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Progress Tests > Pulsenotes > Flashcards

Pulsenotes Flashcards

1
Q

What is CPPD disease also known as?

A

Pseudogout

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2
Q

Aetiology of haemochromatosis

A

Recessive inheritance

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3
Q

Complications of haemochromatosis

A

Arthropathy (50% of patients). Either osteoarthritis-like, inflammatory or pseudogout
Diabetes
Hypopituitarism, hypothyroidism, hypogonadism
Cardiomyopathy

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4
Q

Likely diagnosis in a previously fit and well young adult who has developed malaise and erythema multiforme

A

Mycoplasma pneumoniae

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5
Q

Most common cause of community acquired pneumonia

A

Strep pneumoniae

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6
Q

What patients need follow-up after pneumonia?

A

Smokers over 50 offered a CXR 6 weeks later, as there is a high incidence of lung cancer in these patients

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7
Q

What is G6PD deficiency?

A

G6PD deficiency is an x-linked recessive inherited haemolytic anaemia, which can cause red cell lysis when erythrocytes are put under oxidative stress

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8
Q

Risk factors for idiopathic thrombocytopenic purpura

A

Children under 10 (most common in 2-4 yrs)

Post viral infection

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9
Q

Symptoms of idiopathic thrombocytopenic purpura

A

Increased risk of bleeding (petechiae, purpura, GI bleeding, menorrhagia, retinal haemorrhage, epistaxis) In children, there is usually an abrupt onset and it is self limiting compared to a gradual onset and chronicity seen in adults.

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10
Q

Treatment for idiopathic thrombocytopenic purpura

A

control of any bleeding complications and corticosteroid therapy
In severe cases, immunosuppressive drugs and platelet transfusions

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11
Q

Is Hodgkin lymphoma or non-Hodgkin lymphoma more common?

A

Non-Hodgkin

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12
Q

What defines Hodgkin lymphoma?

A

presence of Hodgkin/Reed-Sternberg cells (HRS cells)

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13
Q

Lymphoma symptoms

A

Lymphadenopathy: Typically painless, firm, enlarged lymph nodes, most commonly found in the neck.
Fever, night sweats and weight loss, fatigue, malaise
Mediastinal mass: May be incidental finding on chest imaging or present with shortness of breath, cough, pain or superior vena cava obstruction.
Pruritis
Hepatosplenomegaly
In extra-nodal disease there may be other symptoms such as CNS, skin or GI symtpoms

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14
Q

Lymphoma diagnosis

A

Excisional biopsy

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15
Q

Management of Hodgkin lymphoma

A

Chemo and radiotherapy

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16
Q

Hodgkin lymphoma prognosis

A

Good

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17
Q

HHS symptoms

A 
Polydipsia and polyuria
Headache
Nausea and vomiting
Abdo pain
Cramps
Late features - confusion, seizures, coma
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18
Q

Mainstay of treatment in HHS

A

Fluids

Monitor glucose and electrolytes and consider insulin

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19
Q

Complications of HHS

A 
Thrombosis (need prophylaxis)
Seizures
Coma
Electrolyte derangement
Cerebral oedema due to fluid resuscitation
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20
Q

What cancers are most at risk for tumour lysis syndrome?

A

Haematological malignancy

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21
Q

What are the main molecules released in tumour lysis syndrome?

A

Phosphate, nucleic acid, calcium

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22
Q

Symptoms of tumour lysis syndrome

A

Nausea and vomiting, lethargy, weakness, spasms or arrhythmias within a few days of starting chemo or radiotherapy

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23
Q

Blood tests results in tumour lysis syndrome

A

Hyperphosphatemia
Hyperkalaemia
Hyperuricaemia
Hypocalcaemia

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24
Q

Diagnosis of tumour lysis syndrome

A

Laboratory diagnosis (hyperphosphatemia, hyperkalaemia, hyperuricaemia, hypocalcaemia) plus clinical diagnosis (raised creatinine, arrhythmias, seizures)

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25
Q

Prevention of tumour lysis syndrome

A

Risk stratification and giving IV fluids (and maybe uric acid lowering agents e.g. allopurinol or raspuricase) to high risk patients

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26
Q

Management of tumour lysis syndrome

A

Correction of electrolytes (calcium gluconate, insulin and dextrose, phosphate binders, uric acid lowering agents e.g. allopurinol or raspuricase, IV hydration)
May need dialysis

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27
Q

Where should patients with acute liver failure be managed?

A

Transplant centre / ITU

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28
Q

Management of acute liver failure

A

Intensive monitoring and supportive management

Liver transplant if eligible

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29
Q

When is the Rockall score used?

A

GI bleeding (after endoscopy to assess risk of death and re-bleeding)

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30
Q

Components of Rockall score

A

Age, BP & HR, Comorbidities, Diagnosis on endoscopy, Endoscopic findings

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31
Q

Management of testicular torsion

A

testicular exploration +/- bilateral orchidopexy +/- orchidectomy

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32
Q

Blood tests results in beta-thalassaemia

A

Microcytic anaemia
Iron studies normal (differentiates it from iron-deficiency anaemia)
Elevated HbA2 as it doesn’t have the HbB to bind to

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33
Q

Symptoms of one allele for beta-thalassaemia

A

Termed beta-thalassaemia minor / trait

Usually have mild, often asymptomatic anaemia

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34
Q

Cause of raised reticulocytes

A

Rapid blood loss (as body is making more)

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35
Q

Cause of lowered reticulocytes

A

Iron deficiency anaemia

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36
Q

Total iron binding capacity in iron deficiency anaemia

A

High

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37
Q

Serum ferritin in iron deficiency anaemia

A

Low

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38
Q

Gold standard for diagnosis of iron deficiency anaemia

A

Low serum ferritin

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39
Q

What type of anaemia is anaemia of chronic disease?

