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Phase 4 Mocks Medschool Flashcards

1
Q

What are common causes of hypoglycaemia ?

A
  • Insulinomas
  • Self-administration of insulin/Sulphonylureas
  • Liver failure
  • Addison’s disease
  • Alcohol
  • Nesidioblastosis (beta cell hyperplasia)
  • Critical illness e.g. sepsis
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2
Q

Which medications can cause hypoglycaemia ?

A
  • Insulin
  • Sulphonylureas e.g. gliclazide
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3
Q

What is the bodies physiological reaction to hypoglycaemia

A
  • Hormonal response  first response is decreased insulin secretion and increased glucagon secretion
  • Growth hormone and cortisol are released but later there is increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the peripheral autonomic nervous system in the central nervous system
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4
Q

What are features of hypoglycemia with a blood sugar <3.3 mol ?

A
  • Autonomic symptoms due to the release of glucagon and adrenaline
  • Sweating, shaking, anxiety, hunger and nausea
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5
Q

What are features of hypoglycemia with blood <2.8mmol

A
  • Weakness
  • Visual changes
  • Confusion
  • Dizziness
  • Severe = convulsions and coma
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6
Q

How could one check for possibility of deliberate excess exogenous insulin ?

A
  • Test C-peptide
  • Its production is absent from exogenous insulin
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7
Q

What would high insulin and high C-peptide suggest ?

A
  • Endogenous insulin production
  • Cause likely to be insulinoma/sulfonylurea use/abuse
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8
Q

What would high insulin and low C-peptide suggest ?

A
  • Exogenous insulin administration
  • Suggesting exogenous insulin overdose/fictitious disorder
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9
Q

What would low insulin and low C-peptide level suggest ?

A
  • Alcohol induced hypoglycemia
  • Critical illness e.g. sepsis
  • Adrenal insufficiency
  • Fasting/starvation
  • Growth hormone deficiency
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10
Q

Management of hypoglycaemia community

A
  • Oral glucose 10-20g liquid, gel or tablet
  • Hypokit can be prescribed containing a syringe and vial of glucagon for IM or SC injection
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11
Q

Management of hypoglycaemia

A
  • If patient is alert then oral glucose 10-20g should be used in liquid, gel or tablet form
  • Unable to swallow then SC or IM glucagon
  • IV glucose 20% 100ml over less than 15 mins
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12
Q

What condition will around 50% of patients with temporal arteritis also have ?

A
  • Polymyalgia rheumatica
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13
Q

Typical features of TA ?

A
  • Typically > 60 YO
  • Rapid onset
  • Headache
  • Jaw claudication
  • Reduced vision
  • Tender, palpable temporal artery
  • Lethargy, depression, low grade fever, anorexia, night sweats
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14
Q

What polymyalgia rheumatica symptoms could present in a patient with TA ?

A
  • Aching
  • Morning stiffness (but not weakness) in proximal limb
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15
Q

What investigations should be done in TA ?

A
  • Inflammatory markers i.e. CRP, ESR
  • Temporal artery biopsy/ultrasound
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16
Q

How is TA treated ?

A
  • High dose glucocorticoids – no visual loss then pred, if visual loss than IV methylprednisolone
  • Urgent ophthalmology review
  • (bisphosphonates are required due to long, tapering course of steroids required)
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17
Q
  1. How does trigeminal neuralgia present ?
A
  • Unilateral brief electric shock like pains with abrupt onset and termination limited to one or more divisions of the trigeminal nerve
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18
Q
  1. What can trigger pain in trigeminal neuralgia ?
A
  • Light touch including washing, shaving, smoking, talking and brushing teeth
  • Frequently occurs spontaneously
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19
Q
  1. What would one consider red flag symptoms in a potential trigeminal neuralgia presentation ?
A
  • Sensory changes
  • Ear/hearing problems
  • Hx of skin or oral lesions
  • Pain only in the ophthalmic division of the trigeminal nerve
  • Bilateral presentation
  • Optic neuritis
  • Fx of MS
  • Age < 40
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20
Q

Trigeminal neuralgia first line management

A
  • Carbamazepine
  • Failure to respond and/or atypical features should prompt referral to neurology
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21
Q

What condition do 5-10% of pts diagnosed with HTN also have ?

A
  • Primary hyperaldosteronism (including Conn’s)
  • Making it the most common cause of secondary HTN
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22
Q

Renal causes of secondary hypertension

A
  • Glomerulonephritis
  • Pyelonephritis
  • Acute polycystic kidney disease
  • Renal artery stenosis
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23
Q

Endocrine disorders that can lead in secondary hypertension

A
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Acromegaly
  • Congenital adrenal hyperplasia
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24
Q

Medications that can cause secondary HTN

A
  • Steroids
  • MOA-I
  • COCP
  • NSAIDs
  • Leflunomide
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25
Q

What features of a patients presentation would indicate a case more likely to be secondary hypertension ?

