Practice Paper 1

Question 1

Which 3 events are acute coronary syndromes?

Answer 1

STEMI
NSTEMI
Unstable Angina

Question 2

What is the aetiology of ACS?

Answer 2

Atherosclerosis

Question 3

What is the mechanism involved in STEMI and NSTEMI?

Answer 3

Stenosed coronary arteries starving the myocardium of oxygen leading to - hypoxic cell death (myocardial infarctions)

Question 4

What is the mechanism involved in unstable angina?

Answer 4

Stenosed coronary arteries starving the myocardium of oxygen

Question 5

How is unstable angina defined?

Answer 5

When rest is no longer adequate to replenish the myocardium with o2.

Question 6

What usually causes acute coronary stenoses?

Answer 6

Usually caused by intimal plaque rupture leading to an intraluminal thrombus

Question 7

What dose of aspiring is given acutely?

Answer 7

300mg

Question 8

How do statins help in the chronic coronary disease patient?

Answer 8

Statins prophylactically lower serum cholesterol and so it its though to reduce plaque formation in the first place

Question 9

Why are beta-blockers and ACEi used in coronary diseases?

Answer 9

They reduce the hearts after-load and the hearts heart rate so the heart does not have to work as hard - this lowers its o2 demand hopefully to prevent hypoxic damage.

Question 10

What would be consistent with Lung collapse on the right upper zone during physical examination?

Answer 10

Reduced breath sounds
Dullness to percussion on affected side
Trachea deviation TOWARDS affected side

Question 11

What is the management of life threatening asthma?

Answer 11

High flow o2 - to get o2sats up
Nebulizers with salbutamol
Steroids oral or iv
IV magnesium sulphate (bronchodilation effect) given if the previous steps had a poor response

Near fatal asthma:
call senior help
IV aminophyline
ITU + Intubate

Question 12

What is a random collapse in a young footballer most likely to be?

Answer 12

Hypertrophic obstructive cardiomyopathy (HOCM)

A congenital disease of the myocardium. The left ventricular myocardium becomes so thick that the outflow tract becomes restricted.
The restricted is mechanically exacerbated by the muscular systolic contraction generated by vigorous exercise.
Hence hard exercise leads to a fall off in output which leads to syncope.
Sufferers are vulnerable to sudden death of which there may be a family history as the disease is autosomal dominant.

Question 13

What would a Hallpike manouevre show to diagnose BPPV?

Answer 13

Delayed onset (a few seconds) torsional nystagmus on descent facing one side only

Question 14

What is a very common cause of diarrhoea symptoms post-hospitalisation?
Tell us more about the bug causing this.

Answer 14

Clostridium difficile infection.

C diff is a major cause of antibiotic-association diarrhoa and hospital morbidity.
Its gram positive commensal bacterium that proliferates with the use of AB.
Specifically broad spectrum antibiotics - (3rd generation cephalosporins)
It produces enterotoxin A and B that cause severe inflammarion of the mucosa and formation of thick fibrous bands in the isntestine.

MX: manage patients fluid and electrolyte balance and prescribe metronidazole or vancomycin.

prevention is key, beware of elderly and hand wash (c diff isnt killed with alcohol hand gel)

Question 15

How does one present with malaria?

Answer 15

Recent travel in africa (tropical countries)

Headaches, fever, flu like symptoms, muscle aches, rigoring

Question 16

What are appropriate investigations for malaria?

Answer 16

Thick/Thin blood film *
Bloods
U&E LFT ABG

Question 17

What does a regularly prolonged PR interval suggest on an ECG?

Answer 17

1st degree heart block

Question 18

Which conditions is associated with UC?

Answer 18

Sclerosing Cholangitis

A condition causing inflammation, fibrosis and stricutre formation of the bile ducts leadgint to cholestasis and eventual cirrhosis

Question 19

What is status epilepticus?

Answer 19

A full body seizure lasting more than 30 mins

Question 20

How do you manage status epilepticus?

Answer 20

ABC approach
Check glucose
Give IV lorazepam or diazepam and repeat again
Consider IV phenytoin if previous steps dont work
Then consider general anesthesia and intubation

Treat the cause: Hypoglycamia, Hyponatremia

** OFTEN CAUSED BY DECREASED COMPLIANCE WITH ANTI-EPILEPTIC MEDICATION IN KNOWN EPILEPTICS ** –> so check blood levels of phenytoin

Question 21

What past medical history aspect would strongly point towards mitral stenosis?

Answer 21

A history of recurrent rheumatic fever would reinforce this diagnosis.

Question 22

How does mitral valve stenosis work?

