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GET AHEAD medicine > Practice Paper 1 > Flashcards

Practice Paper 1 Flashcards

1
Q

Which 3 events are acute coronary syndromes?

A

STEMI
NSTEMI
Unstable Angina

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2
Q

What is the aetiology of ACS?

A

Atherosclerosis

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3
Q

What is the mechanism involved in STEMI and NSTEMI?

A

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

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4
Q

What is the mechanism involved in unstable angina?

A

Stenosed coronary arteries starving the myocardium of oxygen

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5
Q

How is unstable angina defined?

A

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

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6
Q

What usually causes acute coronary stenoses?

A

Usually caused by intimal plaque rupture leading to an intraluminal thrombus

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7
Q

What dose of aspiring is given acutely?

A

300mg

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8
Q

How do statins help in the chronic coronary disease patient?

A

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

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9
Q

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

A

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.

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10
Q

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

A

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

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11
Q

What is the management of life threatening asthma?

A

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

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12
Q

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

A

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.

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13
Q

What would a Hallpike manouevre show to diagnose BPPV?

A

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

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14
Q

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

A

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)

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15
Q

How does one present with malaria?

A

Recent travel in africa (tropical countries)

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

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16
Q

What are appropriate investigations for malaria?

A

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

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17
Q

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

A

1st degree heart block

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18
Q

Which conditions is associated with UC?

A

Sclerosing Cholangitis

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

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19
Q

What is status epilepticus?

A

A full body seizure lasting more than 30 mins

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20
Q

How do you manage status epilepticus?

A

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

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21
Q

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

A

A history of recurrent rheumatic fever would reinforce this diagnosis.

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22
Q

How does mitral valve stenosis work?

A

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)

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23
Q

What signs will you find on examination?

A

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)

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24
Q

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

A

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.

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25
Q

What are common causes of aortic regurg?

A 
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
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26
Q

Signs of aortic regurg on examination?

A

• 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

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27
Q

What is a fluid challenge?

A

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

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28
Q

What are the presenting symptoms of coeliac disease?

A

Steatorrhoea
Abdominal discomfort (bloating)
Diarrhoea
Malaise

Young adults with no recent travel (suggesting infection)

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29
Q

What does the left anterior descending coronary artery usually supply?

A

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

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30
Q

Where does the left anterior descending coronary artery arise from?

A

The left coronary artery

so does the circumflex artery

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31
Q

What does the circumflex artery supply?

A

The posterior and lateral sides of the left centricle

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32
Q

What does the right coronary artery supply?

A

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

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33
Q

When should ACEi be avoided?

A

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.

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34
Q

What morphology is Staph aureus?

A

Gram + cocci

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35
Q

How does a basal cell carcinoma clasically present?

A 
Rolled edge
Pearly appearance
Telangiecstasia
History of sun exposure
slow growing
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36
Q

How do Squamous CC appear?

A

ill defined
keratotic nodules
often ulcerate
faster growing than bcc

RF are the same as BCC

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37
Q

How do keratoacanthomas classically present?

A

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

38
Q

How will a biliary colic clasically present?

A 
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)

39
Q

What are the presenting symptoms of Ankylosing Spondylitis?

A

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

40
Q

How do you diagnose ankylosing spondylitis on examination?

A

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

41
Q

Define Ankylosing spondylitis

A

Seronegative inflammatory arthropathy affecting preferentially the axial skeletal and large proximal joints

seronegative = lack of rheumatoid factor

42
Q

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

A 
5 A's = 
Apical lung fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis (plantar fasciitis)
Amyloidosis
43
Q

What results do you expect on an Xray of AS?

A

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

44
Q

What is the management of AS?

A

Physio
Exercise
Nsaids (slow releasing)

45
Q

With which genotype is AS associated with?

A

HLA-B27

46
Q

What are the findings of mitral stenosis on examination?

A

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

47
Q

What is mitral stenosis pathophysiology?

A

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.

48
Q

What is a trigger for mitral stenosis?