A
  • HTN occurs at a younger age with significantly elevated BP which is often resistant to medication
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26
Q
  1. What examination signs might suggest coarctation of the aorta ?
A
  • Radio-femoral delay
  • Left ventricular heave
  • Weak peripheral pulses in the legs
  • Ejection systolic murmur
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27
Q
  1. How could coarctation of the aorta be diagnosed ?
A
  • Echocardiography
  • CT aorta
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28
Q
  1. How would coarctation of the aorta be managed ?
A
  • Conventional open surgery
  • Ballon angioplasty and stent insertion
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29
Q
  1. What is the law that governs capacity ?
A
  • The Mental Capacity Act of 2005
  • Applies to all adults over the age of 16
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30
Q
  1. What are the 5 key principles of the capacity act ?
A
  • A person must be assumed to have capacity unless it is established that they lack capacity
  • A person should not be treated as unable to make a decision unless all practicable steps to help him to do so have not been taken without success
  • An unwise decision does not mean a person is unable to make a decision
  • An act or decision under this act for or on behalf of a person should be in their best interest
  • Before the act is done or the decision made regard must be taken to make the process as least restrictive of the person’s rights and freedom of action
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31
Q
  1. What must be tested for in a Capacity Assessment ?
A
  • He or she has an impairment or disturbance in the functioning of their mind or brain whether permanent or temporary AND
  • A. Can understand the information
  • B. Can retain the information
  • C. Can use or weight the information
  • D. Communicate the decision
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32
Q
  1. What must occur if a patient lacks capacity ?
A
  • A best interest decision must be made
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33
Q
  1. What must be considered when making a best interest decision ?
A
  • Whether a person is likely to regain capacity and can the decision wait
  • How to encourage and optimise the participation of the person in the decision
  • The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
  • Views of other relevant people
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34
Q
  1. What can be made by a person who could lose their capacity in the future ?
A
  • Lasting Power of Attorney (LPAs)
  • Can make health and welfare decisions and decisions about life-sustaining treatment if the LPA specifies that
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35
Q
  1. What is an advance decision ?
A
  • Can be drawn up by anybody specifying what specific treatments someone would like where they to loose capacity
  • Can be verbal unless they specify refusing life-sustaining treatment
  • ADs cannot demand treatment
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36
Q
  1. In a medical ward what actions could be considered a deprivation of liberty
A
  • Restraint
  • Sedation
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37
Q
  1. What are core requirements that need to be followed to ensure a Deprivation of Liberty Safeguard is valid
A
  • Avoid if possible
  • Act in the patients best interest
  • Only for the immediate intervention required
  • For as short as possible
  • Alternatives need to have been considered
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38
Q
  1. GMC good practice principles
A
  • Making the care of patients the first concern
  • Providing a good standard of practice and care, and working within competence
  • Working in partnership with patients and supporting them to make informed decisions about their care
  • Treating colleagues with respect and help to create an environment that is compassionate, supportive and fair
  • Acting with honesty and integrity and being open if things go wrong
  • Protecting and promoting the health of patients and the public
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39
Q
  1. What laws/acts are used to treat patients in emergency scenarios ?
A
  • Common law: used to treat patients in emergency scenarios
  • Mental Capacity Act: used to treat patients for a physical disorder e.g. delirium/sepsis
  • Mental Health Act: used in patients who require treatment for mental disorders (5(2), 2 or 3)
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40
Q
  1. What is a Section 2 for ?
