx - Aged 25-45 - HIV co-infection

Answer 474

People considered to be at high risk of poor adherence to Tx may have DOT – drug treatment is given under the observation of a key worker

Answer 475

All household members and close contacts should be traced and assessed for latent/active TB Casual contacts should be traced only if the person with TB is particularly infectious OR if casual contacts are at an increased risk of infection

Answer 476

Continue infection control measures until pulmonary / laryngeal disease has been excluded Treat with at least 6 drugs to which it is sensitive

Answer 477

Treat with 3 months of Rifampicin and Isoniazid (with pyridoxine).

Answer 478

Rifampicin => Abnormal LFTs, pink urine Isoniazid => Peripheral neuropathy / encephalopathy => Very rare when prophylactic pyridoxine co-prescribed Pyrazinamide: => Hepatotoxic (rare but severe) Ethambutol => Optic neuritis – assess with colour vision testing

Answer 479

haematogenous spread => some bacilli settle in specific organs and may remain dormant for many years – appearing later to cause disease. Painless lymphadenopathy – Lymphatic TB Monoarthritis – joint / spinal TB Sterile pyuria – Renal TB TB meningitis Erythema nodosum / lupus vulgaris – cutaneous TB TB pericarditis

Answer 480

(AKA hypersensitivity pneumonitis) = immune reactivity in the lungs due to inhaled antigens. Can cause an acute type III hypersensitivity response with immune complex formation. Or with repeated exposure there is a type IV cell mediated hypersensitivity reaction and granuloma formation. The chronic inflammation eventually results in interstitial fibrosis.

Answer 481

Farmer’s Lung => Caused by micopolyspora Bird Fancier’s lung => Caused by proteins in bird droppings Malt worker’s lung => Caused by aspergillus

Answer 482

Features of acute exposure come on 4-6 hours post-exposure. => Fevers, rigors and myalgia. => Dry cough and dyspnoea, possibly wheeze Chronic features are as per idiopathic pulmonary fibrosis

Answer 483

FBC – neutrophilia Serum precipitant levels – only indicate exposure CXR/CT/ lung function tests – confirm interstitial disease Bronchoalveolar lavage – confirm diagnosis => Shows increased T lymphocytes and mast cells

Answer 484

Aim for prevention, with no exposure/face masks/etc. Long-term prednisolone may give physiological improvement Established fibrosis cannot be treated. Compensation available for patients with Farmer’s lung.

Answer 485

SMOKING is the most common risk factor (90% of cases). . Other RFs: - Passive smoking - Urban living - Occupational exposure (asbestos, etc.)

Answer 486

small cell disease (20%) non-small cell disease (80%). => SCC; adenocarcinoma ; large cell anaplastic tumours

Answer 487

NON-SMALL CELL Arise from squamous metaplasia of the normally pseudostratified ciliated columnar epithelium, in response to cigarette smoke exposure. They are usually central and close to the carina => Thus frequently present with collapse/infection secondary to obstruction. May secrete PTH, causing hypercalcaemia. => (Beware as hypercalcaemia can also be due to bone mets) They are relatively slow growing compared to other tumours, and may be resectable.

Answer 488

= partial collapse (or incomplete inflation) of a lung OBSTRUCTIVE => mucous plug , foreign body, mass OTHER => PTX, surfactant deficiency, scarring/fibrosis

Answer 489

NON-SMALL CELL Equal gender incidence, and less related to smoking. Characteristically originate in peripheral locations, potentially in areas of previous lung scarring. (Bronchoalveolar carcinoma is a special type of adenocarcinoma) Accounts for <5%, but a better prognosis.

Answer 490

NON-SMALL CELL Features showing SCC or adenocarcinomatous origins may be seen, but they are not differentiated enough to be classified. Have a poor prognosis Often widely disseminated at diagnosis.

Answer 491

AKA oat cell carcinoma (as the cell nuclei resemble oat grains). Usually centrally located, and rapidly growing. Most highly malignant of all lung cancers. => Often metastasised at diagnosis. Originate from the bronchial epithelium, but differentiate into neuroendocrine cells to secrete active products (ADH / ACTH)

Answer 492

ADH => symptoms of SIADH (i.e. dilutional hyponatraemia) ACTH => Cushing’s syndrome Hypertrophic pulmonary osteoarthropathy Eaton Lambert Syndrome Hyper PTH

Answer 493

Rare - sometimes seen in Pts with small cell lung cancer Myasthenia Gravis-like symptoms => Proximal muscle weakness and reduced tendon reflexes. => Can be accompanied by dry eyes, sexual impotence and neuropathy. !!! Symptoms get better with usage, unlike MG !!!