Answer 22

It restricts the onward flow of freshly oxygenated blood from the lungs.
This back pressure causes pulmonary oedema (inspiratory crackles and frothy pink-white sputum)

Question 23

What signs will you find on examination?

Answer 23

Inspiratory crackles
Frothy pink-white sputum
Loud S1 (due to the mitral valve leaflets shutting abruptly at the start of a systole)
Mid diastolic murmur (turbulent flow of blood through the restricted opening)
Malar flush (possibly)

Question 24

Why is rheumatic fever and mitral valve stenosis associated with each other?

Answer 24

The antibodies formed against the bacterial carbohydrate cell wall cross-react with antigens in the heart, joints, and skin in a process known as molecular mimicry
The immune response in the heart causes myocarditis, pericarditis and endocarditis resulting in valve destruction conduction defects arrhythmia and congestive cardiac failure.

Question 25

What are common causes of aortic regurg?

Answer 25

``` Aortic valve leaflet abnormalities or damage o Bicuspid aortic valve o Infective endocarditis o Rheumatic fever o Trauma Aortic root/ascending aorta dilatation o Systemic hypertension o Aortic dissection o Aortitis o Arthritides (e.g. rheumatoid arthritis, seronegative arthritides) o Connective tissue disease (e.g. Marfan's, EhlersMDanlos) o Pseudoxanthoma elasticum o Osteogenesis imperfecta ```

Question 26

Signs of aortic regurg on examination?

Answer 26

• Collapsing (water-hammer) pulse • Wide pulse pressure • Thrusting and heaving displaced apex beat • Early diastolic murmur over the aortic valve region o Heard better at the left sternal edge when the patient is sitting forward with the breath held at the top of expiration • NOTE: an ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume) • Austin Flint mid-diastolic murmur o Heard over the apex o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis

Question 27

What is a fluid challenge?

Answer 27

A fluid challenge is the rapid administration of a bolus of fluid

Question 28

What are the presenting symptoms of coeliac disease?

Answer 28

Steatorrhoea Abdominal discomfort (bloating) Diarrhoea Malaise Young adults with no recent travel (suggesting infection)

Question 29

What does the left anterior descending coronary artery usually supply?

Answer 29

The anterior wall of the left ventricle and the inter-ventricular septum

Question 30

Where does the left anterior descending coronary artery arise from?

Answer 30

The left coronary artery | so does the circumflex artery

Question 31

What does the circumflex artery supply?

Answer 31

The posterior and lateral sides of the left centricle

Question 32

What does the right coronary artery supply?

Answer 32

The SAN and AVN and right ventricle and inferior part of the left ventricle

Question 33

When should ACEi be avoided?

Answer 33

Renal artery stenosis This is because angiotensins normally increases folmerular capillary perfusion pressure and so when ACEi reduce this ability with a background of already grossly reduced renal perfusion the GFR will fall. Hence avoid ACEi in renal failure patients.

Question 34

What morphology is Staph aureus?

Answer 34

Gram + cocci

Question 35

How does a basal cell carcinoma clasically present?

Answer 35

``` Rolled edge Pearly appearance Telangiecstasia History of sun exposure slow growing ```

Question 36

How do Squamous CC appear?

Answer 36

ill defined keratotic nodules often ulcerate faster growing than bcc RF are the same as BCC

Question 37

How do keratoacanthomas classically present?

Answer 37

Rapidly growing benign tumours that often mimic squamous cell carcinomas. Can become quite large and typically develop a central ulceration and necrosis pattern.

Question 38

How will a biliary colic clasically present?

Answer 38

``` X-month history of intermittent RUQ pain Sharp Radiates to back No other findings on examination Normal LFT's Normal amylase No history of foreign travel (ie; no hep) ``` NOTE: its not a colicky pain its CONstant 5 F's (fat, forty, female, fair, fertile)

Question 39

What are the presenting symptoms of Ankylosing Spondylitis?

Answer 39

Young male Several month history of lower back pain and stifness WORSE IN THE MORNING BETTER WITH EXERCISE Asymmetrical peripheral arthritis symptoms

Question 40

How do you diagnose ankylosing spondylitis on examination?

Answer 40

Schobers test: 2 fingers are places 10 cm apart on the lower back (5cm below and above L5) Then ask patient to flex = This should result in an increase of more than 5cm - this indicates spinal stiffness

Question 41

Define Ankylosing spondylitis

Answer 41

Seronegative inflammatory arthropathy affecting preferentially the axial skeletal and large proximal joints seronegative = lack of rheumatoid factor

Question 42

What are the 5 extra-articular features associated with AS?

Answer 42

``` 5 A's = Apical lung fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis (plantar fasciitis) Amyloidosis ```

Question 43

What results do you expect on an Xray of AS?

