Pass med Questions Flashcards

1
Q

A 23-year-old male presents to you in neurology clinic complaining of excessive daytime somnolence. He describes episodes of sudden onset sleep during the day, and at night often wakes with episodes where he is unable to move his arms or legs and describes seeing figures in the far corner of his bedroom.

Given the likely diagnosis, what is the most appropriate first-line investigation?

A

Multiple sleep latency EEG:

This patient is likely suffering from narcolepsy, which is associated with episodes of sleep paralysis. Here, patients experience episodes of paralysis, sometimes associated with hallucinations (e.g. figures in the corner of the bedroom) upon waking at night.

ECG and echocardiography is not indicated for the diagnosis of narcolepsy.

This patients symptoms are more consistent with narcolepsy over organic pathology, hence and MRI head would not be indicated in this case.

Multiple sleep latency EEG, along with polysomnography are the investigations of choice for narcolepsy.

This patients symptoms are most likely associated with narcolepsy over psychiatric disturbance, hence a psychiatric assessment is not necessary.

24 hour telemetry is typically used to investigate epilepsy over narcolepsy.

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2
Q

When is Abx used for SBP prophylaxis?

A
  • patients who have had an episode of SBP
  • patients with fluid protein <15 g/l and either Child Pugh score of at least 9 or hepatorenal syndrome

NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’

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3
Q

A 47-year-old female presents to her general practitioner with eczematous lesions with flakes on the ears and nose. The lesions began appearing 3 months ago, however, she is now growing increasingly anxious as she can no longer hide them with make-up due to increased dryness. She is otherwise healthy and never experienced anything similar before.

Which one of the following is the most appropriate management?

A

The correct answer is ketoconazole. This patient is suffering from seborrhoeic dermatitis, a very common chronic dermatitis, caused by an inflammatory reaction to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur. The classic symptoms are dandruff and eczematous lesions with flakes on the periorbital, auricular and nasolabial folds. The first-line management for the face and body lesions is ketoconazole, an antifungal, used to decrease the presence of Malassezia furfur.

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4
Q

A 56-year-old lady is referred to rheumatology clinic due to severe Raynaud’s phenomenon associated with arthralgia of the fingers. On examination you note shiny and tight skin of the fingers with a number of telangiectasia on the upper torso and face. She is also currently awaiting a gastroscopy to investigate heartburn. Which one of the following antibodies is most specific for the underlying condition?

A

Limited (central) systemic sclerosis = anti-centromere antibodies.
Important for meLess important
This lady has some features of CREST syndrome. Although ANA is positive in 90% of patients with systemic sclerosis, anti-centromere antibodies are the most specific test for limited cutaneous systemic sclerosis.

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5
Q

A 5-year-old girl is seen in the emergency department following her first seizure. This lasted 5 minutes. Her parents describe her falling to the floor suddenly and jerking her arms. She now feels well in herself and does not remember the incident. She is otherwise well.

Neurological examination is normal. General examination reveals four de-pigmented patches of skin over her torso and areas of thickened leathery skin over her lumbar region.

What is the most likely diagnosis?

A

Tuberous sclerosis

Ash leaf spots and shagreen patches, although not pathognomonic, are often seen in cases of tuberous sclerosis. Most of the manifestations of this disease are neurocutaneous, similarly in the neurofibromatous diseases.

All of the options above may have a seizure component but do not features the skin manifestations described in this case.§

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6
Q

A 28-year-old woman, who is 8 weeks pregnant, recently presented for her booking appointment. A mid-stream urine sample sent to the laboratory has now shown positive cultures. On questioning, she has no urinary symptoms, such as increased frequency, dysuria or haematuria. She is generally well, with no past medical or family history.

Which of the following is the most appropriate next step in the management?

A

Treat with Abx immediately due to a risk of progression to Acute pyelonephritis

It is offered at booking clinic.

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7
Q

Factors that worsen psoriasis?

A

There are multiple triggers for worsening psoriasis including alcohol, smoking, stress, discontinuing steroids or initiating NSAIDs, lithium, antimalarials and beta-blockers such as this patient’s propranolol.

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8
Q

A 55-year-old man with a background of Barrett’s oesophagus is seen in the gastroenterology clinic with the results of his routine surveillance endoscopy. He is still experiencing symptoms of dyspepsia despite regular treatment with high-dose omeprazole. He denies dysphagia or weight loss.

Endoscopy and biopsy results: Columnar epithelium is seen in the distal 5cm of the oesophagus. Dysplastic cells are seen on biopsy in keeping with high-grade dysplasia.

What is the recommended next step in this patient’s management?