Answer 494

Symptoms: - Persistent cough (80%) - Haemoptysis - Dyspnoea - Chest pain - B-symptoms O/E: - Clubbing - Cachexia - Signs of anaemia - Hypertrophic pulmonary osteoarthropathy - Paraneoplastic syndrome – clubbing and painful peri-osteitis of small joints of the hand. - Chest signs of collapse/consolidation/effusion - Signs of metastases.

Answer 495

FBC, LFTs, U&Es, calcium CXR – ANY patient with haemoptysis should have a CXR => Symptomatic tumours are almost always visible. => A normal CXR in a symptomatic patient should warrant further Ix for central tumours. Sputum/pleural fluid cytology Staging CT – head to pelvis Biopsy: - CT guided if peripheral (risk of PTX) - Via bronchoscopy if central. Pulmonary function tests – useful if planning surgery PET scan / radionucleotide bone scan – ?mets

Answer 496

Recurrent laryngeal nerve palsy => Change in voice => If present, indicates inoperability. Phrenic nerve palsy SVC obstruction Pancoast syndrome: - Horner’s syndrome (miosis, ptosis, anhidrosis) - Shoulder pain, radiating along ulnar forearm and into hand - Atrophy of hand/arm muscles - Oedema (due to blodd vessel compression)

Answer 497

Brain, Bone, Liver Adrenal gland

Answer 498

Surgical excision if peripheral enough, with no LNs/metastatic spread; with adjuvant chemotherapy. => Must be >2cm from carina. Curative radiotherapy can be an alternative if poor respiratory reserve, with adjuvant chemotherapy.

Answer 499

Nearly always disseminated at presentation May respond to chemotherapy +/- radiotherapy May have prophylactic cranial radiotherapy

Answer 500

= Interrupted and repeated collapse of the upper airway during REM sleep, associated with hypopnoea/apnoea and desaturations Hypoxia leads to increasing respiratory effort, until the patient overcomes the resistance. The combination of central hypoxia and respiratory effort briefly wakes the patient, leading to excessive daytime sleepiness. The patient is unaware of the awakenings from sleep.

Answer 501

Respiratory Depressants => Opioids, alcohol, sedatives Nasal Obstruction => Adenoids, rhinitis, polyps Encroachment on the pharynx: => Obesity, acromegaly.

Answer 502

Loud snoring during sleep Daytime sleepiness Morning headaches Decreased libido Nocturnal choking Witnessed apnoeic episodes

Answer 503

- Epsworth sleepiness Scale – to distinguish from simple snoring. - Endoscopic examination of the upper airway by ENT - Polysomnography = gold standard for diagnosis => Diagnostic, but rarely used. Diagnosis is made with the occurrence of >15 episodes of apnoea/hypopnoea during one hour of sleep.

Answer 504

Inpatient assessment of variable parameters (EEG, EMG, electro-oculogram, respiratory airflow, thoraco-abdominal movement, ECG, oximetry, snoring sound and video).

Answer 505

Behavioural changes – allow partner to sleep first, sleep on side. Weight reduction Avoidance of alcohol and tobacco CPAP via nasal mask = gold-standard management => Positive pressure keeps the airway open => 50% will not tolerate CPAP Alternatives to CPAP include: - Intra-oral devices - Daytime stimulants – e.g. modafinol - Upper airway surgery – if pressure assessments can localise a level of obstruction.

Answer 506

= disease of the lungs caused by inhalation of dusts, generally used to refer to pathology caused by coal dust The dust is toxic to macrophages (the normal defence for inhaled dusts) => INFLAMMATORY RESPONSE If this becomes chronic, there will also be fibrosis leading to restrictive lung disease.

Answer 507

Presence of small nodules (2-5 mm) on CXR, not associated with any clinically significant impairment of respiratory function. May develop to PMF.

