Monday 27th Flashcards
(101 cards)
1
Q
CI to lung cancer surgery [4]
A
SVC obstruction, FEV < 1.5, MALIGNANT pleural effusion, and vocal cord paralysis
2
Q
When should reinfection with syphilis be suspected in syphilis serology results? [1]
A
Reinfection with syphilis should be suspected if the RPR rises by 4-fold or more
3
Q
If reinfection with syphilis is suspected, how should you manage it? [1]
A
Benzathine penicilli G, IM STAT dose
4
Q
how can serological test be divided? [2]
A
cardiolipin tests (not treponeme specific) treponemal-specific antibody tests
5
Q
How is syphilis Dx? [2]
A
Treponema pallidum is a very sensitive organism and cannot be grown on artificial media. The diagnosis is therefore usually based on clinical features, serology and microscopic examination of infected tissue
6
Q
What are cardiolipin tests? [4]
A
syphilis infection leads to the production of non-specific antibodies that react to cardiolipin
examples include VDRL (Venereal Disease Research Laboratory) & RPR (rapid plasma reagin)
insensitive in late syphilis
becomes negative after treatment
7
Q
What are treponema specific antibody tests? [2]
A
example: TPHA (Treponema pallidum HaemAgglutination test)
remains positive after treatment
8
Q
Following Tx for syphilis, what is the serological results? [2]
A
VDRL becomes negative
TPHA remains positive
9
Q
What is the most common cause of hypothyroidism? [1]
A
Autoimmune thyroiditis (Hashimoto’s) is the most common cause of hypothyroidism and is associated with other autoimmune diseases
10
Q
Goitre in subacute thyroiditis compared to autoimmune thyroiditis [2]
A
Hashimotos = firm, non-tender goitre Subacute = painful goitre
11
Q
How much more common is Hashimotos in women than men? [1]
A
10x
12
Q
Features of Hashimotos [3]
A
features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies
13
Q
Associations with Hashimotos disease [2]
A
other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto’s thyroiditis is associated with the development of MALT lymphoma
14
Q
Features of pulmonary oedema on CXR [6]
A
interstitial oedema
bat’s wing appearance
upper lobe diversion (increased blood flow to the superior parts of the lung)
Kerley B lines
pleural effusion
cardiomegaly may be seen if there is cardiogenic cause
15
Q
Stage 1 hypertension [1]
A
Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
16
Q
Stage 2 hypertension [1]
A
Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
17
Q
Stage 3 hypertension [1]
A
Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg
18
Q
likely Dx for painful erythematous nodosum rash, cough, hilar lymphadenopathy [1]
A
Sarcoidosis
19
Q
Dx of sarcoidosis [2]
A
Although diagnosis is often confirmed on CT imaging, serum ACE is raised in approximately 60% of sarcoid patients at diagnosis and is the most specific autoantibody used in diagnosis.
20
Q
What is C-ANCA commonly associated with? [2]
A
C-ANCA is incorrect. This is most commonly associated with granulomatosis with polyangiitis, raised in 90% of cases.
21
Q
dsDNA associated with? [1]
A
Typically abnormal in lupus eryhtematosus
22
Q
P-ANCA typically raised which conditions? [3]
A
P-ANCA is incorrect. P-ANCA can be raised in several conditions, including but not limited to ulcerative colitis, primary sclerosing cholangitis and rheumatoid arthritis.
23
Q
Define sarcoidosis [2]
A
Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas
24
Q
Which populations sarcoidosis more common in? [2]
A
Young and African descent
25
4 typical features of sarcoidosis [4]
acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: dyspnoea, non-productive cough, malaise, weight loss
skin: lupus pernio
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
26
3 syndromes associated with sarcoidosis [3]
Lofgren's syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
In Mikulicz syndrome* there is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma
Heerfordt's syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis
27
How does pericarditis typically present? [2]
Pericarditis is swelling of the pericardium, and usually presents with chest pain and temperature following a viral illness. The chest pain associated with pericarditis typically is relived on sitting up/leaning forward, making pericarditis the most likely diagnosis in this case.
28
Aetiology and therefore common Tx for pericarditis [1]
Usually the aetiology of pericarditis is viral or idiopathic, and therefore first line treatment is non-steroidal anti-inflammatories (NSAIDs). Antibiotics, such as co-amoxiclav, are not used first line for pericarditis, making this an incorrect answer.
29
When would glyceryl trinitrate typically used? [1]
Glyceryl trinitrate is usually used in the initial management of acute coronary syndrome. Acute coronary syndrome presents typically with crushing left sided chest pain, radiating down the arm and neck, and is typically associated with shortness of breath and nausea
30
Which case of pericarditis would pericardiocentesis be indicated? [2]
Acute cardiac tamponade can occur as a complication of acute pericarditis, and is usually more common with underlying malignancy, TB or purulent pericarditis. This is unlikely to be the case for this patient. Therefore, pericardiocentesis is not indicated in this case.