A

Normocytic (75%) or microcytic (25%)

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40
Q

Total iron binding capacity in anaemia of chronic disease

A

Low

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41
Q

Serum ferritin in anaemia of chronic disease

A

Normal / raised (as it’s an acute phase reactant)

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42
Q

Symptoms of beta-thalassaemia

A

Hepatomegaly
Splenomegaly
Skeletal abnormalities
Symptoms of iron overload form repeated transfusions (hypogonadism, growth failure, diabetes mellitus, hypothyroidism)

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43
Q

Key diagnostic test in beta-thallasaemia

A

Haemoglobin electrophoresis

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44
Q

Management of beta-thallasaemia

A

Blood transfusions

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45
Q

Causes of neutopaenia

A 
Congenital
Infection e.g. HIV / TB
Cancer
Drugs e.g. chemo / carbimazole
Autoimmune
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46
Q

Most common type of lung cancer

A

Adenocarcinoma

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47
Q

CURB-65 score

A 
Confusion
Urea >7
Resp rate >30
BP <90
Age >65
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48
Q

What referral is necessary to consider in iron deficiency anaemia?

A

Upper and lower endoscopy via urgent suspected cancer pathway
Males and post-menopausal women

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49
Q

What part of the lungs is adenocarcinoma usually seen?

A

Peripheries

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50
Q

What part of the lungs is squamous cell lung cancer usually seen?

A

Centrally

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51
Q

Prognosis in small cell lung cancer

A

Very poor

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52
Q

What is a pancoast tumour?

A

Tumour of the lung apex

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53
Q

Definition of multiple endocrine neoplasia

A

Development of many endocrine tumours

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54
Q

Aetiology of multiple endocrine neoplasia

A

Autosomal dominant

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55
Q

What is multiple endocrine neoplasia type 1 (MEN1)?

A

Mutation of MEN1 gene causes tumours of parathyroid, pancreas and pituitary. May also be angiofibromas

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56
Q

What is an angiofibroma?

A

Small cutaneous tumours that are dome shaped and skin coloured

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57
Q

Symptoms of multiple endocrine neoplasia 1 (MEN1)

A

Pituitary tumours - headache, visual disturbance, Cushings, acromegaly, prolactinoma (low libido, galactorrhoea, menstrual irregularity)
Parathyroid hyperplasia - hypercalcaemia (bone pain, renal stones, abdo pain, polyuria, psych issues)
Pancreatic tumours - insulinoma (hypoglycaemia), gastrinoma (peptic ulcer disease)

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58
Q

What is multiple endocrine neoplasia type 2 (MEN2)?

A

Mutation of RET gene causes thyroid cancer and pheochromocytoma

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59
Q

Symptoms of multiple endocrine neoplasia 2 (MEN2)

A

Medullary thyroid cancer - thyroid often removed as prophylaxis
Parathyroid hyperplasia - hypercalcaemia (bone pain, renal stones, abdo pain, polyuria, psych issues)
Pheochromocytoma - flushing, tachycardia, palpitations

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60
Q

Diagnosis of multiple endocrine neoplasia (MEN)

A

Blood tests for increased levels of the hormones involved (e.g. PTH, prolactin, pancreatic polypeptide, gastrin, calcitonin, catecholamines)
Imaging for where tumour is suspected
Genetic testing

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61
Q

Screening for multiple endocrine neoplasia 1 (MEN1)

A

Annual health check looking for tumours in first and second degree relatives

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62
Q

Screening for multiple endocrine neoplasia 2 (MEN2)

A

Health check in relatives looking for tumours

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63
Q

Management of multiple endocrine neoplasia 1 (MEN1)

A

Parathyroid hyperplasia - surgical resection
Pituitary adenoma - surgical resection or medical management
Pancreatic tumours - more difficult to treat, either excision or medications (e.g. PPIs in gastrinoma)

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64
Q

Management of multiple endocrine neoplasia 2 (MEN2)

A

Parathyroid hyperplasia - surgical resection
Pheochromocytoma - adrenalectomy
Medullary thyroid cancer - prophylactic resection

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65
Q

Grading system in acute limb ischaemia

A

Rutherford

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66
Q

Polymyalgia rheumatica symptoms

A

The hallmark is symmetrical muscle aching and stiffness, worse in the morning, that affects the shoulders, hips, neck and torso
May also have systemic features e.g. low fever, fatigue, weight loss, low mood

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67
Q

Signs of polymyalgia rheumatica on examination

A

Reduced range of movement: shoulder, cervical spine, and hips
Synovitis and swelling
Normal power, though pain may make this difficult

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68
Q

Diagnosis of polymyalgia rheumatica

A

The diagnosis of PMR is based on identifying typical clinical features and assessing response to corticosteroids (rapid resolution within 1 week)

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69
Q

Treatment of polymyalgia rheumatica

A

Low dose steroids. Normally dose tapered off after a few weeks but in some patients it is tapered more slowly

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70
Q

Tests needed before starting amiodarone

A

CXR, U&Es, TFTs, LFTs

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71
Q

CLL symptoms

A

Painless enlarged lymph nodes
Constitutional symptoms e.g. weight loss, fever, anorexia, night sweats, lethargy
May have hepatomegaly or splenomegaly

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72
Q

Diagnostic test in CLL

A

Raised lymphocytes on FBC

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73
Q

What is Binet staging used for and what staging system is used?

A

CLL
Stage A: <3 lymphoid sites
Stage B: ≥3 lymphoid sites
Stage C: presence of anaemia and/or thrombocytopaenia

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74
Q

Management of CLL

A

Watch and wait with supportive care e.g. flu vaccine and treating infections
Chemotherapy (chemo, biologics, monoclonal antibodies, steroids)
Stem cell transplant

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75
Q

CLL complications

A

Transformation to more aggressive lymphoma or leukaemia
Infections
Autoimmune conditions
Increased risk of haematological or other cancers

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76
Q

CLL prognosis

A

Good

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77
Q

What is Bell’s palsy?

A

Bell’s palsy is rapid onset (< 72 hours) unilateral facial weakness of unknown cause

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78
Q

Does Bell’s palsy affect the forehead?