Answer 508

Presence of large nodules (>10mm) on CXR, and the disease progresses relentlessly, leading to a mixed obstructive and restrictive pattern. May present long after active exposure to coal dust and culminates in COPD (often with black sputum) Can progress to respiratory failure. Compensation available to patients with PMF

Answer 509

- Asbestos Bodies - Pleural Plaques, Effusion and Thickening - Mesothelioma - Asbestosis There can be a latent period of up to 50 years between exposure and clinical onset of disease. The risk of disease is proportionate to intensity of exposure

Answer 510

Not pathological in themselves, merely act as a marker of asbestos exposure Can only be seen histologically, following lung biopsy => stain golden brown, assuming the shape of fusiform or beaded rods with a translucent centre

Answer 511

Can occur after light exposure and are normally asymptomatic (may be associated with recurrent pleural effusions) There may be mild restrictive deficit on spirometry, with pleural thickening and calcification on CXR Locations most commonly encountered include posterolateral, mediastinal, and diaphragmatic pleura More heavy exposure can cause diffuse pleural thickening (affecting >1/4 of the pleural surface), which will produce restrictive deficits

Answer 512

Caused by light exposure Interval of 20-40 years between exposure and disease onset. Presentation: - Pleuritic chest pain - Increasing dyspnoea - Unilateral pleural effusion on CXR Survival is poor (median survival 2 years from diagnosis).

Answer 513

Caused by heavy exposure Interval of 5-10 years from exposure to disease. Progressive dyspnoea Diffuse bilateral streaky strikes on CXR with honeycombing Outcome is poor – can progress after exposure ceases.

Answer 514

Patients can claim occupational compensation for: bilateral diffuse pleural thickening, asbestosis, mesothelioma asbestos-related bronchial carcinoma.

Answer 515

Contrast injected (usually via a catheter introduced into the femoral artery) Fluouroscopy is then used to visualise the arterial system Risks = contrast reaction, haematoma/ pseudoaneurysm/ AVF formation / arterial occlusion

Answer 516

= now more commonly used to assess the arterial system CTA => carotid/cerebral disease MRA => thoracic, abdominal or limb disease

Answer 517

Tension headache Migraine Cluster headache

Answer 518

Raised ICP Idiopathic intracranial HTN HTN Meningeal irritation (SAH/meningitis) Post-traumatic Giant cell arteritis Sinusitis Metabolic disturbances Drugs (nitrates, vasoactive agents).

Answer 519

Continuous, severe pressure felt bilaterally over the vertex, occiput and eyes. => Can be “band like” and of variable intensity. Classically occurs every day and can persist for year/months Standard analgesics are ineffective, and if used continuously may exacerbate the situation when their effects wear off (analgesic/rebound headache) Few associated symptoms

Answer 520

If episodic (<15 days/ month) => Paracetamol and aspirin/NSAIDs => Advise that can lead to a medication overuse headache. If medications are being used on more than two days per week, consider preventative Tx => Low dose amitriptyline => 75mg initially, titrated upwards if partial response Chronic tension headache is more difficult to treat => Reassurance, relaxation techniques => Addressing underlying stressors => Medication overuse headache and clinical depression should be ruled out/ treated.

Answer 521

Short-lived (30-120 mins) episodes of severe, unilateral pain; typically centred on one eye and come on very suddenly. Associated with AUTONOMIC features on the affected side. - Red eye - Eye/nose watering - Ptosis - Vomiting They may occur several times per day and be recurrent for several weeks/months before the disorder remits Up to 20% will experience an aura; and some may have mild background pain between attacks Alcohol is a common precipitant

Answer 522

Exclude secondary causes, and other causes of eye pain (e.g. angle closure glaucoma). S.C. (or nasal) triptan to take at the start of an attack => Home oxygen for use during the attack => At least 12L/min through a non-rebreather (unless COPD) Oral triptans/oral analgesia not effective for acute attack Prophylactic Tx = alcohol avoidance (and verapamil – off licence).

Answer 523

menstruation OCP use physical exercise alcohol specific food groups (cheese, chocolate, Chinese, red wine, etc) emotional states.

Answer 524

= poorly understood Vasodilation after a period of vasoconstriction (aura phase) is thought to correlate with the onset of headache. Many vasoactive peptides mediate this process.

Answer 525

Migraine headache= throbbing headache with anorexia, N&V, and photophobia is seen. Begins locally and spreads bilaterally. Aggravated by movement Can last several hours/days Neurological Exam is relatively normal

Answer 526

Classical Migraine with Aura Migraine without aura (common migraine) Opthalmoplegic Migraine Hemiparetic/ facioplegic migraine

Answer 527

Starts with sense of ill health (several hours), followed by visual aura in the field of vision opposite to the side of headache. Sensory aura symptoms are less common, speech disturbance is very rare. Thereafter, the headache begins.

Answer 528

Classic visual/sensory aura is absent, however patients may feel non-specifically unwell prior to onset of headache.

Answer 529

Migraine + 3rd or 6th nerve palsy.