A
  • Admission for assessment up to 28 days (cannot be removed)
  • Treatment may be given against the patients wishes
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41
Q
  1. Who can approve a Section 2 ?
A
  • An Approved Mental Health Professional (AMHP) or rarely the nearest relative (NR) makes the application on the recommendation of 2 doctors
  • One of the doctors should be approved under section 12(2) of the Mental Health Act (usually consultant psychiatrist)
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42
Q
  1. What is a Section 3 ?
A
  • Admission for treatment for up to 6 months that can be renewed
  • AMHP along with 2 doctors both of whom which must have seen the patient within the past 24 hours
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43
Q
  1. What is a Section 4 ?
A
  • 72 hour assessment order
  • Used as an emergency, when a section 2 would involve an unacceptable delay
  • A GP or AMHP or nearest relative
  • Often changed to Section 2 upon arrival at hospital
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44
Q
  1. What is a section 5(2) ?
A
  • A patient who is voluntary patient in hospital can be legally detained by a doctor for 72 hours
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45
Q
  1. What is a section 5(4) ?
A
  • Allows a nurse to detain a patient who is voluntarily in hospital for 6 hours
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46
Q
  1. What is a Section 17a ?
A
  • Supervised Community Treatment (Community Treatment Order)
  • Can be used to recall a patient to hospital for treatment if they do not comply with conditions of the order in the community, such as complying with medication
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47
Q
  1. What is a Section 135 ?
A
  • A order to obtained to allow the police to break into a property to remove a person to a Place of Safety
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48
Q
  1. What is a Section 136 ?
A
  • Someone found in a public place who appears to have a mental disorder can be taken by the police to a Place of Safety
  • Can only be used for up to 24 hours whilst a Mental Health Act assessment is arranged
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49
Q
  1. What surgical options are available for patients with severe peripheral artery disease ?
A
  • Angioplasty
  • Sent
  • Bypass graft surgery
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50
Q
  1. What symptoms would present if a patients bypass graft had occluded ?
A
  • Cool and pale foot
  • Absent pulse in graft
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51
Q
  1. How does compartment syndrome present ?
A
  • Swollen, tense and tender calf with a pink foot
  • Pain on dorsiflexion
  • Presence of a pulse does not rule out
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52
Q
  1. When can compartment syndrome occur ?
A
  • Fracture
  • Ischemia reperfusion injury in vascular patients
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53
Q
  1. Which injuries are commonly associated with compartment syndrome ?
A
  • Supracondylar fractures
  • Tibial shaft injuries
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54
Q
  1. How is compartment syndrome diagnosed ?
A
  • Measurement of intercompartmental pressure
  • Excess of 20mmHg are abnormal and >40mmHg is diagnostic
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55
Q
  1. What could be discussed to support and advice a patient with a new diagnosis of metastatic cancer ?
A
  • Sign post to spiritual care
  • Alternative therapies
  • Management of pain
  • Mental health support
  • Palliative care and end of life care
  • Advance directives
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56
Q
  1. What medications can be deprescribed in palliative care ?
A
  • Long term prophylaxis medications
  • Statins
  • Antihypertensives
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57
Q
  1. What can be prescribed in palliative care for agitation ?
A
  • Midazolam
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58
Q
  1. What can be prescribed for respiratory secretions ?
A
  • Hyoscine butylbromide
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59
Q
  1. What can be used to treat muscle spasm and spasticity in palliative care ?
A
  • Baclofen 1st line
  • Diazepam or midazolam 2nd line
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60
Q
  1. What could be prescribed for bowel colic/obstruction in palliative care ?
A
  • Hyoscine butylbromide
  • Also consider laxatives
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61
Q
  1. What can be used to treat constipation in palliative care ?