Answer 43

Sacroilitis Erosion of the corners of the vertebral bodies "Romans lesions" Bony spurs Calcification of spinal ligaments "Bamboo spine"

Question 44

What is the management of AS?

Answer 44

Physio Exercise Nsaids (slow releasing)

Question 45

With which genotype is AS associated with?

Answer 45

HLA-B27

Question 46

What are the findings of mitral stenosis on examination?

Answer 46

Tapping apex beat Peripheral cyanosis Mid-diastolic murmur Bifid P wave on ECG

Question 47

What is mitral stenosis pathophysiology?

Answer 47

It occurs as a result of chronic autoimmune attack on the mitral valves This leads to scar tissue formation which ultimately tethers the leaflets and prevents them from opening fully.

Question 48

What is a trigger for mitral stenosis?

Answer 48

Rheumatic fever (group A streptococcus) antibodies cross react with endocardial tissue.

Question 49

How does mitral stenosis result in cyanosis?

Answer 49

It leads to reduced CO hence peripheral cyanosis

Question 50

Why is there a tapping apex beat in mitral stenosis?

Answer 50

because of the increased force in closing the mitral valve

Question 51

How does Bells palsy usually present?

Answer 51

A few days history of one sided facial weakness. Patient is otherwise fit and well with no history of neurological symptoms No history of preceding infection On examination everything else is normal The forehead is NOT spared. Neurological examination of the limbs is unremarkable Routine investigations are normal

Question 52

What is the most appropriate management plan for Bels palsy?

Answer 52

• Protection of cornea with protective glasses/patches or artificial tears • High-dose corticosteroids is useful within 72 hrs o Only given if Ramsey-Hunt Syndrome is excluded • Surgery - lateral tarsorrhaphy (suturing the lateral parts of the eyelids together) o Performed if imminent or established corneal damage Since there is a possible viral aetiology = antiviral therapy

Question 53

Define Bels palsy

Answer 53

• Idiopathic lower motor neurone facial nerve palsy * IDIOPATHIC * 60% are preceded by an upper respiratory tract infection * This suggests that it has a viral or post-viral aetiology

Question 54

What is bells phenomenon

Answer 54

o Eyeball rolls up but the eye remains open when trying to close their eyes

Question 55

What does forehead sparing or NON-sparing indicate?

Answer 55

Upper motor neuron lesions, such as a stroke, cause contralateral face weakness SPARING the forehead. Lower motor neuron lesions, such as a facial nerve injury, typically cause weakness involving the whole ipsilateral face and are NON-sparing.

Question 56

What is a dangerous complication of Bels palsy

Answer 56

Corneal abrasions - can happen especially during sleep | = eye protection.

Question 57

Define multiple myeloma

Answer 57

There is malignant proliferation of PLASMA cells that secrete monoclonal AB's and light iG chains resulting in bone lesions.

Question 58

How does multiple myeloma present?