Answer 530

Hemiparetic = headache plus temporary hemiparesis. Facioplegic = headache plus unilateral facial weakness

Answer 531

Examine to r/o other differentials: - Signs of focal neurology, raised ICP, meningism, temporal arteritis, retinal haemorrhage (SAH). Headache diary: - Assess frequency, severity of attacks, precipitants, and exacerbating/relieving factors.

Answer 532

1st line is PO NSAID or paracetamol, plus anti-emetic (e.g. metoclopramide). Offer PO triptan (sumatriptan) if attacks are severe - Taken ASAP at the start of symptoms - Can be intranasal if vomiting prevents oral Tx. - Avoid if IHD, uncontrolled HTN, coronary artery spasm. Opioids should NOT be used. Follow up – repeated unsuccessful triptan treatment is rare if the underlying diagnosis is actually migraine.

Answer 533

TRIGGER AVOIDANCE Consider Tx if migraine attacks are causing significant disability (e.g. if >2/month). Topiramate and Propranolol are 1st line => Propranolol in women of child-bearing age. 2nd Line = Amitriptyline/anticonvulsants if these aren’t successful/tolerated Menstrual-related migraines can be treated with mefenamic acid from the first day of menses, throughout menstruation; or triptans started 2 days before expected menses. COCP should be avoided in women with migraine with aura, however contraceptive methods that prevent menstruation can be tried.

Answer 534

In TIAs, the maximum deficit is present immediately, and headache is unusual.

Answer 535

IIH is most common in young obese women Symptoms and signs of raised ICP, but no mass lesion on imaging. It is thought to be a disorder of CSF reabsorption. Most common presentation = visual disturbances (diplopia/obscuration) and headaches. => Sometimes associated with pulsatile tinnitus and 6th nerve palsy. O/E: bilateral papilloedema.

Answer 536

CT/MRI will be normal LP will confirm increased CSF pressure.

Answer 537

Weight loss may facilitate spontaneous remission. A trial of corticosteroids may be successful Definitive Mx is a surgical shunt (necessary to prevent optic atrophy due to prolonged raised pressure).

Answer 538

Compression / pathology (MS) of the trigeminal nerve root. Agonising, sharp pain over the distribution of the nerve on one side, lasting only seconds. Often with a sensory trigger from a certain point

Answer 539

Look for any localising CNS signs, but examination usually normal.

Answer 540

post-herpetic neuralgia - pain is usually less severe and associated with itching/sensory changes. - patient will have had shingles previously

Answer 541

Simple analgesics are ineffective Carbamazepine offers good symptom control Sometimes TCAs (e.g. amitryptiline used)

Answer 542

Episodic aching in non-anatomical distributions of the head/neck. Commonly associated with depression/anxiety. May respond to antidepressants.

Answer 543

= LMN weakness of muscles supplied by cranial nerves with cell bodies in the medulla (i.e. the “bulb”) => CN IX, X and XII Most commonly degenerative (MND) or vascular (stroke) in origin. More rare causes are inflammatory (Guillain-Barre), infective (botulism), neoplastic (brainstem tumours) or congenital.

Answer 544

Inspect the tongue – wasted, flaccid and fasciculation, can be moved rapidly. Ask about dysphagia (do not test unless controlled environment) Ask the patient to say “AHHH” – look for poor elevation of the soft palate. Ask the patient to repeat sentences – quiet, nasal speech Assess jaw jerk/gag reflex – may be absent.

Answer 545

= Bilateral UMN disease of the medullary cranial nerves. Most common causes are degenerative (MND) and vascular (stroke). Also seen in MS and can follow head trauma.

Answer 546

Inspect the tongue – stiff/spastic tongue with slow movements, not wasted. Ask about dysphagia Ask the patient to say “AHHH” – normal elevation of the soft palate. Ask the patients to repeat sentences – gravelly, “Donald duck” speech Assess jaw jerk/gag reflex – preserved, may be exaggerated jaw jerk. May be mood disturbances

Answer 547

Cerebral lesions lead to impairment in higher function – the type of function affected gives clues to the location affected. FRONTAL - Intellectual impairment, personality change, urinary incontinence and monoparesis/hemiparesis. - Broca’s aphasia (if left frontal area). LEFT TEMPORO-PARIETAL (dominant hemisphere): - Agraphia, alexia, acalculia - Wernicke’s aphasia - Contralateral sensory neglect RIGHT TEMPORO-PARIETAL: - Failure of face recognition - Contralateral sensory neglect. OCCIPITAL: - Visual field defects - Visuospatial defects