A

Yes (a way to differentiate it from stroke)

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79
Q

Bell’s palsy prognosis

A

The majority of patients with Bell’s palsy will make a full recovery within four months.

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80
Q

Bell’s palsy management

A

Mostly reassurance and advice on supportive care e.g. eye care
Prednisolone if presenting within 72 hours of symptom onset

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81
Q

Inheritance of Lynch Syndrome

A

Autosomal dominant

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82
Q

Haemorrhoids treatment

A

Treatment is commonly conservative. It aims to prevent or reduce constipation and symptoms. Symptomatic relief involves simple analgesics and topical anaesthetics.
Refractory disease may require treatment with rubber band ligation, sclerotherapy, diathermy and haemorrhoidectomy.

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83
Q

What is multiple myeloma?

A

A malignant disorder of plasma cells which will secrete monoclonal antibodies

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84
Q

Symptoms of multiple myeloma

A

Constitutional features e.g. weight loss, fatigue, night sweats, anorexia
Bone disease (typically lytic lesions that can lead to fractures)
Renal impairment
Anaemia
Hypercalcaemia
Recurrent infections

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85
Q

What cancer is hyperviscosity syndrome particularly associated with?

A

Multiple myeloma

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86
Q

Symptoms of hyperviscosity syndrome

A

Blurred vision, headaches, mucosal bleeding and dyspnoea

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87
Q

Treatment of hyperviscosity syndrome

A

Urgent plasma exchange

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88
Q

Tests to diagnose multiple myeloma

A

Protein electrophoresis to look for monoclonal antibodies
Immunofixation may be used to look for monoclonal antibodies
May do urine electrophoresis to look for Bence-Jones protein (free light chains in the urine)
May do bone marrow biopsy

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89
Q

Treatment principles in multiple myeloma

A

The four key areas of management include: induction therapy (chemotherapy and steroid), autologous stem cell transplantation (ASCT), maintenance therapy (chemotherapy) and managing relapse or refractory disease.

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90
Q

Prognosis in multiple myeloma

A

Variable but usually poor
Beta-2 microglobulin is often used as a prognostic tool
Most patients will have a period of remission then relapse

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91
Q

Acute pulmonary oedema management

A

furosemide 40mg IV
high-flow Oxygen
nitrates (Sublingual / infusion)
diamorphine IV

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92
Q

Non-massive vs sub-massive PE

A

Non-massive: haemodynamically stable and no evidence of right heart strain
Sub-massive: haemodynamically stable, but evidence of right heart strain on imaging (e.g. CT, ECHO) or biochemistry (e.g. elevated troponin)

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93
Q

Treatment in minimal change disease

A

Steroids first line
Other immunosuppressants may be used in adults with recurrent disease
ACE inhibitors / ARBs to manage HTN and diuretics to manage oedema

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94
Q

Most common cause of nephrotic syndrome in adults

A

Membranous glomerulonephropathy

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95
Q

First line in focal epliepsy

A

Carbamazepine

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96
Q

Staging sarcoidosis

A

Stage 0: Normal CXR
Stage I: Bilateral hilar lymphadenopathy
Stage II: Bilateral hilar lymphadenopathy and infiltrates
Stage III: Infiltrates alone
Stage IV: Pulmonary fibrosis (volume loss predominantly in the upper zones)

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97
Q

What is sarcoidosis?

A

Sarcoidosis is a rare multisystem granulomatous inflammatory disorder of unknown aetiology

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98
Q

Age of onset of sarcoidosis

A

20-40

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99
Q

Symptoms of sarcoidosis

A

Asymptomatic
Lungs most commonly involved: will have signs of fibrosis e.g. fine crackles, restrictive spirometry, exertional breathlessness, may have right heart strain
Eyes may be affected: uveitis
Skin may be affected: papules / erythema nodosum
Other manifestations e.g. renal disease or hypercalcaemia

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100
Q

Management of sarcoidosis

A

Often no management needed
If severe, may have steroids (high dose then tapered to low dose) or other immunosuppressants if steroids not tolerated
Lung transplant if very severe

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101
Q

Prognosis in sarcoidosis

A

Good prognosis and it often regresses spontaneously

Pulmonary disease may increase mortality

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102
Q

CXR findings in sarcoidosis

A

Bilateral hilar and mediastinal lymphadenopathy
Reticulonodular / airspace opacities
Pulmonary fibrosis
Normal in 20%

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103
Q

Most common causes of hypercalcaemia

A

Malignancy or hyperparathyroidism

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104
Q

Pathophysiology of malignant hypercalcaemia

A

Parathyroid hormone related peptide (PTHrP) secretion from tumours
Osteolytic lesions (release calcium)
Secretion of activated vitamin D (rarer)

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105
Q

Medications that can be used to manage hypercalcaemia

A

Bisphosphonates

Calcitonin

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106
Q

Most common organism in acute otitis media

A

Strep pneumoniae

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107
Q

What is eosinophilic oesophagitis?

A

Eosinophilic oesophagitis is a chronic immune-mediated disease, characterised by eosinophil-predominant inflammation of the oesophagus

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108
Q

Risk factors for eosinophilic oesophagitis

A

Male
30s-40s
Other allergic conditions such as asthma, atopic dermatitis, food or environmental allergies

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109
Q

Symptoms of eosinophilic oesophagitis

A

Dysphagia (often slow eating needing lots of water to help swallow food)
May have heartburn / dyspepsia / chest pain

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110
Q

Diagnosis of eosinophilic oesophagitis

A

Endoscopy with biopsy to show raised eosinophils

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111
Q

Management of eosinophilic oesophagitis

A

Conservative: diet modification
Medical: PPI, steroids (either inhaled or a slurry to make it topical)
May need endoscopic surgery e.g. to treat strictures

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112
Q

Drug to treat spasticity

A

Baclofen

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113
Q

Definition of MS

A

Multiple sclerosis (MS) is a demyelinating neuroinflammatory condition, which affects the central nervous system (CNS). Focal areas of demyelination are known as plaques

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114
Q

Risk factors for MS

A

Women
Onset 20-40
Genetics
Environmental e.g. EBV infection

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115
Q

Commonly sites of lesions in MS

A

Optic nerves
Spinal cord
Brainstem
Cerebellum

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116
Q

Most common course of MS

A

Relapsing-remitting (90% of MS)

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117
Q

pattern in relapsing-remitting MS

A

Relapses of more severe symptoms followed by periods of full or partial recovery with few symptoms

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118
Q

Pattern in primary progressive MS

A

Sustained progression of disease severity from onset. May also have relapses

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119
Q

Pattern in secondary progressive MS

A

Starts as relapsing and remitting pattern then becomes a pattern with sustained progression

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120
Q

What is clinically isolated syndrome with respect to MS?