A

Management
endoscopic surveillance with biopsies
high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited

Endoscopic surveillance
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years

If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
endoscopic mucosal resection
radiofrequency ablation

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9
Q

A 36-year-old male presents to the general practitioner with a 2-month history of generalised weakness and headaches.

Observations show:

Respiratory rate 16 breaths/min
Heart rate 63 beats/min
Blood pressure 168/132mmHg
Temperature 37.2ºC
Oxygen saturations 98% on room air

Blood results include:

Na+	169 mmol/L	(135 - 145)
K+	2.9 mmol/L	(3.5 - 5.0)
Bicarbonate	34 mmol/L	(22 - 29)
Urea	4.2 mmol/L	(2.0 - 7.0)
Creatinine	74 µmol/L	(55 - 120)

A plasma aldosterone/renin ratio is subsequently performed which suggests a peripheral cause of the patient’s presentation.

What is investigation could be used to further differentiate the likely underlying diagnosis?

A

This patient is presenting with symptoms of lethargy and headache, accompanied by hypertension, hypokalaemia, hypernatraemia and high serum bicarbonate (caused by metabolic alkalosis). This is a classical presentation of primary hyperaldosteronism, otherwise known as Conn syndrome. The first-line investigation of this condition is with an aldosterone/renin ratio, which in this case indicates a peripheral source of excess aldosterone secretion, suggesting an underlying aetiology of either unilateral adrenal adenoma or bilateral adrenal hyperplasia. These two peripheral causes of hyperaldosteronism can be distinguished with adrenal venous sampling. An adrenal adenoma will show excess aldosterone in only one adrenal vein, whereas levels will be raised in both adrenal veins in cases of bilateral adrenal hyperplasia.

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10
Q

A 41-year-old man develops itchy, polygonal, violaceous papules on the flexor aspect of his forearms. Some of these papules have coalesced to form plaques. What is the most likely diagnosis?

A

Lichen

planus: purple, pruritic, papular, polygonal rash on flexor surfaces. Wickham’s striae over surface. Oral involvement common
sclerosus: itchy white spots typically seen on the vulva of elderly women

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11
Q

A 52-year-old male is referred to urology clinic with impotence. He is known to have hypertension. He does not have any morning erections. On further questioning the patient reports pain in his buttocks, this worsens on mobilising. On examination there is some muscle atrophy. The penis and scrotum are normal. What is the most likely diagnosis?

A

Leriche syndrome

Classically, it is described in male patients as a triad of symptoms:

  1. Claudication of the buttocks and thighs
  2. Atrophy of the musculature of the legs
  3. Impotence (due to paralysis of the L1 nerve
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12
Q

What are the circumstances in which rythm control would be first line in AF management?

A
  • New onset AF (<48 hrs)
  • AF with reversible cause
  • AF leading to HF
  • AF remaining symptomatic despite adequate rate control
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13
Q

What is the QRISK score?

A

QRISK 3 gives the risk of a stroke or MI for a patient in the next 10 years if it is over 10% then a low dose statin should be started

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14
Q

All patients with CKD or T1DM for more then 10 years should be offered what?

A

A statin

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15
Q

What monitoring is needed after initiating a statin?

A

 Check lipid levels at 3 months and increase the dose to aim for a 40% reduction in the HDL cholesterol. (always check adherence before increasing dose)
 Also check LFTs within 3 months of starting the statin and at 12 months to make sure that they are normal- they can cause a mild transient rise in ALT/AST in the first few weeks, only needing stopping if they hit abnormal ranges.

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16
Q

Stages of HTN and their blood readings?

A

Stage 1: >140/90 or >135/85
Stage 2: >160/100 or >150/95
Stage 3: >180/120

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17
Q

Give 5 Contraindications to the Combined oral contraceptive pill?

A

more than 35 years old and smoking more than 15 cigarettes/day
migraine with aura
history of thromboembolic disease or thrombogenic mutation
history of stroke or ischaemic heart disease
breast feeding < 6 weeks post-partum
uncontrolled hypertension
current breast cancer
major surgery with prolonged immobilisation
positive antiphospholipid antibodies (e.g. in SLE)

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18
Q

Give 5 situations in which the risks of taking the COCP would outweigh the benefits?

A

more than 35 years old and smoking less than 15 cigarettes/day
BMI > 35 kg/m^2*
family history of thromboembolic disease in first degree relatives < 45 years
controlled hypertension
immobility e.g. wheel chair use
carrier of known gene mutations associated with breast cancer (e.g. BRCA1/BRCA2)
current gallbladder disease

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19
Q

ALARMS symptoms?