Answer 548

cause IPSILATERAL pathological signs Broad, ataxic gait Titubation – rhythmic head tremor Dysarthria - Slurred, staccato speech Nystagmus - Course and horizontal, towards the side of the lesion Hypotonia Mild hyporeflexia Dysmetria – imprecise movements/coordination => Finger to nose test – misses target, may be intention tremor which worsens as the patient approaches the target. Dysdiadochokinesis – clumsy rapid alternating movements

Answer 549

Ask the patient to repeat “British constitution” / “baby hippopotamus” Staccato speech - each syllable will be pronounced individually

Answer 550

- Dysdiadochokinesia - Ataxia (gait and posture) - Nystagmus - Intention tremor - Slurred, staccato speech - Hypotonia/heel-shin test To complete cerebellar examination – perform a full neurological examination of the CNS and PNS.

Answer 551

Rolling, broad ataxic gait Difficulty standing and sitting unsupported => Cannot perform Romberg’s test with eyes open or closed => Ask the patient to sit forward with arms across their chest. Vertigo and vomiting if extension into fourth ventricle.

Answer 552

BILATERAL Alcohol Drugs – phenytoin, anti-epileptics Paraneoplastic cerebellar degeneration UNILATERAL MS Stroke Tumour => Especially acoustic neuroma, meningioma

Answer 553

Anti-neuronal antibodies = +ve

Answer 554

Bradykinesia (can progress to akinesia) Muscle rigidity Involuntary movements - Tremor - Dystonia – spasms/abnormal muscle contractions - Athetosis – writhing involuntary movements of hands/face/tongue - Chorea – jerky involuntary movements - Hemiballismus – violent involuntary movements, restricted to proximal muscles of one arm

Answer 555

= inflammation of the leptomeninges (i.e. the arachnoid and pia mater, and underlying CSF).

Answer 556

Outside of the neonatal period, 70% of acute bacterial meningitis cases are caused by: Neisseria meningitidis Streptococcus pneumoniae Other: - Listeria monocytogenes – common in the elderly/immunosuppressed - Haemophilus influenzae - Staph aureus - TB - Viral causes: Enteroviruses, HSV, VZV - Fungal causes (in immunosuppressed patients)

Answer 557

Most commonly caused by blood-borne spread of M. tuberculosis to the brain following primary infection or miliary TB RFs – immunosuppression, malnourishment, multiple comorbidities, recent contact with TB May present as per acute bacterial meningitis, but more commonly as an insidious illness with fever, weight loss, and progressive confusion/cerebral irritation, eventually leading to coma

Answer 558

Blood-borne Para-meningeal suppuration => e.g. otitis media, sinusitis Direct spread through a defect in the dura => e.g. post-surgery, trauma => CSF leaking out of the nose/ear is a sign of a defect in the dura Direct spread through the cribriform plate => rare

Answer 559

Meningitic syndrome Triad: 1. Headache 2. Neck stiffness 3. Fever (+/- rigors) Other symptoms include: - Photophobia - Vomiting - Intense malaise (coming on over hours) - Confusion / altered mental state - Seizures O/E: - Kernig’s Sign positive - Brudzinski’s sign positive - Signs of raised ICP and/or cranial nerve palsies In uncomplicated meningitis, consciousness will remain intact

Answer 560

Flex the hip and knee extending the knee causes pain

Answer 561

Passive flexion of the neck leads to flexion of the knees/hip

Answer 562

Progressive drowsiness, lateralising signs or cranial nerve lesions - Venous sinus thrombosis - Severe cerebral oedema - Hydrocephalus

Answer 563

Bloods: - FBC, U&E, clotting, glucose, lactate - Cultures (prior to ABX if possible, but do not delay). Serum PCR for pneumococcal and meningococcal antigens LP – if no clinical suspicion of mass lesion / raised ICP - Send for MCS, protein, glucose and meningococcal / pneumococcal viral PCR - Do not delay LP unless signs of raised ICP CT prior to LP – if ?raised ICP Throat swabs – 1 for virology, 1 for bacteriology.