A

CIS describes the first clinical episode of suspected MS.

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121
Q

Symptoms of MS

A

Optic nerve involvement: visual symptoms e.g. vision loss / blurring or pain
Cerebellar lesions: ataxia, gait disturbance, cerebellar signs
Brainstem lesions: cranial nerve palsies
Spinal cord lesions: movement / sensory disorders
Others: pain, sexual dysfunction, bowel / bladder dysfunction, depression

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122
Q

Diagnosis of MS

A

2 or more bouts
2 or more locations (seen as plaques on MRI)
If diagnosis uncertain can look for oligoclonal bands in CSF

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123
Q

Management of MS

A

General: help with bladder or bowel dysfunction e.g. catheters for retention / meds for incontinence / laxitives, meds / CBT for depression, walking aids, meds for neuropathic pain, physio / meds for spasticity
Treatment of relapses: Steroids
Long term treatment: Biologics may be indicated as disease modifying therapy

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124
Q

Indication for punch biopsy

A

Biopsy in sensitive areas e.g. face to see if it needs excision

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125
Q

Diagnostic test of choice in BCC

A

Excisional biopsy

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126
Q

Definition of BCC

A

Slow growing locally invasive malignant skin tumour with very limited metastatic potential

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127
Q

Prognosis in BCC

A

Good

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128
Q

What does a classic BCC look like?

A

Telangiectasia (small blood vessels)
Ulceration
Rolled edges
Pearly edge

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129
Q

Definition of SCC

A

Malignant fast growing tumour of epidermis with metastatic potential. Typically occurs in sun exposed areas

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130
Q

What does a classic SCC look like?

A

Indurated, nodular, keratinising or crusted tumour with or without ulceration

131
Q

Management of skin cancer

A

Surgery: excisional / destructive (if biopsy not needed)

Non-surgical: Topical immunotherapy (low risk cancer), cryotherapy (low risk cancer), radiotherapy

132
Q

What sort of rash is typhoid associated with?

A

Small red dots often on chest

133
Q

is C.diff gram positive or negative?

A

Positive

134
Q

Most common pathogen in prostatitis

A

E. coli

135
Q

Acute bacterial prostatitis symptoms

A

Pain (abdominal, rectal, pelvic or back pain)
Dysuria, urinary frequency or retention
Systemic signs of infection e.g. fever, rigors, myalgia, tachycardia

136
Q

What cultures and screening are important in acute bacterial prostatitis?

A

Blood, urine and semen cultures

STI screen

137
Q

Imaging in acute bacterial prostatitis

A

MRI (look for abscesses)

138
Q

What prophylactic medication should patients with HHS be started on and why?

A

Prophylactic LMWH as dehydration predisposes to thrombosis

139
Q

Oesophagitis scoring system

A

Los Angeles

140
Q

Risk factors for variocele

A 
Adolescence
Malignancy (rare)
141
Q

Symptoms of variocele

A 
Testicular swelling (described as "bag of worms", may be better on lying down and worse with the valsalva manoeuvre)
Classically painless but some patients experience pain or discomfort
142
Q

Complications of variocele

A

Infertility

Testicular atrophy

143
Q

Indications for referral in variocele

A

Symptomatic
Doesn’t drain on lying down
Isolated on the right side
Testicular atrophy in adolescents

144
Q

Management of variocele

A

Yearly observation if asymptomatic

If symptomatic may have surgery

145
Q

Demographic of myasthenia gravis

A

Younger females

Older males

146
Q

Myasthenia gravis is associated with pathology of which organ?

A

Thymus gland (thymoma, thymic hyperplasia, atrophy)

147
Q

Result of ice pack test in myasthenia gravis

A

Improves with ice

148
Q

Main antibodies in myasthenia gravis

A

AChR-Ab (antibodies against acetylcholine receptor)

149
Q

Treatment for myasthenia gravis

A

Acetylcholine esterase inhibitors first line (e.g. pyridostigmine)
Corticosteroids second line
Immunosuppressants third line
Thymectomy can improve symptoms if there is a thymoma

150
Q

Key monitoring in patients with myasthenic crisis

A

FVC

151
Q

Treatment in myasthenic crisis

A

IVIG (IV immunoglobulins)
Steroids
Plasma exchange if severe

152
Q

Most common organism in native valve endocarditis

A

Streptococci

153
Q

What syndrome does anca associated vasculitis cause?