A

RF for dyspepsia:

Anaemia (IDA), Loss of weight, Anorexia, Recent onset, Maleana, Swallowing issues.

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20
Q

What drug is given alongside isoniazide to prevent Peripheral neuropathy?

A

Pyridoxine

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21
Q

What are the ECG changes in hyperkalaemia

A
  • Tall tented T waves
  • Prolonged PR interval (>200 ms)
  • Widened QRS complex (>120 ms)
  • Small/absent P waves
  • SINE WAVE PATTERN
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22
Q

GnRH analogue, GnRH antagonist

A
Goserelin goserelin (Zoladex) or leuprorelin (Prostap), use for short periods in fibroids.
Relugolix
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23
Q

What are the triad needed for endocarditis?

A

Endothelial damage, platelet adhesion, Microbial Adherence.

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24
Q

Dukes modified criteria?

A
•	For diagnosis:
o	2 major or
o	1 major 3 minor or
o	5 minor
•	Major:
o	Positive blood culture for endocarditis (from 2 separate cultures)
o	Evidence of endocardial involvement:
	Postive ECHO suggestive of IE
•	Minor:
o	Predisposition (CHD, surgery)
o	Fever
o	Vascular phenomena (Emboli, infarcts…)
o	Immunologic phenomena (Glomerulonephritis, Oslers nodes, Roth spots, RF)
o	Microbiological evidence 
o	Echo findings
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25
Q

What are the four components of tetralogy of fallot?

A
  • VSD
  • Overriding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
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26
Q

Which bacteria is important in acne?

A

Propionibacterium acnes

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27
Q

Mild moderate and severe acne?

A
  • Mild: Open and closed comedones with/without sparse inflammatory markers
  • Moderate: Widespread non-inflammatory lesions and numerous papules and pustules
  • Severe: Extensive inflammatory lesions, may include nodules, pitting and scarring.
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28
Q

Steroid ladder for exczema?

A

Hydrocortisone (0.5,1.0, 2.5%)
Eumovate (clobetasone butyrate 0.05%)
Betnovate (Beclamethasone 0.1%)
Dermovate (clobetasone propranoate 0.05%)

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29
Q

• Two products with a potent steroid and a vit D analogue that are commonly prescribed and need to know about:

A

o Dovobet

o Enstilar

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30
Q

When would you admit a child with bronchiolitis?

A
o	Apnoea
o	Persistent sat of <92% on air
o	Clinical dehydration
o	50-75 % usual fluid intake! 
o	Severe resp distress signs:
	Recession 
	Grunting 
	RR over 70 B/M
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31
Q

What scoring system is used for croup?

A

Westley croup score

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32
Q

What are the 3 cardinal pahtophysiological features of asthma?

A

Chronic airway inflammation
Airway hyperresponsiveness
Reversible airway obstruction

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33
Q

What are the structural changes in asthma?

A

o Thickening of the epithelial reticular basement membrane (collagen deposition)
o Hypertrophy and airway smooth muscle hyperplasia
o Extracellular matrix deposition
o Hypertrophy of mucus secreting glands

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34
Q

Prehn sign positive

A

Elevation of the testes relieves pain in epididymitis

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35
Q

Which cells produce surfactant?

A

Type II pneumocytes

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36
Q

Di george

A

22q11- deletion causes cardiac defects, facial issues, absent thymus and hypocalcaemia.

Lack of thymus leads to underdeveloped T cells.

CATCH 22

C- Congenital HD
A- Abnormal faces
T- Thymus gland missing 
C- cleft palate
H- Hypoparathyroidism leading to hypocalcaemia

22nd chromosome effected

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37
Q

Wiskott aldrich?

A
•	Wiskott-Aldrich syndrome is an X-linked recessive condition with a mutation of the WAS gene. It causes abnormal functioning of the T cells. 
•	Other features:
o	Thrombocytopenia
o	Neutropenia
o	Eczema 
o	Recurrent infections 
o	Chronic bloody diarrhoea.
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38
Q

Ataxic Telangiesctasia:

A

• Ataxic telangiaectasia is an AR condition affecting the gene that codes for the ATM serine/threonine kinase protein on chromosome 11.
• This is key for several functions of DNA coding, meaning that the single mutation can lead to issues with this gene leads to issues with the coding of many other genes.
• There are various features associated with this condition:
o Low numbers of T-cells and immunoglobulins, causing immunodeficiency and recurrent infections.
o Ataxia: Issues with coordination, due to cerebellar impairment
o Telangiectasia, particularly in the sclera and damaged areas of the skin.
o Predisposition to cancers: particularly haem
o Slow growth and delayed puberty
o Accelerated aging
o Liver failure.