A
  • Stimulant laxatives e.g. Bisacodyl or Senna 1st line
  • Add osmotic laxatives e.g. macrogol 3350 or lactulose 2nd line
  • Add Docusate sodium 3rd line
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62
Q
  1. What can treat dysphagia in palliative care ?
A
  • Dexamethasone
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63
Q
  1. What should be prescribed for nausea and vomiting associated with gastric issues in palliative care ?
A
  • Metoclopramide 1st
  • Domperidone 2nd
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64
Q
  1. What can be prescribed for nausea and vomiting with chemical causes (hypercalcemia, morphine use or renal failure) in palliative care ?
A
  • Haloperidol
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65
Q
  1. What anti-emetic can be used in palliative care associated with raised intracranial pressure ?
A
  • Cyclizine (in conjunction with dexamethasone)
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66
Q
  1. What can haloperidol be used to treat in palliative care ?
A
  • Nausea and vomiting (associated with chemical causes)
  • Agitation/delirium
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67
Q
  1. What can be prescribed for patients with anxiety in palliative care ?
A
  • Months left to live – SSRIs
  • Weeks – diazepam or lorazepam
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68
Q
  1. What can be used to treat seizures in palliative care ?
A
  • Levetiracetam
  • Midazolam may be preferred in last days
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69
Q
  1. How can hiccups be treated in palliative care ?
A
  • Prokinetic e.g. Metoclopramide
  • Peppermint oil
  • PPI e.g. Lansoprazole
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70
Q
  1. What can help treat noisy respiratory secretions in a patients last days ?
A
  • Hyoscine butylbromide
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71
Q
  1. How could a malodourous fungating tumour be treated ?
A
  • Topical metronidazole in conjunction to systemic treatment
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72
Q
  1. How can pruritus be treated in palliative care ?
A
  • Emollients
  • Levomenthol if resistant
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73
Q
  1. What kind of sickle cell crisis’s can there be ?
A
  • Thrombotic ‘vaso-occlusive’ and ‘painful crises’
  • Acute chest syndrome
  • Anaemia (aplastic or sequestration)
  • Infection
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74
Q
  1. What can precede a thrombotic sickle cell crisis ?
A
  • Infection, dehydration, deoxygenation
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75
Q
  1. How is a thrombotic crisis diagnosed ?
A
  • Clinically – no specific test
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76
Q
  1. What is acute chest syndrome sickle cell crisis
A
  • Vaso-occlusion within the pulmonary microvasculature  Infarction in the lung parenchyma
  • Presents with dyspnoea, chest pain, pulmonary infiltrates on chest x-ray and low pO2
77
Q
  1. How is an acute chest syndrome sickle cell crisis treated ?
A
  • Pain relief
  • Respiratory support e.g. high flow oxygen
  • ABxs
  • Transfusion
78
Q
  1. What is an aplastic crises in sickle cell ?
A
  • Infection with parvovirus
  • Causing a sudden fall in haemoglobin
  • Bone marrow suppression causes a reduced reticulocyte count
79
Q
  1. What is a sequestration crises in sickle cell ?
A
  • Sickling within organs such as the spleen or lungs causing pooling of blood with worsening of anaemia
  • Associated with an increased reticulocyte count
80
Q
  1. General management of a sickle cell crisis
A
  • Analgesia e.g. opiates
  • Rehydrate and keep warm
  • Oxygen
  • Consider Abx
  • Blood transfusion if severe
  • Exchange transfusion if vaso-occlusive crisis (i.e. stroke, acute chest syndrome, multi-organ failure)
81
Q
  1. Long term management of sickle cell
A
  • Hydroxyurea
  • Pneumococcal polysaccharide vaccine every 5 years
82
Q
  1. What is ascites ?
A
  • An abnormal collection of fluid in the abdomen
83
Q
  1. What can cause ascites with a SAAG > 11g/L
A
  • Indicates portal hypertension
  • Liver disorders e.g. cirrhosis/alcoholic liver disease, acute liver failure and liver metastases
  • Cardiac – right heart failure or constrictive pericarditis
  • Other – Budd-Chiari syndrome, portal vein thrombosis, veno-occlusive disease or myxoedema
84
Q
  1. What can cause ascites with SAAG < 11g/L
A
  • Hypoalbuminemia e.g. nephrotic syndrome or severe malnutrition
  • Malignancy – peritoneal carcinomatosis
  • Infections – tuberculous peritonitis