A

Nephritic

154
Q

Symptoms of granulomatosis with polyangiitis

A

Vasculitic rash
AKI
Nasal features e.g. epistaxis

155
Q

Autoantibody present in granulomatosis with polyangiitis

A

cANCA

156
Q

Symptoms in microscopic polyangiitis

A

Vasculitic rash
AKI
Peripheral neuropathy

157
Q

Autoantibody present in microscopic polyangiitis

A

pANCA

158
Q

Symptoms of eosinophilic granulomatosis with polyangiitis

A

Adult onset asthma

Allergic features

159
Q

Autoantibody present in eosinophilic granulomatosis with polyangiitis

A

cANCA or pANCA

160
Q

Pathophysiology of tubulointerstitial nephritis

A

Hypersensitivity causes inflammation of the kidney tubules. Often caused by drugs e.g. abx or diclofenac

161
Q

Symptoms of tubulointerstitial nephritis

A

Fever, rash, eosinophilia, arthralgia, myalgia

162
Q

Treatment in tubulointerstitial nephritis

A

Discontinue drugs that may have caused it
Dialysis if severe
May give steroids if severe

163
Q

Renal artery stenosis symtoms

A

severe HTN
variable renal function
recurrent pulmonary oedema

164
Q

Renal artery stenosis diagnosis

A

doppler ultrasound

CT

165
Q

Management of renal artery stenosis

A 
HTN management (but ACE inhibitors contraindicated)
Manage comorbidities
166
Q

Diagnosis of Parkinson’s

A

Step 1: Parkinsonism (bradykinesia with either rigidity, postural instability or resting tremor)
Step 2: Considering differentials (e.g. stroke / trauma / encephalitis)
Step 3: Supportive features (progressive, unilateral onset, asymmetry, responds well to levodopa)

167
Q

What are parkinson plus syndromes:

A

Other conditions that can present similarly to Parkinsons (multisystem atrophy, progressive supranuclear palsy, corticobasal degeneration, lewi body dementia)

168
Q

What is multisystem atrophy?

A

A parkinson plus syndrome
MSA is an adult-onset, rapidly progressive disease that is characterised by profound autonomic dysfunction leading to severe postural hypotension, urogenital dysfunction and other features including cerebellar and corticospinal features. There is a poor response to treatment.

169
Q

What is progressive supranuclear palsy?

A

A parkinson plus syndrome
PSP is a neurodegenerative disorder that typically begins at age 50-60 years and is characterised by vertical gaze dysfunction, dysarthria and cognitive decline. Tremor is rare in this condition.

170
Q

What is corticobasal degeneration?

A

A parkinson plus syndrome
CBD is a neurodegenerative disorder that is characterised by a progressive dementia, parkinsonism and limb apraxia. Apraxia refers to problems with motor planning (i.e. unable to wave hello).

171
Q

Paraneoplastic syndromes associated with squamous cell carcinoma

A

PTH release

Cushings

172
Q

Paraneoplastic syndromes associated with small cell lung cancer

A

SIADH

Cushings

173
Q

Symptoms of renal cell cancer

A 
Haematuria
Flank pain
Flank mass
Constitutional symptoms e.g. fever / night sweats / malaise / weight loss
Variocele
Paraneoplastic syndromes
174
Q

Imaging in renal cell cancer

A

CT first line
MRI if CT contraindicated
May be picked up on ultrasound

175
Q

Management of renal cell carcinoma

A

Partial / total nephrectomy

Chemotherapy in advanced disease and palliative care if necessary

176
Q

Management of combined B12 and folate deficiency

A

Correct B12 first

177
Q

Kernig’s sign

A

Kernig’s sign describes an inability to fully extend at the knee when the hip is flexed at 90º due to pain
Suggests meningism

178
Q

Brudzinski’s sign

A

Brudzinski’s sign describes spontaneous flexion of the knees and hips on active flexion of the neck due to pain
Suggests meningism

179
Q

Grey Turner’s sign

A

bruising in both flanks due to retroperitoneal haemorrhage (characteristic in acute pancreatitis)

180
Q

Battle’s sign

A

bruising over the mastoid bone suggestive of basal skull fracture

181
Q

Hutchinson’s sign

A

herpetic lesion on the tip of the nose, which can be an early warning of ocular herpes zoster

182
Q

Muller’s sign

A

visible pulsation or bobbing of uvula seen in aortic regurgitation

183
Q

Factors that can artificially increase PSA

A

Vigorous exercise in previous 48 hours
Ejaculation in previous 48 hours
Urinary / prostatic infection
Prostate biopsy

184
Q

Management of BPH

A

Watchful waiting
Medical (alpha blockers e.g. Tamsulosin or 5-alpha reductase inhibitors e.g. finasteride)
Surgical resection (transurethral resection or incision or laser techniques)

185
Q

Complications of surgical procedures for BPH

A

Retrograde ejaculation (up to 75% for a transurethral resection), urinary infection, need for urinary catheter are all relatively common. Occasionally clot retention, urinary incontinence, urethral stricture and erectile dysfunction may occur.

186
Q

First line imaging in BPH

A

Ultrasound

187
Q

Management of an infective exacerbation of COPD

A

nebulisers, steroids and antibiotics. Controlled oxygen therapy should be given to patients if required.

188
Q

Symptoms of optic neuritis

A

Pain behind the eye which is worse on eye movement
Reduced visual acuity
Blurred vision
Central scotoma
May have reduced ability to see the colour red
Optic disc swelling on fundoscopy

189
Q

Drug to treat erectile dysfunction

A

Sildenafil

190
Q

Pathophysiology of primary TB

A

A Ghon focus develops composed of tubercle-laden macrophages

In immunocompetent people, this usually heals by fibrosis.

191
Q

Monitoring of lithium

A

Serum-lithium monitoring should be performed weekly after initiation and after each dose change until concentrations are stable, then every 3 months for the first year, and every 6 months thereafter.

192
Q

Indication for lithium

A

Mood disorders (bipolar)

193
Q

What condition are pencil cells associated with?

A

Iron deficiency anaemia

194
Q

What condition are Howell-Joly bodies associated with?

A

Splenectomy

195
Q

What condition are spherocytes associated with?

A

Hereditary shperocytosis

196
Q

What condition are schistocytes associated with?