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39
Q

C1 Esterase Inhibitor Deficiency (HEA):

A
  • Bradykinin is part of the inflammatory response.
  • It is responsible for causing BV dilation and increased permeability, leading to angioedema.
  • Part of the action of C1 esterase is to inhibit bradykinin.
  • An absence of C1 esterase leads to intermittent angioedema in response to minor triggers, such as viral infection or stress, or without any clear trigger at all.
  • Angioedema often affects the lips or face but can occur anywhere in the body, including the resp and GI tracts.
  • The swelling can last a few days before self resolving.
  • Angioedema can occur in the airway and compromise the patients airways
  • Patients can be treated with IV C-1 esterase inhibitor before dental appointments/surgical procedures or in response to acute attacks of HAE.

Key point- test C4 levels in recurrent angioedema

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40
Q

Kawasaki disease findings?

A

• A key feature that should lead to you considering Kawasaki disease is a PERSITENT high fever (>39) for OVER 5 DAYS.
• Children will be unhappy and unwell
• The key skin findings are:
o Widespread maculopapular rash
o Desquamation of the palms and soles (2-5 days after onset)
• Other features include:
o Strawberry tongue (red with large papillae)
o Cracked lips
o Cervical lymphadenopathy
o Bilateral conjunctivitis (2-4 days after onset)
• May also have inflammation of their BCG vaccine scar

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41
Q

Measels features

A
•	Prodrome:	
o	Irritable child
o	Fever
o	Conjunctivitis
•	Koplik spots (before the rash): white spots “grains of salt” rash on the buccal mucosa PATHOGENOMIC
•	Rash:
o	Starting behind the ears 
o	Then spreads to the whole body 
o	Discrete maculopapular rash which becomes blotchy and confluent.
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42
Q

CI to lumbar puncture?

A
o	Focal neuro signs
o	Papilledema
o	Sig. bulge of the fontanelle
o	DIC
o	Signs of cerebral herniation
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43
Q

What test on CSF?

A
o	Bacterial culture
o	Viral PCR
o	Cell count
o	Protein 
o	Glucose
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44
Q

HIV transmission at birth?

A

• Mode of delivery is determined by the mothers viral load:
o Normal < 50 copies/ml
o C section >50 copies /ml and in all over 400 copies/ml
o IV Zidovudine should be given with C-section if the viral load is unknown or there are >1000 copies/ml
• Prophylaxis treatment may be given to the baby depending on the mothers V.load:
o Low risk babies, where mums viral load is <50 copies per ml, should be given Zidovudine for 4 weeks
o High risk babies, where the mum’s viral load is >50 copies per ml, should be given zidovudine, Lamivudine and nevirapine for 4 weeks.

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45
Q

Testing for HIV in children of HIV (+) mothers?

A

Testing for HIV in children of (+) Mothers:
 Babies to HIV (+) are tested 2x for HIV:
o HIV Viral load test:
 At 3 months
 If this is (-) then the child has not developed HIV at birth and will not develop it without further exposure
 With 2 negative results, at least 2 weeks after ART= not infected then confirmed with Ab test after 18 months.
o HIV Ab test:
 At 24 months
 Assess if they have contracted HIV since their 3 month viral load test, ie via breast feed.
 If the 3 month test was (-) and they are not breast fed the test should be (-)
 Note that the Ab test can be (+) in children who do not have HIV until 18 months of age, due to maternal Ab.

46
Q

Management of hyperkalaemia?

sine wave ecg

A

This is a medical emergency. Treatment is with 10ml 10% calcium gluconate for cardioprotection, followed by 10 units of fast acting insulin (with 50ml 50% dextrose) to drive potassium into the intracellular space. Inhaled salbutamol has a similar effect if there is no IV access. Bicarbonate 50ml IV can also be given. Ultimately total body potassium needs to be decreased – in this case urgent dialysis or haemofiltration is indicated.

47
Q

What is Brugada syndrome and the management?

A

No it is certainly not normal. This ECG is characteristic of Brugada Syndrome (Type 1). In leads V1 – V3 there is >2mm ST elevation, the T waves are inverted and the ST segment has a characteristic ‘coved’ shape. This condition has a high risk of sudden death from ventricular fibrillation (VF). Treatment is with an implantable cardioverter-defibillator (ICD).§

48
Q

What is the mangement of TCA OD?