  • Other – pancreatitis, bowel obstruction, biliary ascites
85
Q
  1. How is ascites managed ?
A
  • Reducing dietary sodium
  • Fluid restriction if sodium < 125
  • Aldosterone antagonist e.g. spironolactone
  • Often add loop diuretics e.g. furosemide
  • Drainage if tense ascites (with albumin cover)
  • Prophylactic antibiotics – oral ciprofloxacin if ascitic protein 15g/l
  • Transjugular intrahepatic portosystemic shunt in some patients
86
Q
  1. Which blood tests best examine synthetic liver function ?
A
  • INR
  • Albumin
87
Q
  1. Name potential causes for confusion in a patient with cirrhosis
A
  • Hepatic encephalopathy
  • Intracerebral bleed
  • Electrolyte or vitamin deficiency
  • Alcohol withdrawal (Wernicke’s encephalopathy)
  • Sepsis
  • Medication or intoxication
  • Spontaneous bacterial peritonitis
  • GI bleed
88
Q
  1. In audiograms what should the results be above on the x axis ?
89
Q
  1. In sensorineural hearing loss what type of hearing is impaired ?
A
  • Air and bone condition
90
Q
  1. In conductive hearing loss what type of hearing is impaired ?
A
  • Air conduction
91
Q
  1. How is Weber’s test performed ?
A
  • Strike the tunning fork
  • Place at centre of the patients forehead
  • Ask the patient if they can hear the sound and in which ear is it loudest
92
Q
  1. How will Weber’s test present in sensorineural hearing loss ?
A
  • Sound will be louder in the normal ear as it is better at sensing the sound
93
Q
  1. How will Weber’s test present in conductive hearing loss ?
A
  • The sound will be louder in the affected ear
  • When the tuning fork’s vibration is transmitted directly to the cochlea, rather than having to be conducted, the increased sensitivity makes it sound louder in the affected ear.
94
Q
  1. What does Weber’s Test test ?
A
  • Which ear is affected
  • Is it conductive hearing loss ?
95
Q
  1. How is Rinne’s Test Performed ?
A
  • Strike a tunning fork
  • Place the flat end on the mastoid process (tests boney conduction)
  • Ask the patient when they can no longer hear the noise
  • When yes move the tunning fork and hover 1cm from ear
  • Ask patient if they can now hear (tests air conduction)
96
Q
  1. What is a normal Rinne’s test ?
A
  • The pt can hear the sound when the fork is moved from the mastoid process to the ear
  • It is normal for air conduction to be better than bone conduction
  • This is Rinne’s positive
97
Q
  1. What is an abnormal Rinne’s test ?
A
  • When bone conduction is better than air conduction
  • This suggests a conductive cause for the hearing loss
  • Sound can still be transmitted through the bones whoever sound is less able to travel through the air, ear canal, tympanic membrane and middle ear to the cochlea due to a conductive problem
98
Q
  1. What are causes of sensorineural hearing loss ?
A
  • Presbycusis (age related)
  • Nosie exposure
  • Meniere’s disease
  • Labyrinthitis
  • Acoustic neuroma
  • Neurological conditions e.g. stroke, MS or brain tumour
  • Infections e.g. meningitis
  • Medications e.g. furosemide, gentamicin or chemo medications
99
Q
  1. What are causes of conductive hearing loss ?
A
  • Ear wax
  • Infection e.g. otitis media or otitis externa
  • Fluid in the middle ear
  • Eustachian tube dysfunction
  • Perforated tympanic membrane
  • Otosclerosis
  • Cholesteatoma
  • Exostoses
  • Tumours
100
Q
  1. How would a right sided labyrinthitis present on hearing tests ?
A
  • Labyrinthitis is a sensorineural hearing loss
  • Weber’s test = the tunning fork is heard loudest in the unaffected ear e.g. left ear
  • Rinne’s test will be normal in both ears
101
Q
  1. Which parts of the ear mediate conductive hearing ?
A
  • The outer and middle ear
102
Q
  1. Which part of the ear mediates sensorineural hearing loss ?
A
  • The inner ear
103
Q
  1. X-ray changes associated with osteoarthritis
A
  • LOSS
  • Loss of joint space
  • Osteophytes (bone spurs)
  • Subarticular sclerosis (increased density of the bone along the joint line)
  • Subchondral cysts (fluid-filled holes in the bone)
104
Q
  1. Hand signs of Osteoarthritis
A
  • Heberden’s nodes (DIP joints)
  • Bouchard’s nodes (PIP joints)
  • Squaring at the base of the thumb (CMC joint)
  • Weak grip
  • Reduced range of motion
105
Q
  1. Hand signs seen in advanced RA
A
  • Z-shaped deformity (thumb)
  • Swan neck deformity (hyperextended PIP and flexed DIP)
  • Boutonniere deformity (hyperextended DIP and flexed PIP)
  • Ulnar deviation if the fingers at the MCP joints
106
Q
  1. X-ray Changes in RA
A
  • Periarticular osteopenia
  • Boney erosions
  • Soft-tissue swelling
  • Joint destruction and deformity (in more advance disease)