A

Metallic valve replacement or some haemolytic anaemias

197
Q

Management of asymptomatic gallstones

A

Nothing

198
Q

Fibroadenoma examination findings

A

smooth, hard, painless lump in the outer upper quadrant of the breast

199
Q

Management of fibroadenoma

A

Referral for triple assessment to exclude breast cancer. Consider urgent suspected cancer referral if over 30 or other features of breast cancer)
Once fibroadenoma is confirmed no management is needed (but should advise to check breasts regularly)

200
Q

Age range associated with fibroadenomas

A

Young women

201
Q

Most common cause of primary aldosteronism

A

Bilateral idiopathic hyperplasia

202
Q

Symptoms of primary aldosteronism

A

Asymptomatic
Hypertension (may present with CKD, cerebrovascular disease, heart failure or retinopathy)
Hypokalaemia (may present with muscle weakness, paraesthesia, mood disturbance and polyuria)

203
Q

Who to test for primary hyperaldosteronism

A

Hypertension with hypokalaemia
Severe hypertension (systolic > 150, diastolic > 100)
Hypertension resistant to treatment
Hypertension and:
Adrenal incidentaloma
Sleep apnea
Family history of early onset hypertension
Family history of early onset CVA
Primary aldosteronism affecting all 1st degree relatives with hypertension

204
Q

Testing for primary aldosteronism

A

Aldosterone: Renin ratio (will be raised)
If raised, CT adrenals
May do adrenal vein sampling prior to surgery to determine if it is bilateral or unilateral

205
Q

Management of primary aldosteronism

A

Unilateral: Surgery or mineralocorticoid receptor antagonists
Bilateral: Mineralocorticoid receptor antagonists

206
Q

Most common organism in IVDU infective endocarditis

A

Staph aureus

207
Q

Most common organism in native valve infective endocarditis

A

Streptococcus

208
Q

Most common organism in prosthetic valve infective endocarditis

A

Staphylococcus if early or streptococcus if late

209
Q

What are Roth spots? What do they signify?

A

Haemorrhage on the retina due to emboli

Associated with infective endocarditis

210
Q

Criteria used to diagnose infective endocarditis

A

Duke criteria

211
Q

What is Zollinger-Ellison syndrome?

A

Zollinger-Ellison syndrome is characterised by multiple peptic ulcers secondary to hypergastrinaemia in patients with a gastrinoma.

212
Q

Formula used to calculate fluid replacement in burns

A

Parkland formula

213
Q

Which patients with ADPKD get screening for berry aneurisms?

A
  • Personal or family history of intracerebral haemorrhage
  • Anticoagulation
  • High-risk occupations
  • Patients needing major surgery
214
Q

Symptoms of anaphylactoid reaction

A

nausea, vomiting, urticarial rash, angioedema, tachycardia, and bronchospasm but shock is uncommon

215
Q

Management of suspected DVT if doppler ultrasound not available within 4 hours

A

Start interim anticoagulation

216
Q

Management of patient with suspected DVT but negative doppler ultrasound

A

Stop anticoagulation
D-dimer
If negative, consider alternate diagnosis
If positive, stop anticoagulation and re-ultrasound in a week

217
Q

DVT management

A

DOAC first line

LMWH if DOAC not suitable

218
Q

Symptoms of post-thrombotic syndrome

A

chronic swelling, pain and skin changes within 2 years of a DVT

219
Q

Scoring system to assess risk in confirmed PE

A

PESI score

220
Q

Properties of TB pathogen

A

aerobic, acid-fast, slow-growing bacteria

221
Q

Definition of primary-progressive TB

A

Progressive-primary TB: primary infection is not suppressed, and prolonged infection occurs.

222
Q

What is a Gohn complex?

A

A small caseating lung lesion with an associated enlarged lymph node indicative of TB (primary or latent)

223
Q

TB symptoms

A

weight loss, malaise, fever
Pulmonary symptoms e.g. cough, SOB, haemoptysis
Enlarged lymph nodes
Other organs may be effected with a range of other symptoms e.g. epididymo-orchitis, meningitis, back pain, lupus vulgaris, pericardial effusion, Addison’s, terminal ileitis

224
Q

Who should be screened for latent TB?

A

Close contacts of patients with active TB
Immunocompromised patients
Prior to starting meds that may cause reactivation (e.g. biologics)
Entry to UK from areas of high prevalence

225
Q

Principle of Mantoux test

A

The Mantoux test Involves an intradermal injection of tuberculin, a purified protein derivative from M. tuberculosis. If a patient has had exposure to TB they exhibit a delayed (type IV) hypersensitivity reaction. Diagnosis is based on the degree of the local epidermal reaction.

226
Q

Limitation of Mantoux test

A

BCG vaccination affects results

227
Q

Principle of interferon gamma release assay testing for TB

A

These assays detect the bodies cellular immune response to TB. It tests for the T-cell interferon gamma response to M. tuberculosis antigens.

228
Q

Tests for latent TB

A

Mantoux or interferon gamma release assay

229
Q

Key investigations in active TB

A

CXR
3x early morning sputum for culture
Others for extra-pulmonary TB (e.g. CSF culture or other imaging)

230
Q

Efficacy of BCG vaccine

A

Poor

231
Q

Indication for treating latent TB

A

Under 65 without hepatic impairment and with contact with active or drug resistant TB

232
Q

Treatment for latent TB

A

6 months isoniazid or 3 months isoniazid and rifampicin

233
Q

Treatment for active TB (without CNS involvement)

A

isoniazid and rifampicin for 6 months

pyrazinamide and ethambutol for 2 months

234
Q

Treatment for active TB with CNS involvement

A

isoniazid and rifampicin for 12 months
pyrazinamide and ethambutol for 2 months
Steroids weaned down over 4-8 weeks

235
Q

Testing for drug resistant TB (Who to test and how?)

A

Previous TB
Contact with resistant TB
Born / Lived in country with high prevalence of resistant TB
Test with nucleic acid amplification

236
Q

Treatment for drug resistant TB

A

Specialist, usually a combination of at least 6 meds

237
Q

Cholesterol emboli risk factors

A

Cardiac angiography or initiation of thrombolysis 1-2 weeks previously

238
Q

Cholesterol emboli symptoms

A

Worsening renal function
Blue toes
Red-blue skin mottling
Necrosis if severe

239
Q

Management of cholesterol emboli

A

Analgesia
Some meds but limited evidence
Amputation if severe

240
Q

What is the name of the variant of T1DM that onsets in adulthood?