Answer 58

``` It's a multi system disease that may present with lethargy bone pain pathological fracture renal failure amyloidosis pancytopenia marrow infiltration ``` • Bone Pain o Usually in the back and ribs o Sudden and severe bone pain may be caused by a pathological fracture • Infections - which are often recurrent ``` • General o Tiredness o Thirst o Polyuria o Nausea o Constipation o Mental change (due to hypercalcaemia) ``` • Hyperviscosity o Bleeding o Headaches o Visual disturbance

Question 59

Whats the aetiology of multiple myeloma?

Answer 59

UNKOWN | possible viral trigger

Question 60

What are the signs of multiple myeloma on examination?

Answer 60

* Pallor * Tachycardia * Flow murmur * Signs of heart failure * Dehydration * Purpura * Hepatosplenomegaly * Macroglossia * Carpal tunnel syndrome * Peripheral neuropathies

Question 61

What are appropriate investigations of multiple myeloma?

Answer 61

• Bloods o FBC M low Hb, normochromic normocytic o High ESR (and possible high CRP) o U&Es M high creatinine, high Ca2+ o Normal ALP • Blood Film o Rouleaux formation with bluish background (suggests high protein) • Serum or Urine Electrophoresis o Serum paraprotein o Bence-Jones protein (monoclonal immunoglobulin light chain that's found in the urine and suggests multiple myeloma) • Bone Marrow Aspirate and Trephine o High plasma cells (usually > 20%) • Chest, Pelvic or Vertebral X-Ray o Osteolytic lesions without surrounding sclerosis o Pathological fractures

Question 62

Define HIV

Answer 62

• Infection with the human immunodeficiency virus (HIV)

Question 63

What is the aetiology and risk factors of HIV?

Answer 63

• HIV is transmitted by: o Sexual intercourse • Heterosexual intercourse is the MOST COMMON mode of transmission • Homosexuals are at greater risk in the West o Blood (and other bodily fluids) • Mother to child (intrauterine, childbirth, breastfeeding) • Needles • Blood transfusions • Organ transplantation

Question 64

What is the pathophysiology of HIV?

Answer 64

o HIV enters CD4+ lymphocytes by binding to their gp120 receptors o Reverse transcriptase allows the incorporation of HIV genetic material into the host genome o This leads to dissemination of HIV, cell death and eventual T-cell depletion

Question 65

What is the epidemiology of HIV?

Answer 65

Increasing in Africa and Asia

Question 66

What are the 3 phases of HIV?

Answer 66

• There are THREE phases of HIV: ``` SEROCONVERSION: • Self- limiting • Fever • Night sweats • Generalised lymphadenopathy • Sore throat • Others: oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea ``` EARLY ASYMPTOMATIC: • Apparently well • Some may have persistent lymphadenopathy • Progressive minor symptoms (e.g. rash, oral thrush, weight loss) AIDS • Syndrome of secondary diseases resulting from immunodeficiency

Question 67

What are the effects of HIV infection?

Answer 67

o Neurological: polyneuropathy, dementia o Lung: lymphocytic interstitial pneumonitis o Heart: cardiomyopathy, myocarditis o Haematological: anaemia, thrombocytopaenia o GI: anorexia, wasting o Eyes: cotton wool spots

Question 68

What are the secondary effects of HIV infection?

Answer 68

o Bacterial Infection: TB, skin infections, pneumococcal infections o Viral: CMV, HSV, VZV, HPV, EBV o Fungal: pneumocystic jirovecii pneumonia, Cryptococcus, candidiasis, invasive aspergillosis o Protozoal: toxoplasmosis, cryptosporidia o Tumours: Kaposi sarcoma, SCC, nonMHogkin's lymphoma, Hodgkin's lymphoma

Question 69

What are the appropriate investigations for HIV infection?

Answer 69

HIV TESTING: o HIV antibodies, PCR for viral RNA, CD4 count, viral load OTHERS: o Pneumocystic pneumonia - CXR o Cryptococcal meningitis - brain CT or MRI, LP o CMV (colitis) - colonoscopy and biopsy o Toxoplasmosis - brain CT or MRI o Cryptosporidia - stool microscopy

Question 70

Define achalasia

Answer 70

• A condition in which the normal muscular activity of the oesophagus is disturbed (absent or uncoordinated) due to FAILURE OR INCOMPLETE RELAXATION OF THE LOWER OESOPHAGEAL SPHINCTER.

Question 71

What causes achalasia?

Answer 71

Degeneration of the ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause.

Question 72

What is Chagas disease?

Answer 72

Oesophageal infection with Trypanosoma cruzi seen in Central/South America produces a similar disorder

Question 73

What are the PC of achalasia?

Answer 73

* Intermittent dysphagia involving solids and liquids * Difficulty belching * Regurgitation (particularly at night) * Heartburn * Chest pain (atypical/cramping, retrosternal) * Weight loss (because they are eating less)

Question 74

What are the appropriate investigations for achalasia?

Answer 74

CXR: o Widened mediastinum o Double right heart border (dilated oesophagus) o Air-fluid level in the upper chest o Absence of the normal gastric air bubble BARIUM SWALLOW: o Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped) ENDOSCOPY to exclude malignancy (which could mimic achalasia) MANOMETRY (used to assess pressure at the LOS) may show: o Elevated resting LOS pressure (> 45 mm Hg) o Incomplete LOS relaxation o Absence of peristalsis in the smooth muscle portion of the oesophagus • NOTE: you may do serology for antibodies against T. cruzi if CHAGAS DISEASE is a possibility (and blood film may detect parasites)

Question 75

Define thalassaemia

Answer 75

• A group of genetic disorders characterised by reduced globin chain synthesis

Question 76

Explain the aetiology of thalassaemia

Answer 76

* Autosomal recessive * Result in an imbalance of globin chain production and deposition in erythroblasts and erythrocytes ``` • This leads to: o Ineffective erythropoiesis o Haemolysis o Anaemia o Extramedullary haematopoiesis ```

Question 77

What are the types of thalassaemia?

Answer 77

ALPHA THALASSEMIA Reduction in alpha-globin chain synthesis. There are FOUR alpha-globin genes on the chromosome. • 4 gene deletion = Haemoglobin Barts Hydrops Fetalis (intrauterine death) • 3 gene deletion = Haemoglobin H --> microcytic hypochromic anaemia and splenomegaly • 2 gene deletion = Alpha - thalassemia --> microcytic hypochromic red cells, NO ANAEMIA • 1 gene deletion = Alpha+ thalassemia --> microcytic hypochromic red cells, NO ANAEMIA BETA THALASSEMIA • Beta Thalassemia Major (homozygous beta thalassemia) --> little or no beta-chain synthesis • Beta Thalassemia Intermedia - mild defect in beta-chain synthesis leads to: ! Microcytic anaemia ! Reduced alpha-chain synthesis ! Increased gamma-chain synthesis • Beta Thalassemia Trait (heterozygous carrier state) ! ASYMPTOMATIC ! Mild microcytic anaemia ! Increased red cell count

Question 78

What is thalassemia epidemiology

Answer 78

* WORLDWIDE | * Most common in the MEDITERRANEAN and areas of the MiddleEast

Question 79

What are the presenting symptoms of thalassaemia?

Answer 79