107
Q
  1. How is C. difficle tested for ?
A
  • Stool sample for PCR/microscopy and culture
  • Also test stool sample for C.difficle toxin
108
Q
  1. List indications for ICU admission in a deteriorating patient with pneumonia
A
  • Respiratory or metabolic acidosis (pH < 7.26)
  • Persistent hypotension
  • PaO2 <8 despite inspire O2
  • PaCo2 >6.5
  • Serial ABGs indicating respiratory failure
  • Exhaustion, drowsiness, LOC
  • Evidence of septic shock
109
Q
  1. Management of low severity CAP
A
  • Amoxicillin 500 mg TDS for 5 days
  • Doxycycline or clarithromycin if pen allergy
110
Q
  1. Management of high severity CAP
A
  • Co-Amoxiclav
111
Q
  1. Moderate CAP with suspected atypical micro cause
A
  • Amoxicillin Plus
  • Clarithromycin (erythromycin if pregnancy)
112
Q
  1. What is the most common cause of hypercalcemia in outpatients ?
A
  • Primary hyperparathyroidism
113
Q
  1. What is the most common cause of primary hyperparathyroidism ?
A
  • Solitary adenoma (85%)
114
Q
  1. What is a good pneumonia for hypercalcemia ?
A
  • Bones, stones, groans and moans
115
Q
  1. How can hypercalcemia present ?
A
  • Polydipsia and polyuria
  • Depression
  • Anorexia, nausea and constipation
  • Peptic ulceration
  • Pancreatitis
  • Bone pain/fracture
  • Renal stones
  • Hypertension
116
Q
  1. How can primary hyperparathyroidism be investigated ?
A
  • Bloods – raised Ca2+, low phosphate, PTH may be raised or normal (if face of high Ca2+ this is abnormal)
  • Technetium-MIBI subtraction scan
  • X-ray – pepperpot skull, osteopenia
117
Q
  1. How is primary hyperparathyroidism managed ?
A
  • Definitive = total parathyroidectomy
  • Cinacalcet can be used if not suitable for surgery
118
Q
  1. How does hypercalcemia present ?
A
  • Bones, stones, groans and moans
  • Corneal calcification
  • Hypertension
  • Shortened QT interval on ECG
119
Q
  1. How does hypercalcemia present on ECG ?
A
  • Shortened QT interval on ECG
120
Q
  1. How is hypercalcemia managed ?
A
  • Rehydration with NaCl 1000ml 4 hours
  • Bisphosphonates can also be used after rehydration
121
Q
  1. How is hypercalcemia associated with malignancy managed ?
A
  • Calcitonin (salmon)
122
Q
  1. What are essential questions when taking a Hx for testicular torsion ?
A
  • Trauma
  • Sexual history
  • Urinary symptoms
  • Previous hx
  • Systemic symptoms
  • Speed of onset
123
Q
  1. What would one find on examination of a testicular torsion ?
A
  • Cord is most tender
  • Testical is retracted
  • Absence of cremasteric reflex
124
Q
  1. What is epididymis-orchitis ?
A
  • Infection of the epididymis +/- the testes resulting in pain and swelling
  • Most commonly caused by local spread of infections from the genital tract (Chlamydia trachomatis and Neisseria gonorrhoeae in young adults and E.coli in older adults)
125
Q
  1. What would one find on examination of epididymis-orchitis ?
A
  • Erythema and warmth
  • Involvement of the scrotal sac
  • Prehn’s sign (alleviation of scrotal pain by lifting the testical)
126
Q
  1. What is testicular torsion ?
A
  • The twisting of the spermatic cord resulting in testicular ischemia and necrosis
  • Most common in males between 10 and 30 with peak incidence 13-15 years
127
Q
  1. What are the presenting features of testicular torsion ?
A
  • Sudden onset severe pain which may referrer down to the lower abdomen
  • Nausea and vomiting
  • Swollen and tender testis retracted upwards
  • Loss of cremasteric reflex and no Prehn’s sign
128
Q
  1. What are features of Epididymo-orchitis ?
A
  • Unilateral testicular pain and swelling
  • Urethral discharge may be present but urethritis is often asymptomatic
  • Prehn’s sign
  • Cremasteric reflex present (lost in TT)
129
Q
  1. How is Epididymo-orchitis investigated ?
A
  • In younger patients assess for STI e.g. urethral swabs, NATT testing for GN
  • In older adults with low-risk sexual history send a mid-stream urine sample for culture
130
Q
  1. How is Epididymo-orchitis managed ?
A
  • Chlamydia – doxycycline 7 days course
  • Gonorrhea – IM ceftriaxone once
  • Enteric organism ofloxacin
131
Q
  1. What are DDs of peritonsillar abscess ?
A
  • Tonsilitis
  • Glandular fever
  • Tonsillar cancer
132
Q
  1. General symptoms of tonsillitis
A
  • Sore throat
  • Painful swallowing
  • Fever
  • Neck pain
  • Referred ear pain
  • Swollen tender lymph nodes
133
Q
  1. Specific signs that suggest peritonsillar abscess
A
  • Trismus (unable to open mouth)
  • Change in voice
  • Swelling and erythema in area beside tonsils
134
Q
  1. What causes trismus in peritonsillar abscess ?
A