A

LADA (latent onset autoimmune diabetes in adults)

241
Q

What is the name for monogenic diabetes?

A

MODY (maturity onset diabetes of the young)

242
Q

Management of Budd-Chiari syndrome

A

recanalisation of the hepatic veins using anticoagulation, thrombolysis, stents or a transjugular intrahepatic portacaval shunt (TIPS)
Transplantation if severe

243
Q

Symptoms of post-coital headache

A

Severe headache during / shortly after intercourse / orgasm. Typically occipital and lasts 1-24 hours. Important to exclude sub-arachnoid haemorrhage

244
Q

Overview of diffuse large B cell lymphoma

A

Most common non-Hodgkin lymphoma
Aggressive
Usually presents as rapidly enlarging mass

245
Q

Overview of follicular lymphoma

A

A type of B cell non-Hodgkin lymphoma
Second most common non-Hodgkin lymphoma
Indolent (non-aggressive)
Usually presents with gradual lymphadenopathy

246
Q

Overview of Burkitt’s lymphoma

A

A type of B cell non-Hodgkin lymphoma
Fairly rare but commonly affects children
Aggressive
Usually presents as rapidly enlarging tumour in the jaw with lymphadenopathy and there may be abdominal symptoms

247
Q

Inheritance of Wilson’s disease

A

Autosomal recessive

248
Q

Symptoms of Wilsons disease

A

Kayser-Fleischer rings
Liver complications e.g. acute liver disease, chronic hepatitis or cirrhosis
Neurological complications e.g. akinesis / tremor / ataxia
Psychiatric complications e.g. behaviour changes / depression / psychosis
Anaemia
Others e.g. cataracts / renal failure / osteoarthritis / infertility

249
Q

Definition of Wilson’s disease

A

Genetic condition of abnormal copper deposition

250
Q

Key tests in Wilson’s disease

A

Serum caeruloplasmin: main carrier of copper in the blood. It tends to be decreased in patients with Wilson’s.
Serum copper: Tends to be decreased though it may be normal or elevated in acute liver failure
Serum ‘free’ copper: tends to be elevated.
24-hour urinary copper: Tends to be elevated.

251
Q

Screening for Wilson’s disease

A

Siblings and children

252
Q

Management of Wilson’s disease

A

Conservative (counselling, lifestyle advice, follow-up)
Meds (D-penicillamine first line)
Liver transplant may be indicated

253
Q

Definition of haemochromatosis

A

Genetic condition of excess iron in the body with abnormal deposition

254
Q

Inheritance of haemochromatosis

A

Autosomal recessive

255
Q

Age of onset in Wilson’s disease

A

Older children / Young adults

256
Q

Ago of onset of haemochromatosis

A

Middle age - old age (typically after menopause in females)

257
Q

Symptoms of haemochromatosis

A 
Fatigue
Arthritis
Bronze pigmentation of skin
Hair loss
Erectile dysfunction / amenorrhoea
Memory problems or mood disturbance
258
Q

Diagnosis of haemochromatosis

A

Raised serum ferritin
Raised transferrin saturation
Genetic testing

259
Q

Serum ferritin in haemochromatosis

A

High

260
Q

Transferrin saturation in haemochromatosis

A

High

261
Q

Complications of haemochromatosis

A

T1DM
Liver damage and cirrhosis or hepatocellular carcinoma
Endocrine / sexual problems e.g. hypogonadism / hypothyroidism
Cardiomyopathy
Arthritis

262
Q

Management of haemochromatosis

A

Weekly venesection to remove excess iron

263
Q

Conservative management of epistaxis

A

Pinch fleshy part of nose and lean forward over sink for 20 mins
Spit out blood in the mouth
Ice packs on forehead and neck
Consider anticoagulant reversal (senior decision)

264
Q

When to involve ENT in epistaxis

A

If conservative measures failed after 20 mins

265
Q

What bloods to do in epistaxis and when

A

FBC, clotting screen and group and save if conservative measures failed after 20 mins

266
Q

Management of epistaxis if conservative measures failed

A

Local anaesthetic
Cautery with silver nitrate
Prophylactic naseptin topical abx

267
Q

Management of epistaxis if cautery failed

A

Nasal packing

268
Q

Care of patient with nasal packing

A

Admit under ENT for monitoring
Analgesia
Make NBM incase surgery needed
Prophylactic abx according to local guidelines

269
Q

Management of posterior epistaxis

A

Senior ENT help

Catheterisation of posterior nasal cavity

270
Q

Post epistaxis advice

A

Topical naseptin abx

Avoid blowing / picking nose, hot drinks, heavy lifting or lying flat for 1-2 days

271
Q

When to refer in epistaxis

A 
Under 2 (epistaxis uncommon and consider NAI)
Recurrent nosebleeds and risk factors for underlying cancer / condition
272
Q

Posterior stroke symptoms

A

Balance issues
Visual disturbance
Cranial nerve involvement

273
Q

Symptoms of strangulated hernia

A

Hernia symptoms
Bowel obstruction symptoms
Severe pain

274
Q

Imaging in hernias

A

Not usually necessary for diagnosis
USS may be done if there is diagnostic uncertainty
CT if there are complications e.g. strangulation

275
Q

Indications for urgent referral in hernias

A

Strangulation / bowel obstruction (emergency referral)
Female
Irreducible

276
Q

Management of asymtpomatic herniae

A

Watchful waiting and education on signs of strangulation

277
Q

Management of symptomatic hernias

A

Surgery (open or laparoscopic)

278
Q

Management of ADPKD

A

BP control with ACE inhibitors

Renal replacement therapy (dialysis / transplant) in end-stage disease

279
Q

Criteria to describe Barratt’s oesophagus

A

Prague (split into two components: circumferential extent and maximal length)

280
Q

What are Heberden’s nodes?