Answer 564

Gram positive intracellular diplococci = pneumococcus Gram negative cocci = meningococcus. Ziehl-Neelsen stain for acid-fast bacilli = TB Indian Ink = fungi

Answer 565

Leucocytes - VERY HIGH Protein - HIGH Glucose - LOW (normal = 50-80% of blood level)

Answer 566

Leucocytes - SLIGHTLY RAISED Protein - SLIGHTLY RAISED Glucose - NORMAL (normal = 50-80% of blood level) Appearance = yellow/turbid

Answer 567

Leucocytes - SLIGHTLY RAISED Protein - SLIGHTLY RAISED Glucose - NORMAL (normal = 50-80% of blood level) Appearance = clear

Answer 568

Leucocytes - RAISED Protein - RAISED Glucose - VERY LOW (normal = 50-80% of blood level) Appearance = yellow/viscous

Answer 569

If meningitis is suspected => LP within 1 hour If this cannot be achieved, empirical ABX should be given immediately after blood cultures. Meningitis is managed with: * Antibiotics * Adequate oxygenation * Prevention of hypoglycaemia and hyponatraemia * Anticonvulsants – if patient is fitting * Decrease intracranial hypertension – prevent brain herniation * Notifiable Disease – inform public health of ALL cases.

Answer 570

If non-blanching rash: => Benzylpenicillin 1.2g IM => 2.4mg 4-hourly is then the treatment of choice in hospital => Cefotaxime can be used in penicillin allergic patients If <60 and not immunosuppressed: => IV ceftriazone 2g BD (IV chloramphenicol in penicillin allergic patients) => IV dexamethasone given with 1st dose of ABX and 2nd dose after 6 hours If >60 or immunosuppressed: - IV ceftriaxone 2g BD - IV amoxicillin 2g 4-hourly - IV dexamethasone Add IV acyclovir if ?HSV encephalitis (i.e. if drowsy, mood changes)

Answer 571

Meningococcal meningitis contacts: => Single dose of ciprofloxacin given to all close contacts as prophylaxis.

Answer 572

= inflammation of the brain parenchyma, usually viral (similar organisms to viral meningitis). HSV-1 => causes necrotising encephalitis, affecting the temporal lobes. HSV-2 => causes meningitis in adults

Answer 573

Normally mild => Headache, drowsiness, fever, malaise and confusion. Rarely, serious illness can occur: => High fever, mood changes, progressive drowsiness over hours/days; leading to seizures and coma => Most commonly caused by HSV-1 => Carries a mortality of 20%

Answer 574

Head CT/MRI => Diffuse oedema, classically in the temporal lobes Lumbar puncture: => Raised opening pressure, Raised lymphocytes, Raised protein => Normal glucose => Positive viral PCR Viral serology: => Blood and CSF culture

Answer 575

Clinical features as for viral encephalitis CSF PCR = diagnostic Mx = IV acyclovir for >10 days Mortality = 20%

Answer 576

ACUTE: - Sepsis - DIC - Hydrocephalus - Adrenal haemorrhage (Waterhouse-Friedrichsen syndrome) LONGER-TERM: - Brain abscesses - Seizure disorders - CN palsies – sensorineural hearing loss or gaze palsies - Ataxia / muscular hypotonia Long-term sequelae are most common in pneumococcal meningitis

Answer 577

Generally very rare, most commonly complicating otitis media/paranasal sinus infections or secondary to bacterial endocarditis. May be a Hx of head trauma/neurosurgery Presentation: - Features of expanding mass lesion - Fever - Possible systemic illness

Answer 578

Surgical drainage Broad-spectrum ABX High dose corticosteroids Mortality is high; and many of those who survive go on to develop epilepsy.

Answer 579

Presents with fever, back pain and later spinal root lesions Caused by S. aureus Requires emergency imaging, ABX and surgical decompression

Answer 580

= the continuing tendency to have recurrent, unprovoked seizures.

Answer 581

1. Generalised: - Tonic clonic - Absence - Myoclonic - Tonic - Atonic 2. Focal: - Temporal - Frontal - Occipital - Parietal

Answer 582

- Discharge from both hemispheres - No warning - Always have LOC

Answer 583

- Discharge from ONE part of ONE hemisphere - May have a preceding aura - May or may not have LOC - May lead to generalised tonic-clonic seizure if LOC

Answer 584

TONIC PHASE - body becomes rigid for up to a minute, usually fall to the ground - Accompanied by tongue biting and incontinence - holds breath (cyanosis) CLONIC PHASE - lasts seconds to minutes - rhythmical jerking - irregular breathing, cyanosis, salivation - tongue biting, incontinence POST-ICTAL PHASE - drowsiness/ sleep / LoC (up to several hours)