  • Pus causes the pterygoid muscle to go into spasm preventing the opening of the mouth
135
Q
  1. What bacteria are associated with peritonsillar abscess ?
A
  • Streptococcus pyogenes (group A strep)
  • Staphylococcus aureus
  • Haemophilus infuenza
136
Q
  1. How are patients with peritonsillar abscess managed ?
A
  • Referral to hospital under ENT for needle aspiration or surgical incision and drainage
  • IV penicillin and metronidazole
  • ENT surgeons can use dexamethasone to settle inflammation
137
Q
  1. What are the components of a CURB 65 score ?
A
  • Confusion
  • Urea (>7mmol/L)
  • RR > 30
  • Systolic BP < 90 or diastolic < 60
  • Age >65
138
Q
  1. Risk factors for pyelonephritis
A
  • Female sex
  • Structural urological abnormalities
  • Vesico-ureteric reflux
  • DM
139
Q
  1. MCC of pyelonephritis
140
Q
  1. How is pyelonephritis investigated ?
A
  • Urine dipstick
  • Midstream urine for microscopy, culture and sensitivity testing is essential to establish causative organism
  • Blood tests – FBC and inflammatory markers
  • CT or ultrasound KUB
141
Q
  1. How is Pyelonephritis managed ?
A
  • Referral to hospital is symptoms of sepsis
  • 1st line = Abxs for 7-10 days
  • Absx Cefalexin, co-amoxiclav, trimethoprim or ciprofloxacin depending on cultures
142
Q
  1. What is the sepsis 6 ?
A
  • Out – lactate, blood cultures and urine output
  • In – oxygen, abxs, IV fluids
143
Q
  1. What could be DDs of pyelonephritis if pt does not respond to treatment ?
A
  • Renal abscess
  • Kidney stones
144
Q
  1. Causes of transudate effusion (< 30g/L protein)
A
  • HF
  • Hypoalbuminemia (liver disease, nephrotic syndrome, malabsorption)
  • Hypothyroidism
  • Meig’s syndrome (benign ovarian tumours (+ ascites)
145
Q
  1. Causes of exudate (> 30g/L protein)
A
  • MCC is pneumonia
  • TB
  • Connective tissue disease (RA, SLE)
  • Neoplasia e.g. lung cancer
  • Pancreatitis
  • PE
146
Q
  1. What tests should be performed on a exudate effusion fluid ?
A
  • Microscopy, culture, sensitivity and cytology
147
Q
  1. What investigations would you order for an exudate pleural effusion ?
A
  • CT thorax
  • Ultrasound guided biopsy
148
Q
  1. What question would you ask a 8 week pregnant pt with pain and bleeding ?
A
  • Bleeding volume
  • Bleeding colour e.g. fresh red or brown or dark
  • Intensity of pain
  • Location of pain
  • Pregnancy symptoms
149
Q
  1. What is a missed miscarriage ?
A
  • Fetus is no longer alive but no symptoms have occurred
150
Q
  1. What is a threatened miscarriage ?
A
  • Vaginal bleeding with closed cervix and a fetus that is alive
151
Q
  1. What is an inevitable miscarriage ?
A
  • Vaginal bleeding with an open cervix
152
Q
  1. What is an incomplete miscarriage ?
A
  • Retained products of conception remain in the uterus after the miscarriage
153
Q
  1. What is complete miscarriage ?
A
  • A full miscarriage has occurred and there are no products of conception left in the uterus
154
Q
  1. What is an anembryonic pregnancy ?
A
  • A gestational sac is present but contains no embryo
155
Q
  1. What are 3 key features looked at on a transvaginal US when investigating miscarriage ?
A
  • Mean gestational sac diameter
  • Fetal pole and crown-rump length
  • Fetal heartbeat
156
Q
  1. At what crown-rump length is a heartbeat expected ?
A
  • 7mm
  • If a heartbeat isn’t found in a 7mm pregnancy the scan is repeated after 1 week before confirming a non-viable pregnancy
157
Q
  1. When is a fetal pole expected ?
A
  • Once the mean gestational sac diameter is 25 mm or more
  • Once 25 mm or more without a fetal pole the scan is repeated after 1 week before confirming an anembryonic pregnancy
158
Q
  1. How is a potential miscarriage managed when less than 6 weeks ?
A
  • Expectantly managed (providing no pain or complications e.g. previous ectopic)
  • This means awaiting the miscarriage without investigation or treatment
  • Repeat urine pregnancy test after 7-10 days and if negative confirm miscarriage
159
Q
  1. How is a potential miscarriage managed when more than 6 weeks ?
A
  • Referral to an early pregnancy assessment service
  • Transvaginal US to confirm location and viability of pregnancy
  • 3 options expectant, medical or surgical management
160
Q
  1. When should a urine pregnancy test be performed post-expectant management decision ?
A
  • 3 weeks after bleeding and pain have settled
161
Q
  1. What does medical management of a missed miscarriage involve ?
A
  • Oral misoprostol (prostaglandin analogue)
  • 48 hours later vaginal, oral or sublingual misoprostol
162
Q
  1. How is a incomplete miscarriage medically managed ?
A