``` Beta Thalassemia Major o Anaemia o Presenting at 3-6 months • This is when the change from HbF to HbA takes place • Failure to thrive • Prone to infection ``` Alpha or Beta Thalassemia Trait o May be ASYMPTOMATIC o Detected during routine blood tests or due to family history

Question 80

Signs of thalassemia on examination

Answer 80

``` Beta Thalassemia Major o Pallor o Malaise o Dyspnoea o Mild jaundice o Frontal bossing o Thalassaemia facies (facial features caused by marrow hyperplasia) o Hepatosplenomegaly (due to erythrocyte pooling and extramedullary haematopoiesis) ``` Patients with beta-thalassemia INTERMEDIA may also have these signs

Question 81

Appropriate investigations for thalassaemia

Answer 81

``` BLOODS o FBC • Low Hb • Low MCV (microcytic anaemia) • Low MCH ``` ``` BLOOD FILM o Hypochromic microcytic anaemia o Target cells o Nucleated red cells o High reticulocyte count HB ELECTROPHORESIS o Absent or reduced HbA o High HbF ``` BONE MARROW o Hypercellular o Erythroid hyperplasia GENETIC TESTING (rarely used) SKULL XRAY o 'Hair on end' appearance in beta thalassemia major • This is caused by expansion of marrow into the cortex

Question 82

Define septic arthritis

Answer 82

Infection of one or more joints caused by pathogenic bacteria.

Question 83

Whats the aetiology of septic arthritis

Answer 83

Direct bacterial inoculation | Haematogenous spread

Question 84

What are the RF for septic arthritis

Answer 84

Pre-existing joint disease (e.g. RA) Immunosuppression (e.g. DM, iatrogenic) Prosthetic joints IVDU

Question 85

How does a patient typically present with septic arthritis?

Answer 85

Previously fit and well pt (or immunosupressed) Limps into emergency room Acutely red, hot, swollen, very tender knee Tachycardic Febrile This presentation of acute monoarthritis and systemic signs suggestive of infection is septic arthritis until proven otherwise.

Question 86

How do you manage and investigate septic arthritis?

Answer 86

Urgent joint aspiration: Gram stain & culture White blood cell count (also to relive pressure) Bloods: ESR/CRP, WCC, Blood cultures Imaging: X-ray, MRI Manage: Start on IV AB's stat. Analgesia Consider joint washout under GA

Question 87

Which organisms commonly cause septic arthritis?

Answer 87

``` Staphylococcus aureus (60%) Neisseria gonorrhoea (in young sexually active - (**BUZZ**) ```

Question 88

Which drugs can cause opiate overdose?

Answer 88

``` o Codeine o Diamorphine o Dihydrocodeine o Fentanyl o Loperamide o Methadone o Morphine ```

Question 89

How does a patient typically present with opiate overdose?

Answer 89

``` • Constipation (if chronic) • Nausea and vomiting • Loss of appetite • Sedation • Craving the next dose • Drowsiness (if acute overdose) OR FOUND UNRESPONSIVE ```

Question 90

What are the signs on physical examination of opiate overdose?

Answer 90

* Respiratory depression * Hypotension and tachycardia * Pinpoint pupils

Question 91

Identify appropriate investigations for opiate overdose

Answer 91

* Toxicology screen * Paracetamol blood level (should be considered in patients who have self-poisoned) * If in doubt, give a small test dose of NALOXONE