A

A,B,C,D,E (ventilation may be required)
Bloods including paracetamol level; ABG (likely metabolic acidosis)
Activated charcoal if within 8hrs of ingestion
Sodium bicarbonate (50ml of 8.4%)
Give if any arrhythmia or QRS>110
Further options:
If ventricular tachycardia: lignocaine (avoid beta blockers, amiodarone and calcium blockers)
If seizures: benzodiazepines

49
Q

Acute interstitial nephritis:

A

The clinical picture points to a diagnosis of acute interstitial nephritis, secondary to the amoxicillin. Penicillins are some of the most common causes of drug-induced interstitial nephritis, so it is always important to look out for any new drugs with any presentation of new-onset renal impairment.

Acute interstitial nephritis essential causes an ‘allergy’-type reaction, so look out for urticarial-like rashes and a fever. Arthralgia is also a common feature. Classically urine shows elevated white cell counts and eosinophils. IgE is also often elevated.

50
Q

Adverse affects of lithium?

A
  • nausea/vomiting, diarrhoea
  • fine tremor
  • nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus
  • thyroid enlargement, may lead to hypothyroidism
  • ECG: T wave flattening/inversion
  • weight gain
  • idiopathic intracranial hypertension
  • leucocytosis
  • hyperparathyroidism and resultant hypercalcaemia
51
Q

Monitoring of lithium?

A
  • inadequate monitoring of patients taking lithium is common - NICE and the National Patient Safety Agency (NPSA) have issued guidance to try and address this. As a result it is often an exam hot topic
  • when checking lithium levels, the sample should be taken 12 hours post-dose
  • after starting lithium levels should be performed weekly and after each dose change until concentrations are stable
  • once established, lithium blood level should ‘normally’ be checked every 3 months
  • after a change in dose, lithium levels should be taken a week later and weekly until the levels are stable.
  • thyroid and renal function should be checked every 6 months
  • patients should be issued with an information booklet, alert card and record book
  • This patient is on lithium therapy to manage their bipolar I disorder - characterised by manic episodes, with or without major depressive episodes. Lithium is a mood stabiliser, and the gold standard treatment for bipolar I disorder, used as prophylaxis to prevent significant mood swings (in particular manic episodes), as well as treating acute mania.

Patients are required to have lithium levels taken every 3 months to ensure the dosing is within a narrow therapeutic window, ensuring dosing is sufficient to ensure efficacy as well as minimising the risk of side effects if at toxic levels. Levels are taken 12 hours post-dose to capture the ‘trough level’ - the lowest serum concentration of lithium in a dosing cycle.

Multiple attempts before a successful venepuncture, with prolonged tourniquet use, may result in a haemolysed sample. However, this would not affect the lithium levels or their calculation in a laboratory.

Fasting is not required prior to specimen collection for lithium levels.

Alcohol consumption does not impact lithium levels, unless it leads to significant dehydration which may increase lithium levels.

Venepuncture is normally performed using an aseptic technique.

52
Q

What is section 2 of the MHA?

A

Duration – 28 days (cannot be renewed)
Purposes – assessment (although treatment can be given without patients’ consent)
Professionals involved - 2 doctors (one S12 approved), AMHP
Evidence required:
a) The patient is suffering from a mental disorder of a nature or degree that warrants detention in hospital for assessment; and
b) The patient ought to be detained for his or her own health or safety, or the protection of others

53
Q

What is section 3 of the MHA?

A

Duration – 6 months (and can be renewed)
Purposes – treatment
Professionals involved – 2 doctors, 1 AMHP
Evidence required:
(a)The patient is suffering from mental disorder of a nature or degree which makes it appropriate for the patient to receive medical treatment in a hospital; and
b) The treatment is in the interests of his or her health and safety and the protection of others; and
c) Appropriate treatment must be available for the patient

54
Q

What is section 4 of the MHA?

A

Duration – 72 hrs
Purposes – only in an “urgent necessity” when waiting for a second doctor would lead to “undesirable delay”
Professionals required – 1 doctor and 1 AMHP
Evidence required –
a) The patient is suffering from a mental disorder of a nature or degree that warrants detention in hospital for assessment; and
b) The patient ought to be detained for his or her own health or safety, or the protection of others
c) There is not enough time for 2nd doctor to attend (risk)

NOT COMMONLY USED

55
Q

What is section 5(4)?

A

For a patient ALREADY admitted (can be psychiatric or general hospital) but wanting to leave
Nurses’ holding power until doctor can attend
6 hours
Cannot be treated coercively whilst under section

56
Q

What is section 5(2)?