31
Clinical features of acute pericarditis [4]
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia
32
Give a few causes of pericarditis [3]
```
viral infections (Coxsackie)
tuberculosis
uraemia (causes 'fibrinous' pericarditis)
trauma
post-myocardial infarction, Dressler's syndrome
connective tissue disease
hypothyroidism
malignancy
```
33
ECG changes seen in pericarditis
the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events
'saddle-shaped' ST elevation
PR depression: most specific ECG marker for pericarditis
34
Mx of pericarditis [2]
treat the underlying cause
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
35
What can be given pericarditis if first-line Tx doesn't work? [1]
Low-dose COC
36
Features of intrahepatic cholestasis of pregnancy [3]
```
pruritus, often in the palms and soles
no rash (although skin changes may be seen due to scratching)
raised bilirubin
```
37
When is cholestasis typically seen in pregnancy? [1]
Intrahepatic cholestasis of pregnancy (also known as obstetric cholestasis) occurs in around 1% of pregnancies and is generally seen in the third trimester. It is the most common liver disease of pregnancy.
38
Mx of cholestasis in pregnancy [3]
- ursodeoxycholic acid is used for symptomatic relief
- weekly liver function tests
- women are typically induced at 37 weeks
39
Cx of cholestasis in pregnancy [1]
Complications include an increased rate of stillbirth. It is not generally associated with increased maternal morbidity
40
Features of acute fatty liver disease in pregnancy [3]
```
Non-specific symptoms:
abdominal pain
nausea & vomiting
headache
jaundice
hypoglycaemia
severe disease may result in pre-eclampsia
```
41
How common is acute fatty liver in pregnancy and when may it occur? [2]
Acute fatty liver of pregnancy is rare complication which may occur in the third trimester or the period immediately following delivery.
42
Mx of acute fatty liver pregnancy [1]
support care
| once stabilised delivery is the definitive management
43
What is HELLP syndrome? [3]
Haemolysis, Elevated Liver enzymes, Low Platelets
44
What does ANCA stand for? [1]
Anti-neutrophil cytoplasmic antibodies
45
What are ANCA antibodies associated with? [3]
- granulomatosis with polyangiitis
- eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
- microscopic polyangiitis
46
What increases the likelihood of ANCA associated vasculitis? [1]
Increasing age
47
Which systems does ANCA associated vasculitis affect? [1]
Renal, respiratory, systemic, skin [rash], ENT
48
Renal and respriatory Sx of ANCA associated vasculitis [3]
```
renal impairment
- caused by immune complex glomerulonephritis → raised creatinine, haematuria and proteinuria
respiratory symptoms
- dyspnoea
- haemoptysiis
```
49
Systemic, skin and ENT Sx of ANCA associated vasculitis
```
systemic symptoms
fatigue
weight loss
fever
vasculitic rash: present only in a minority of patients
ear, nose and throat symptoms
sinusitis
```
50
General approach to first-line Ix for ANCA associated vascultis [3]
urinalysis for haematuria and proteinuria
bloods:
urea and creatinine for renal impairment
full blood count: normocytic anaemia and thrombocytosis may be seen
CRP: raised
ANCA testing (see below)
chest x-ray: nodular, fibrotic or infiltrative lesions may be seen
51
What are two main types of ANCA associated vasculitis? [1]
cytoplasmic (cANCA) and perinuclear (pANCA)
52
As a general rule of thumb, distinction between two types of ANCA
cANCA - granulomatosis with polyangiitis
| pANCA - eosinophilic granulomatosis with polyangiitis + others (see below)
53
target cANCA vs pANCA
```
cANCA = serine proteinase 3 [PR3]
pANCA = myeloperoxidase [MPO]
```
54
Associated conditions to cANCA vs pANCA
```
None cANCA
pANCA:
Ulcerative colitis (70%)
Primary sclerosing cholangitis (70%)
Anti-GBM disease (25%)
Crohn's disease (20%)
```
55
General approach to ANCA therapy [1]
Once suspected, ANCA associated vasculitis should be managed by specialist teams (e.g. renal, rheumatology, respiratory) to allow an exact diagnosis to be made. Kidney or lung biopsies may be taken to aid the diagnosis.
The mainstay of management is immunosuppressive therapy.
56
Aching, morning stiffness, proximal muscle weakness but in absence of weakness.
Blood test results increased ESR with normal CK. Dx? [1]
Polymylagia rheumatica
57
Tx for polymyalgia rheumatica
Treatment
prednisolone e.g. 15mg/od
patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis
58
Action of dexamethasone [1]
Dexamethasone is another type of steroid medication. It has very high glucocorticoid activity but minimal mineralocorticoid activity. It has many uses, including in the diagnosis of Cushing's syndrome.
59
Which condition is MTX used first-line for? [1]
Methotrexate is the first-line treatment for rheumatoid arthritis.