A

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

49
Q

How does mitral stenosis result in cyanosis?

A

It leads to reduced CO hence peripheral cyanosis

50
Q

Why is there a tapping apex beat in mitral stenosis?

A

because of the increased force in closing the mitral valve

51
Q

How does Bells palsy usually present?

A

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

52
Q

What is the most appropriate management plan for Bels palsy?

A

• 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

53
Q

Define Bels palsy

A

• 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
54
Q

What is bells phenomenon

A

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

55
Q

What does forehead sparing or NON-sparing indicate?

A

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.

56
Q

What is a dangerous complication of Bels palsy

A

Corneal abrasions - can happen especially during sleep

= eye protection.

57
Q

Define multiple myeloma

A

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

58
Q

How does multiple myeloma present?

A 
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

59
Q

Whats the aetiology of multiple myeloma?

A

UNKOWN

possible viral trigger

60
Q

What are the signs of multiple myeloma on examination?

A
  • Pallor
  • Tachycardia
  • Flow murmur
  • Signs of heart failure
  • Dehydration
  • Purpura
  • Hepatosplenomegaly
  • Macroglossia
  • Carpal tunnel syndrome
  • Peripheral neuropathies
61
Q

What are appropriate investigations of multiple myeloma?

A

• 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

62
Q

Define HIV

A

• Infection with the human immunodeficiency virus (HIV)

63
Q

What is the aetiology and risk factors of HIV?

A

• 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

64
Q

What is the pathophysiology of HIV?

A

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

65
Q

What is the epidemiology of HIV?

A

Increasing in Africa and Asia

66
Q

What are the 3 phases of HIV?

A

• 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

67
Q

What are the effects of HIV infection?

A

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

68
Q

What are the secondary effects of HIV infection?

A

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

69
Q

What are the appropriate investigations for HIV infection?

A

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

70
Q

Define achalasia

A

• 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.

71
Q

What causes achalasia?

A

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

72
Q

What is Chagas disease?

A

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

73
Q

What are the PC of achalasia?

A
  • 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)
74
Q

What are the appropriate investigations for achalasia?

A

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)

75
Q

Define thalassaemia

A

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

76
Q

Explain the aetiology of thalassaemia

A
  • 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
77
Q

What are the types of thalassaemia?

A

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

78
Q

What is thalassemia epidemiology

A
  • WORLDWIDE

* Most common in the MEDITERRANEAN and areas of the MiddleEast

79
Q

What are the presenting symptoms of thalassaemia?

A 
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

80
Q

Signs of thalassemia on examination

A 
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

81
Q

Appropriate investigations for thalassaemia

A 
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

82
Q

Define septic arthritis

A

Infection of one or more joints caused by pathogenic bacteria.

83
Q

Whats the aetiology of septic arthritis

A

Direct bacterial inoculation

Haematogenous spread

84
Q

What are the RF for septic arthritis

A

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

85
Q

How does a patient typically present with septic arthritis?

A

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.

86
Q

How do you manage and investigate septic arthritis?

A

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

87
Q

Which organisms commonly cause septic arthritis?

A 
Staphylococcus aureus (60%) 
Neisseria gonorrhoea (in young sexually active - (**BUZZ**)
88
Q

Which drugs can cause opiate overdose?

A 
o  Codeine  
o  Diamorphine   
o  Dihydrocodeine  
o  Fentanyl 
o  Loperamide  
o  Methadone  
o  Morphine
89
Q

How does a patient typically present with opiate overdose?

A 
•  Constipation (if chronic)  
•  Nausea and vomiting  
•  Loss of appetite 
•  Sedation 
•  Craving the next dose  
•  Drowsiness (if acute overdose)  
OR FOUND UNRESPONSIVE
90
Q

What are the signs on physical examination of opiate overdose?

A
  • Respiratory depression
  • Hypotension and tachycardia
  • Pinpoint pupils
91
Q

Identify appropriate investigations for opiate overdose

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

GET AHEAD medicine (6 decks)

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