A

For a patient ALREADY admitted (can be psychiatric or general hospital) but wanting to leave
Doctors’ holding power – 72 hours
Allows time for Section 2 or Section 3 assessment
Cannot be coercively treated

57
Q

Section 135/136?

A

Police sections:
S136 – person suspected of having mental disorder in a public place
S135 – needs court order to access patient’s home and remove them to

Place of Safety (local psychiatric unit or police cell)- 72 hrs
Further assessment - ??? Need Section 2 or 3

58
Q

Lithium interactions?

A
  • Increased plasma concentration: ACE-I, NSAIDS, SSRIs, Antiepileptics, Aps
  • Decreased plasma concentration: Antacids, theophylline
  • Other interactions: Anti-arrythmics (e.g. amiodarone- increase risk of hypothyroidism), anti-diabetics (may impair glucose tolerance), antipsychotics (increased risk of ESPE’s)
59
Q

Lithium toxicity?

A
o	Usually upper is 12 hr post dose serum lithium level is 1.2mmol/L (>1.5 mmol/L have symptoms if >2.0 can be fatal
o	Early signs and symptoms:	
	Marked tremor
	Anorexia
	N+V or diarrhoea
	Dehydration and lethargy
o	As rises:
	Neuro complications:
•	Restless
•	Muscle fasiculations 
•	Hypertonicity
	Progress to:
•	Ataxia
•	Dysarthria 
•	Increased lethargy
•	Confusion and delirium 
•	Hypotenison and arrhythmia preced collapse emerging seizure, stupor and coma.
60
Q

Schneiders 1st rank symptoms?

A

• Auditory hallucinations:
o Voices repeating words out loud (Thought echo-gedankenlautwerden)
o 2+ hallucinatory voices discussing a subject or arguing about them in the srd person
o Voices commentating on the patients thoughts or behaviours
• Thought insertion and thought withdrawal
• Thought broadcasting
• Somatic passivity: Patient believes that sensations are being imposed on their body by and outside force.
• Made acts and feelings:
o Made acts: patient experiences his action as he will to be under the control of an outside force.
o Made feelings: The patient has the experience that his feelings are not his own and have been opposed upon him.
o Made impulses: The patient acts on a compelling impulse which they believe is not their own.
• Delusional perception: Normal event to which a delusion is attached

61
Q

Management of Hypotension?

A

1st line is fludrocortisone, unless HF or RF

2nd line is midodrine (sympathinomimetic)

62
Q

Refeeding syndrome

A

• Describes the metabolic abnormalities which occur when a person is fed following a period of starvation.
• It occurs when an extended period of catabolism ends abruptly with the need to switch to a carbohydrate metabolism.
• The metabolic consequences:
o Hypophosphatemia
o Hypokalaemia
o Hypomagnesaemia
o Abnormal fluid balance
• The body is used to fat metabolism so when there is a sudden increase in insulin in response to glucose, this forces potassium, magnesium and phosphate into cells. (the patient may have overall low levels hidden until this happens), this causes fluid to shift to the intracellular compartment
o Leads to:
 Cardiac failure/arrythmia
 Resp insufficiency
 Death (now rare)
• These abnormalities can lead to organ failure

63
Q

RF for Refeeding

A

• Patients are considered high risk with one of the following:
o BMI <16 kg/m^2
o Unintentional WL >15% over 3-6 months
o Little nutritional intake over 10 days
o One of the ion imbalances pre feeding
• If they have 2+ of:
o BMI <18.5 kg/M^2
o Unintentional WL >10% over 3-6 months
o Little nutritional intake over 5 days
o Hx of: Alcohol abuse, drug therapy, chemotherapy, diuretics

64
Q

What is the most common cause of cervical cancer?

A

Squamous cell carcinoma

65
Q

Initial management of closed angle glaucoma?

A

• NICE CKS 2019- need to be reviewed on the same day by an ophthalmologist. If there is a delay in admission, or while waiting for an ambulance:
o Lie patient on their back without a pillow
o Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
o Give acetazolamide 500 mg orally
o Give analgesia and antiemetics as required.
• Pilocarpine acts on the muscarinic receptors in the sphincter muscles of the iris and cause the constriction of the pupils.
o Therefore it is a miotic agent
o It also causes ciliary muscle contraction.
o Theses 2 effects cause the pathway for flow of the aqueous humour from the ciliary body, around the iris and trabecular meshwork to open up
• Acetazolamide is a carbonic anhydrase inhibitor. Reduces the production of aqueous humour.