Answer 585

"blanking out" / staring Absence of motor symptoms Brief onset and termination

Answer 586

repetitive, jerky movements

Answer 587

generalised increase in tone => fall

Answer 588

loss of muscle tone => fall

Answer 589

Aura - fear/deja vu sensation Smell / taste / sound distortions Lip smacking / chewing

Answer 590

Clonic movements spread proximally

Answer 591

Visual disturbances

Answer 592

Contralateral sensory disturbance Tingling/numbness

Answer 593

= when focal seizures are associated with temporary paresis of the originally affected limb after the attack

Answer 594

EPILEPTIC = Seizure due to excessive, hyper-synchronous neuronal discharge in the cerebral cortex NON-EPILEPTIC = Seizures not involving abnormal electrical activity in the brain

Answer 595

a type of non-epileptic seizure Caused by mental or emotional processes, rather than by a physical cause. => E.g. Seizure can happen as a cut-off mechanism to prevent bad memories being relived. Often caused by traumatic events - Such as major accidents, bereavement, psychological stress (e.g. divorce), physical or sexual abuse, bullying.

Answer 596

1. History = MOST IMPORTANT - Frequency, triggers, length, symptoms - Any impairments, educational/psychological/social impacts - Video of seizure if possible 2. Examination: - CNS and PNS - CVS and resp - Skin markers for neurocutaneous syndromes 3. EEG - Can show neuronal excitability in epilepsy (sharp waves/complexes). - NB – may be normal in epilepsy or abnormal in non-epilepsy - If normal, consider sleep-deprived EEG/24hr ambulatory 4. Imaging - MRI/CT – if neuro signs between seizures (r/o tumour or CVD) - PET/SPECT – detect areas of hypo/hypermetabolism 5. Tests to r/o other causes - ECG – cardiac causes - Bloods – metabolic disturbances - FBC, U&Es, LFTs, Ca, Mg, glucose. - Toxicology/drug screen if indicated.

Answer 597

Most seizures will only last a few minutes and end spontaneously – best immediate management: - Place the patient in the recovery position - Remove harmful objects around them If the seizure lasts over 3 minutes, or starts outside of hospital and is still ongoing once in hospital – treat as status epilepticus: - ABCDE => 100% oxygen, IV access, bloods including glucose, magnesium and calcium, VBG/ABG, ECG. => If hypoglycaemia, give IV glucose. => If any suspicion of alcohol withdrawal, give IV pabrinex. IV/PR/SL Lorazepam => 2-4mg bolus, repeated after 5 mins if no response. In females of childbearing age, perform pregnancy test. If seizure is continuing despite x2 doses of lorazepam – initiate 2nd anti-convulsant. => Often IV phenytoin 15mg/kg slow infusion with continuous ECG monitoring. If seizure is continuing 20 minutes from first presentation, then ICU should be called. => They may choose to intubate under GA. => Thiopentone = agent of choice.

Answer 598

TRIGGER AVOIDANCE = VERY IMPORTANT => Common triggers are lack of sleep, alcohol/drugs, hypoglycaemia, caffeine, stress, flashing lights. Most specialists will start AED treatment after 2 seizures, after ruling out organic causes. Drug depends on type of seizure: GENERALISED: - 1st line is valproate (or Lamotrigine in females of child-bearing age). - Adjuncts may be clobazam, carbamazepine or Levetiracetam - Ethosuximide is generally 1st line for Absence seizures. FOCAL: - 1st line is Carbamazepine (or Lamotrigine in females of child-bearing age). - Multiple adjuncts are used.

Answer 599

Withdrawal from AEDs may be considered if Pt is seizure free for 2-4 years. Drug should be dose-reduced every 4 weeks Patient has to stop driving for the withdrawal.

Answer 600

Weight gain Hair loss Teratogenic

Answer 601

Agranulocytosis Teratogenic CYP140 inducer Hyponatraemia

Answer 602

Increased gum growth Nystagmus Enzyme inducer Zero order kinetics, thus requires TDM

Answer 603

Ideally patients should withdraw from AEDs if possible prior to conception. However, treatment is preferable to hypoxic seizures during pregnancy Carbamazepine, Valproate, and Phenytoin all lead to NTDs (although carbamazepine has the lowest risk of the 3) Lamotrigine is now 1st line in a woman of child-bearing age and in pregnancy for generalised seizures. Any drug should be given with 5mg folic acid daily in the 1st trimester and vitamin K in the 3rd trimester (due to risk of neonatal bleeding).