  • A single dose of misoprostol (vaginal, oral or sublingual)
163
Q
  1. How do prostaglandins works ?
A
  • Soften the cervix and stimulate uterine contractions
164
Q
  1. How can miscarriage be managed surgically ?
A
  • Vacuum aspiration (local as outpatient)
  • Surgical management (under GA in theatre)
165
Q
  1. Why is Rhesus status checked during the booking scan in pregnancy ?
A
  • If a Rh -ve mother delivers a Rh +ve child a leak of fetal red blood may occur
  • This causes anti-D IgG antibodies to form in the mother
  • In later pregnancies these can cross the placenta and cause haemolysis in fetus
  • Can also occur in the 1st pregnancy due to leaks
166
Q
  1. How is Rhesus negative mothers managed ?
A
  • NICE advises anti-D to non-sensitised Rh -ve mothers at 28 and 34 weeks
167
Q
  1. What are Rhesus sensitising events ?
A
  • Delivery of Rh +ve infant (alive or stillborn)
  • Any termination of pregnancy
  • Miscarriage if gestation > 12 weeks
  • Ectopic if managed surgically
  • External cephalic version
  • Antepartum haemorrhage
  • Amniocentesis, chronic villus sampling, fetal blood sampling
  • Abdominal trauma
168
Q
  1. What is the pathophysiology of hyperosmolar hyperglycemic state
A
  • ↑ serum osmolality → osmotic diuresis → severe volume depletion
169
Q
  1. What are precipitating factors for HHS ?
A
  • Intercurrent illness
  • Dementia
  • Sedative drugs
170
Q
  1. What is the timescale of the development of HHS ?
A
  • Days
  • Hence the metabolic and dehydration are worse than DKA
171
Q
  1. What is typically seen that would suggest HHS ?
A
  • Hypovolemia
  • Marked hyperglycemia (>30 mmol/L)
  • Significant raised serum osmolarity (> 320 mosmol/kg)
  • No significant hyperketonemia (<3 mmol/L)
  • No significant acidosis (bicarbonate > 15 or pH > 7.3)
172
Q
  1. How is serum osmolarity calculated ?
A
  • 2*Na + glucose + urea
173
Q
  1. How is HHS managed ?
A
  • NaCl 0.9% 0.5-1L/h
  • Monitor potassium
  • Insulin should not be given unless BM stops falling while giving IV fluids
  • VTE prophylaxis
174
Q
  1. How does hypokalemia present ?
A
  • Muscle weakness and hypotonia
  • On ECG – U waves, small or absent T waves, prolonged PR interval, ST depression and long GQ
175
Q
  1. What signs may present on physical examination of a patient with hypokalemia ?
A
  • Hypotension
  • Irregular pulse
  • Bradycardia or tachycardia
  • Hypoventilation
  • Lethargy
  • Muscle fasciculations, tetany, decreased muscle power, diminished tendon reflexes
  • Hypoactive bowel sounds
176
Q
  1. RFs for Hodgkin’s lymphoma
177
Q
  1. Classic features of Hodgkin’s lymphoma
A
  • Lymphadenopathy
  • B symptoms
  • Mediastinal lymphadenopathy on chest x-ray
178
Q
  1. How can Hodgkins lymphoma be investigated ?
A
  • Normocytic anaemia
  • Eosinophilia
  • LDH raised
  • Lymph node biopsy – Reed-Sternberg Cells
179
Q
  1. What physical signs may be found on physical examination of a patient with Hodgkin’s lymphoma ?
A
  • Cervical or axillary lymphadenopathy
  • Hepatosplenomegaly or splenomegaly
180
Q
  1. How does one convert from codeine to morphine ?
A
  • Divide by 10
181
Q
  1. How does one get from oral morphine to SC ?
A
  • Divide by 2
  • Then if need be calculate for 24 hours
182
Q
  1. What is the ‘double effect doctrine’
A
  • Sometimes it is permissible to cause a harm as a side effect of brining about a good result, provided the side effect was not the intended outcome
183
Q
  1. What pharmacological options are available to a pregnant patient in pain ?
A
  • Paracetamol
  • Codeine may be useful where paracetamol is not
  • Systemic NSAIDs are avoided from 20 weeks and contraindicated after 28 weeks
184
Q
  1. In the last weeks of pregnancy which drugs should be avoided and why ?
A
  • NSAIDs – risk of oligohydramnios
  • Opioids – risk of neonatal respiratory depression
185
Q
  1. What are the 4 common types of leukaemia
A
  • Acute myeloid leukaemia
  • Acute lymphoblastic leukaemia
  • Chronic myeloid leukaemia
  • Chronic lymphoblastic leukaemia
186
Q
  1. What is a key identifying feature of acute lymphoblastic leukaemia ?
A
  • Most common in children and is associated with Down syndrome
187
Q
  1. What is a key identifying feature of chronic lymphoblastic leukemia ?
A
  • Smudge cells
  • CLL can transform (Richter’s transformation) into a high-grade B cell lymphoma
  • Typically affects adults over 60 years
188
Q
  1. What is a key identifying feature of chronic myeloid leukemia ?
A
  • Philadelphia chromosome
189
Q
  1. What is a key identifying feature of acute lymphoblastic leukemia ?
A
  • Blast cells and Auer Rods

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