66
Q

• Diabetic retinopathy can be split into 3 broad categories, based on the fundoscopic findings:

A

o Non proliferative (background/preproliferative)
 Mild- microaneurysms
 Moderate- microaneurysms, blot haemorrhages, hard exudates, cotton wall spots and venous bleeding
 Severe- Blot haemorrhages plus microaneurysm in 4 quadrants, venous bleeding in 2 quadrants, intraretinal microvascular abnormality in any quadrant.
o Proliferative
 Neovascualarisation
 Vitreous haemorrhage
o Diabetic Maculopathy
 Macular oedema
 Ischaemic maculopathy

67
Q

Crystal arthorpathy?

A

Negative bifringent needle - Gout

Positively bifringent Crystal- Pseudo gout

68
Q

Pembertons Sign?

A

Pemberton’s sign involves bilateral arm elevation, and a positive sign results in facial engorgement. The exam manoeuvre is useful for detecting superior vena cava (SVC) obstruction. Renal cell carcinoma is a rare cause of SVC syndrome from tumour metastasis compression of the vein.

69
Q

Key Ab to test for in nephritis?

A

ANCA and Anti-GBM

70
Q

Nephritic syndrome?

A

Nephritic syndrome- Group of symptoms not a diagnosis. It means that they fit the clinical picture of having inflammation of their kidney, it does not present a specific diagnosis or give an underlying cause. No set criteria, but the following are associated.
o Haematuria- either microscopic or macroscopic
o Oliguria- reduced UO
o Proteinuria (less than 3g/24 hrs- any more –> nephrotic)
o Fluid retention

71
Q

Nephrotic syndrome?

A

Nephrotic syndrome:

A group of symptoms without specific underlying cause. Must fulfil the following criteria:
	Peripheral oedema
	Proteinuria (more than 3g/24 hrs)
	Serum albumin under 25g/L
	Hypercholersteraemia
72
Q

Nephrotic syndrome key points?

A

Usually present with oedema.
May notice frothy urine (proteinuria). Predisposes patients to thrombosis, HTN and high cholesterol
o Most common cause:
 MCD- idiopathic and treated with steroid- children
 Focal segmental glomerulosclerosis- adults

73
Q

• Membranous glomerulonephritis

A

o Most common type of glomerulonephritis overall
o Bimodal peak of age in the 20s and 60s
o Histology shows “IgG and complement deposits on the basement membrane”
o The majority (-70%) are idiopathic
o Can be secondary to malignancy, Rheumatoid disorders and drugs (NSAIDs)

74
Q

Good pastures?

A

Anti-GBM ab attack the glomerulus and the pulmonary basement membranes- cause glomerulonephritis and pulmonary heamorrhage. In your exam, there may be a patient with AKI and haemoptysis

75
Q

Hyponatraemia signs and symptoms?

A

Early: nausea, Headache, malaise

Late (quick): Confusion, Seizures, coma)

76
Q

Hypervolaemic hyponatraemia?

A

Failure (liver, renal, heart)

Nephrotic syndrome

77
Q

Hypervolaemic hyponatraemia?

A

Urinary sodium:

High (renal):
Addisons
Diuretic
CKD diuresis

Low (extra renal):
Burns
Diarrhoea
Vomiting 
Stoma
78
Q

Euvolaemic hyponatraemia?

A

Urinary osmolality:

Low (under 500)
Psychogenic
Hypothyroid

High (over 500):
SIADH

79
Q

What are the 3 histological findings on Biopsy of IgA nephritis?

A

Mesangial proliferation, C3 and IgA deposition

80
Q

Features of AP syndrome?

A

C- Coagulopathy
L- Levido reticularis
O- Obs issues
T- Thrombocytopenia

81
Q

Dermatomyositis skin features?

A
  • Gottron lesions (scaly erythematous patches) on the knuckles, elbows and kness
  • Photosensitive erythematous rash on the back, shoulders and neck.
  • Purple rash on the face and eyelids  Heliotrope
  • Periorbital oedema (swelling around the eyes)
  • SC calcinosis
82
Q

What are the symptoms of Acromegaly?

A
Bitemporal hemionopia
Large spade like hands
Sweating 
Macroglossia
OSA
HTN 
Headache
Voice change 
Carpal tunnel syndrome
83
Q

Multiple myeloma?

A

Over expression of the B-lymphocyte cells, leading to over production of commonly IgG

84
Q

Supportive care in AML?

A
  • Blood transfusions for anaemia
  • Pt transfusions for thrombocytopenia
  • Abx for Leuco/Neutropenia
  • Counselling on Dx and Tx
85
Q

Endoscopic findings of CD, UC?