A

Bony swellings on the distal interphalangeal joints

281
Q

What are Bouchard’s nodes?

A

Bony swellings on the proximal interphalangeal joints

282
Q

What is Pemberton’s sign?

A

Pemberton’s sign describes an increase in facial plethora, venous dilation and respiratory distress on raising the arms above the head for 1-2 minutes.
Suggests SVCO

283
Q

Most common type of prostate cancer

A

Adenocarcinoma

284
Q

First line imaging in prostate cancer

A

MRI

285
Q

Scoring system for likelihood of prostate cancer based on MRI

A

Likert (out of 5)

286
Q

Management of low risk prostate cancer

A

Surveillance, radiotherapy or prostatectomy

287
Q

Management of intermediate risk prostate cancer

A

Radiotherapy or prostatectomy. May also have hormone therapy

288
Q

Management of high risk prostate cancer

A

Radiotherapy or prostatectomy. May also have hormone or chemo therapy

289
Q

Age of onset of Eosinophilic granulomatosis with polyangiitis

A

40s

290
Q

What is Churgg-Strauss syndrome known as?

A

Eosinophilic granulomatosis with polyangiitis

291
Q

What is Wegeners granulomatosis known as?

A

Granulomatosis with polyangiitis

292
Q

What is pseudoxanthoma elasticum?

A

a rare condition characterised by progressive calcification and fragmentation of elastic fibres. It can cause gastrointestinal haemorrhage

293
Q

What faecal test can assess pancreatic function?

A

Faecal elastase

294
Q

Symptoms of sickle cell anaemia

A

Increased infections
Anaemia
Acute painful episodes (typical sites are back, chest, abdomen and extremities)
Acute chest syndrome (acute respiratory symptoms)
Organ damage

295
Q

Symptoms of acute chest syndrome

A 
Fever
Chest pain
Hypoxaemia
Wheezing
Cough
Respiratory distress
296
Q

Conservative management in sickle cell

A 
Education
Close follow-up
Folate supplements
Prophylactic abx
Immunisations
297
Q

Types of transfusion in sickle cell

A 
Top-up transfusions (give donor blood)
Exchange transfusions (remove some blood then give donor blood)
298
Q

Medication to reduce sickling in sickle cell

A

Hydroxycarbamide/Hydroxyurea (various indications)

299
Q

What can precipitate acute painful episode in sickle cell?

A

hypoxia, infection, dehydration, cold weather or even pregnancy

300
Q

Management of acute painful episode in sickle cell

A

ABCDE and obs
Check sickle care plan (personalised care plan for patients to manage painful episodes)
Analgesia (usually morphine)
Regular observation
Managing exacerbating factors (ensure well hydrated, treat concurrent infections and provide oxygen as needed)
Haematology referral

301
Q

Acute chest syndrome on X-ray

A

Pulmonary infiltrates

302
Q

Management of acute chest syndrome

A 
Abx
O2
Pain relief
IV fluids
VTE prophylaxis
May need ventilation
May need rapid transfusion
303
Q

Treatment of pseudogout with 2 joints or less affected

A

Intraarticular steroid injection (may also add lidocaine)

304
Q

Treatment of pseudogout with more than 2 joints affected

A

NSAID
Colchicine is an alternative
Steroids if severe

305
Q

What does silver wiring on ophthalmoscopy indicate?

A

Vessel sclerosis

306
Q

What is von-Hippel Lindau syndrome?

A

autosomal dominant syndrome associated with numerous malignancies including renal cell carcinoma

307
Q

Colour of gram positive organisms on gram stain

A

violet

308
Q

Colour of gram negative organisms on gram stain

A

pink

309
Q

Classification of renal cysts

A 
Bosnaik classification
(I - simple, II - minimally complex, III - intermediate, IV - malignant)
310
Q

What is haptoglobin

A

Haptoglobin is an acute phase plasma protein, which binds to free haemoglobin within the blood.

311
Q

What does low haptoglobin indicate?

A

Intravascular haemolysis (as the haptoglobin mops up the Hb)

312
Q

Driving restrictions after a stroke

A

Don’t drive for 1 month (longer for HGVs)

313
Q

Frequency of endoscopic screening in Barratt’s oesophagus

A

Dysplasia- 6 months
Long segment metaplasia - 3 years
Short segment metaplasia - 5 years

314
Q

Most common cause of tubulointerstitial nephritis

A

Drugs

315
Q

Symptoms of tubulointerstitial nephritis

A 
Asymptomatic
Nausea & vomiting
Oliguria
Malaise
Arthralgia
Fever
Rash (maculopapular and typically starts on trunk)
316
Q

Management of tubulointerstitial nephritis

A

Remove causative drug (or treat infection or systemic illness that has caused it)
Observation
Steroids if severe
Dialysis if very severe

317
Q

What is a jerky pulse associated with?

A

HOCM

318
Q

Meningitis contacts prophylaxis

A

A single dose of ciprofloxacin (500 mg) should be offered to patients, relatives and healthcare workers who have been in contact

319
Q

Treatment of IgA nephropathy

A

ACE inhibitors / ARBs for HTN and proteinuria

Immunosuppressants if severe and ongoing

320
Q

Complications of epididymo-orchitis

A

Testicular abscess
Testicular infarction
Subfertility

321
Q

Treatment of epididymo-orchitis

A

Simple analgesia
Advise on abstinence from sexual activity
Antibiotics (if STI-related, IM dose of ceftriaxone followed by course of oral doxycycline. if UTI-related, course of ofloxacin or levofloxacin)

322
Q

Referral in epididymo-orchitis

A

Referral to urology for outpatient USS to exclude tumour

323
Q

What cancers does Lynch syndrome increase risk of?

A

bowel, endometrial, ovarian, gastric, small bowel, urothelial, hepatobiliary and brain

324
Q

Treatment in testicular cancer

A

Orchidectomy

Progress Tests (17 decks)

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