60
First-line Tx for OA? [1]
Paracetamol and topical NSAIDs are the first-line treatment for osteoarthritis. This would present as unilateral pain, usually in a large joint (such as the knee) that gets better with usage. In this case, the stiffness is bilateral and gets better with usage.
61
How does pregabalin work?
Gabapentinoid that inhibits the calcium channels
62
Which joint condition is pregabalin used for?
Fibromyalgia
63
Features of PMR [4]
Features
typically patient > 60 years old
usually rapid onset (e.g. < 1 month)
aching, morning stiffness in proximal limb muscles
weakness is not considered a symptom of polymyalgia rheumatica
also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
64
Ix for polymyalgia rheumatica [2]
Investigations
raised inflammatory markers e.g. ESR > 40 mm/hr
note creatine kinase and EMG normal
65
When should nitrates be used with caution and why? [2]
If patient is hypotensive
| They are powerful vasodilators.
66
Initial drug therapy for patients with ACS [1]
MONA
67
dose aspirin in ACS Tx [1]
300mg
68
when to give O2 in patients with ACS [1]
If under 94%
69
When should morphine be given in ACS? [1]
morphine should only be given for patients with severe pain
previously IV morphine was given routinely
evidence, however, suggests that this may be associated with adverse outcomes
70
How can nitrates be given in ACS? [3]
can be given either sublingually or intravenously
useful if the patient has ongoing chest pain or hypertension
should be used in caution if patient hypotensive
71
What is the next step in ACS Mx after MONA? [1]
The next step in managing a patient with suspected ACS is to determine whether they meet the ECG criteria for STEMI. It is, of course, important to recognise that these criteria should be interpreted in the context of the clinical history.
72
STEMI criteria [4]
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)
73
What are the two types of coronary repercussion therapy? [1]
PCI and fibrinolysis
74
When can can PCI be offered? [2]
should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
75
Can PCI still be offered if the patient presents past 12h? [1]
if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
76
Which access preferred in PCI? [1]
radial access is preferred to femoral access
77
When should fibrinolysis be offered in ACS? [1]
should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
78
Which further anti platelet intervention can b e offered with a STEMI? What factor does this depend on? [2]
this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel
79
Drug therapy during PCI [2]
patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
patients undergoing PCI with femoral access:
bivalirudin with bailout GPI
80
Further drug therapy patient with NSTEMI/unstable angina [2]
antithrombin treatment
fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately
if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given
81
Which tool is used to risk assess and inform whether patient has coronary angiography or conservative Mx? [1]
Global registry of acute coronary events [GRACE]
82
Primary coronary intervention for patients with NSTEMI/unstable angina [3]
Further drug therapy
unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI
if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
if taking an oral anticoagulant: clopidogrel
83
Further drug management for patients with NSTEMI/unstable angina [2]
Further drug therapy
further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)
if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrel
84
Visual hallucinations with dementia Dx? [1]
Lewy body
85
Differentiation between LBD and PD timeline [2]
This is suggested by the presence of detailed visual hallucinations on a background of fluctuating cognition, inattention, REM sleep disorder and recent onset of parkinsonian features. The timeline of symptoms is important and differentiates it from Parkinson's disease, which would typically present with a movement disorder, before cognitive changes.
86
Parkinsonian triad key features [1]
Tremor, rigidity and bradykinesia
87
What is FTD also known as? [1]
Pick's disease
88
Signs of FTD [2]
Frontotemporal dementia, also known as 'pick's disease' is associated with disinhibition, socially inappropriate behaviour and emotional lability.
89
Features of LBD [3]
progressive cognitive impairment
in contrast to Alzheimer's, early impairments in attention and executive function rather than just memory loss
cognition may be fluctuating, in contrast to other forms of dementia
usually develops before parkinsonism
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
90
Dx of LBD [2]
usually clinical
single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%
91
Which drugs can be used in LBD? [2]
both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer's. NICE have made detailed recommendations about what drugs to use at what stages.
92
Which drugs should be avoided in LBD? [1]
neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent
93
Which drugs commonly cause SS? [4]
monoamine oxidase inhibitors
SSRIs
ecstasy
amphetamines
94
Which SSRI taken OTC can cause SS? [1]
St John's Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome
95
Features of SS [3]
```
neuromuscular excitation (e.g. hyperreflexia, myoclonus, rigidity)
autonomic nervous system excitation (e.g. hyperthermia)
altered mental state
```
96
Mx of SS
supportive including IV fluids
benzodiazepines
more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine
97
What is NMS caused by and how to differentiate it? [2]
Caused by antipsychotics
| Slower onset, normal pupils [vs dilated], 'lead-pipe' rigidity
98
Mx severe cases of NMS vs SS [2]
more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine in SS
Dantrolene in NMS
99
What is the NYHA classification system? [1]
The NYHA classification is based on the severity of cardiac failure symptoms (e.g. shortness of breath on exertion, angina pain, palpitations, fatigue).
100
NYHA class I and II [2]
NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
101
NYHA class III and IV [2]
NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