A

o Transmural lesion- Crohns
 Non-caseating epithelioid cell granulomata- hallmark only found in 30% of samples

o Superficial lesion- UC
 Histology reveals mucosal inflammation, crypt damage (cryptitis, architectural distortion, abscesses and crypt loss), and ulceration

86
Q

Main cause of stroke/TIA?

A

Carotid artery stenosis- treated with carotid endarectomy

87
Q

What are the 2 forms of gall stones?

A

Bile salt,

Cholesterol

88
Q

Risk of Catheter high outpu?

A

Post obstructive diuresis, high volume Output so monitor hourly UO and ensure adequate fluid rehydration.

89
Q

Criteria for screening?

A
Course of the disease should be known 
Acceptable screen availabel
Treatment available for all
Treatment protocol in place
Cost effective 
Prompt treatment benegit over delayed
90
Q

TURP syndrome?

A

Irrigant fluid (glycine) enters the prostates vascular bed and then the IV space, expaning to cause fluid overload and hyponatraemia

91
Q

Ulcer?

A

Break in the epithelial layer

92
Q

Addisons bloods?

A

Increased K+ low Na2+

neutrophilia

93
Q

Young man + WL fatigue and abdo pain?

A

Addisons- also low bp and hyperpigmentation. Bloods will show that the patient has hyponatraemia and hyperkalaemia

94
Q

Parkland formula?

A

Used in burns to caclulate fluids in the next 24 hrs:
4 * % burn * Weight- 24 hrs
Then give half in 8 hrs and the other half for 16 hrs.

95
Q

Dementia bloods?

A
FBC, CRP and ESR
U and E
Ca 2+
LFT 
Glucose
TFT
B12
Folate
Vit D
96
Q

3 areas to address immediately in demetia pt?

A

Social- is she safe at home
Physical- ?infection
Nutrition assessment

97
Q

Drugs for dementia

A

Memantine- monoamine oxidase inhibitor

Donepezil- AChesterase inhibitor

98
Q

4 point holistic care plan tension headache?

A
  1. Arrange CBT/ health education intervention
  2. Address medication use and self help
  3. Consider accupuncture
    4.
99
Q

What is the paediatric sepsis 6?

A

GOSH sepsis 6.

  1. Give high flow oxygen
  2. Obtain Access IV/Bone Take cultures and lactate
  3. Give IV/IO Abx
  4. Give IV/IO fluids +Measure UO- Catheter
  5. Consider Ionotropes
  6. Senior r/v immediate
100
Q

Signs and symptoms of SLE?

A
M alar rash
D iscoid rash
S erositis (pericarditis, Pleural effusion)
O ral/ nasal ulcers 
A rthralgia (>2)
P hotosensitive 
B Lood disorders (pancytopenia)
R enal disease (lupus nephritis)
A NA (+)
I mmunological (Anti DSDNA, Anti-SM)
N euro (seizures)
101
Q

Mx of SLE?

A

Flair- steroids and NSAIDs
Chronic- Hydroxychloroquine
Severe- Rituximab (anti CD20)-B cells

Severe flair- IV hydrocortisone and IV cyclophosphamide

102
Q

PE Wells score?

A
Clinical features of DVT
Tachycardia
Haemoptysis
Cancer (active/ <6 months)
PE is most likely diagnosis 
Previous DVT/PE
recent immobilisation (<3 days)
Surgery ( <4 weeks)
103
Q

Prognosis in PE?

A

PE severity Index

104
Q

Pre PE D/C

A
  1. Arrange Anti Coag F/U
  2. Verbal and written info on anti Coag
  3. Give pt anticoag alert card
  4. Provide written and verbal info on PE.
105
Q

Pt now has Met diagnosis?

A

Treatment is now palliative not for cure

Any ADR or LPA/DNA CPR etc

If patient wants control- advice them to make ADR, plan finances and wills,

106
Q

What are the three parts of a health economics evaluation?

A

Comparitive (of the 2 interventions)
Costs
Benefits

107
Q

2 features of a QALY?

A

Number of years expected to gain and the expected quality of life (0-1) score in those years.

108
Q

What system do Healthcare economists use to evaluate disability?

A

Disability adjusted life years (years of life lost due to premature mortality and years lived with disability

109
Q

Define healthcare econimics efficacy?

A

Effect of the intervention operating in ideal conditions.

Efficiency - maximising benefit for any cost or reducing cost for any benefit.

110
Q

Cmn causes of Coma?

A
  • Hypoglycaemia
  • Hypothermia
  • narcotic OD
  • Hypovolaemia
  • Subdural haematoma
111
Q

Which 2 services do you need to report never events too?

A

National reporting and learning system

Strategic Executive Information system