Answer 604

Patients must tell the DVLA immediately and stop driving if they have had a seizure. If the attack was whilst awake and involved LOC, the license will be revoked. Patients can apply for their license back if they haven’t had a seizure for 6 months (after one seizure) After repeated attacks (true epilepsy), you can reapply after 1 year being seizure free. Patients with sleep-related epilepsy can drive if they have only had seizures while sleeping during the past 3 years.

Answer 605

1. Evidence of memory loss 2. At least one of: * Language impairment * Impaired executive function (e.g. problem solving, emotions). * Apraxia (difficulty motor planning) * Agnosia (difficulty recognising objects) 3. No other medical or psychiatric explanation 4. Present for at least 6 months

Answer 606

= evidence of early memory decline on formal memory tests (e.g. MMSE) without clinical evidence of the other features of dementia.

Answer 607

1. Alzheimer’s Disease – 2/3rd 2. Vascular Dementia – 20% 3. Lewy Body Dementia – 5% 4. Frontotemporal Dementia – 2% 5. Other rarer causes

Answer 608

Characteristic beta-amyloid plaques and neurofibrillary tangles. Brain atrophy, particularly the hippocampus. Enlarged ventricles Tends to be a gradual, progressive decline.

Answer 609

= Progressive memory loss that affects function. - Forgets names, people, places - Repeat themselves - Cannot remember new info - Misplace items - Confusion about time of day - Problems finding words - Mood/behaviour problems

Answer 610

Early onset (<65) there is some familial risk Association with APO-E gene Association with CVD risk factors.

Answer 611

= 2nd most common type of dementia. Caused by reduced blood supply to the brain => Due to diseased blood vessels Usually stepwise progression => Stable and then sudden decline – e.g. after a stroke. Risk factors – HTN, cholesterol, alcohol, smoking, DM, male, etc.

Answer 612

= problems with memory, thinking and reasoning. Problems planning/organising/decision making/problem solving. Difficulty following steps/instructions Slower thought speed (Often overlaps with symptoms of Alzheimer’s)

Answer 613

Characterised by alpha-synuclein deposits in the brain. Cause is unknown.

Answer 614

Early stages – hallucinations and delusions, mood swings/ short tempered, short attention span, fluctuating alertness. Late stages – Motor deterioration, similar to Parkinson’s.

Answer 615

Different Variants: - Behavioural (2/3) - Progressive non-fluent aphasia - Semantic dementia Symptoms of behavioural variant: - Loss of inhibition – rude and compulsive - Personality changes – loss of interest in people, loss of sympapthy/empathy - Crave food – often sweet/fatty, eat until vomit. - Speech, language difficulties - (A cognitive deficit is not so obvious).

Answer 616

- Wernicke-Korsakoff Syndrome - Down’s Syndrome - Huntington’s - Multiple Sclerosis - Parkinson’s Disease Dementia - Creuzfeldt-Jakob disease - Pugilistic Dementia (repetitive head trauma).

Answer 617

Detailed History (often collateral) => Duration of Sx, effects on ADLs => r/o dementia mimics – e.g. delirium/depression Physical examination => CNS/PNS, gait, CVS, thyroid. Blood tests +/- lumbar puncture => “Confusion bloods” = FBC, CRP, U&E, LFT, TFT, glucose, calcium, B12, folate. Medication Review => Look for any correlation of medications and duration of symptoms Cognitive tests – e.g. MMSE/MOCA CT/MRI => To exclude other causes.

Answer 618

= FBC, CRP, U&E, LFT, TFT, glucose, calcium, B12, folate.

Answer 619

There is NO CURE – eventually progresses to dependence and palliative care. 1. Referral to Psychiatric Services => Memory clinic, Rapid response Liaison Psychiatry (RRLP) 2. Pharmacological – alleviate symptoms/slow progression 3. Non-pharmacological - Social services care plan - OT input - Consider capacity – organise ADs/LPAs/DNACPRs while the patient still has capacity. - Cognitive Stimulation Therapy – may slow decline.

Answer 620

Cholinesterase Inhibitors – e.g. donepezil, rivastigmine, galantamine. => Alzheimer’s, LBD and Parkinson’s (mild-moderate disease). NMDA Receptor Antagonists – e.g. Memantine => Alzheimer’s only (moderate-severe disease). NB – there is no treatment for vascular/FT dementia. For behavioural/psychological symptoms, consider – anti-depressants, antipsychotics, laxatives, analgesia.

Answer 621

can drive a car as long as they have hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. They are required to check their blood glucose levels every 2 hours when driving.

Medicine 1 Flashcards

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