2017 (Paper 2) Flashcards
Lady with falciparum. Other than doxycycline, what other abx would you give her?
Options:
Chloroquine
Quinine
Proguanil
Pyrimethamine
Quinine
Non-artemisinin based combinations: Quinine plus tetracycline/doxycycline
Feature of severe malaria
- schizonts on a blood film
- parasitaemia > 2%
- hypoglycaemia
- acidosis
- temperature > 39 °C
- severe anaemia
- complications:
- cerebral malaria: seizures, coma
- acute renal failure: blackwater fever, secondary to intravascular haemolysis, mechanism unknown
- acute respiratory distress syndrome (ARDS)
- hypoglycaemia
- disseminated intravascular coagulation (DIC)
Uncomplicated falciparum malaria
- strains resistant to chloroquine are prevalent in certain areas of Asia and Africa
- the 2010 WHO guidelines recommend artemisinin-based combination therapies (ACTs) as first-line therapy
- examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine, artesunate plus sulfadoxine-pyrimethamine, dihydroartemisinin plus piperaquine
Severe falciparum malaria
- a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state
- intravenous artesunate is now recommended by WHO in preference to intravenous quinine
- if parasite count > 10% then exchange transfusion should be considered
- shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse
Which of the DMARDs cause retinopathy?
Options:
Hydroxychloroquine
Prednisolone
Sulfasalazine
Leflunomide
Hydroxychloroquine
Rheumatoid arthritis drug side effects
- Hydroxychloroquine
- Retinopathy
- Corneal deposits
- Methotrexate
- Myelosuppression
- Liver cirrhosis
- Pneumonitis
-
Sulfasalazine
- Rashes
- Oligospermia
- Heinz body anaemia
- Interstitial lung disease
- Leflunomide
- Liver impairment
- Interstitial lung disease
- Hypertension
- Prednisolone
- Cushingoid features
- Osteoporosis
- Impaired glucose tolerance
- Hypertension
- Cataracts
- Gold
- Proteinuria
- Penicillamine
- Proteinuria
- Exacerbation of myasthenia gravis
- Etanercept
- Demyelination
- Reactivation of tuberculosis
- Infliximab
- Reactivation of tuberculosis
- Adalimumab
- Reactivation of tuberculosis
- Rituximab
- Infusion reactions are common
- NSAIDs (e.g. naproxen, ibuprofen)
- Bronchospasm in asthmatics
- Dyspepsia/peptic ulceration
Which of the DMARDs cause azoospermia and bone marrow suppression?
Options:
Sulfasalazine
Azathioprine
Methotrexate
Leflunomide
Sulfasalazine
- Hydroxychloroquine
- Retinopathy
- Corneal deposits
- Methotrexate
- Myelosuppression
- Liver cirrhosis
- Pneumonitis
- Sulfasalazine
- Rashes
- Oligospermia
- Heinz body anaemia
- Interstitial lung disease
- Leflunomide
- Liver impairment
- Interstitial lung disease
- Hypertension
- Prednisolone
- Cushingoid features
- Osteoporosis
- Impaired glucose tolerance
- Hypertension
- Cataracts
- Gold
- Proteinuria
- Penicillamine
- Proteinuria
- Exacerbation of myasthenia gravis
- Etanercept
- Demyelination
- Reactivation of tuberculosis
- Infliximab
- Reactivation of tuberculosis
- Adalimumab
- Reactivation of tuberculosis
- Rituximab
- Infusion reactions are common
- NSAIDs (e.g. naproxen, ibuprofen)
- Bronchospasm in asthmatics
- Dyspepsia/peptic ulceration
Lady with tremor, weight loss, proptosis and exophthalmos. Has ophthalmoplegia. What is likely cause?
Options:
Rectus muscle thickening
Retrobulbar tumour
Cavernous sinus syndrome
Rectus muscle thickening
as seen in thyroid eye disease
Pathophysiology: it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation –> glycosaminoglycan and collagen deposition in the muscles
(frequently: inferior rectus > medial rectus > superior rectus) sparing their tendinous insertions, and is usually bilateral and symmetrical.
Features
- the patient may be eu-, hypo- or hyperthyroid at the time of presentation
- exophthalmos
- conjunctival oedema
- optic disc swelling
- ophthalmoplegia
- inability to close the eye lids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
Prevention
- smoking is the most important modifiable risk factor for the development of thyroid eye disease
- radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease. In a recent study of patients with Graves’ disease around 15% developed, or had worsening of, eye disease. Prednisolone may help reduce the risk
Management
- topical lubricants may be needed to help prevent corneal inflammation caused by exposure
- steroids
- radiotherapy
- surgery
69 year old guy with two previous TIAs and AF. What do you start him on?
Option:
Warfarin
Aspirin
Clopidogrel
Aspirin + Modified release dipyridamol
Warfarin or NOAC (Dabigatran, Rivaroxaban, Apixaban)
nb Direct oral anticoagulants (direct thrombin/Xa inhibitors) are used in the prevention of stroke secondary to non-valvular AF
Post ischaemic stroke prophylaxis:
- clopidogrel is now recommended by NICE ahead of combination use of aspirin plus modified release (MR) dipyridamole in people who have had an ischaemic stroke
- aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated, but treatment is no longer limited to 2 years’ duration
- MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated, again with no limit on duration of treatment
- Stoke secondary to AF:
- following a stroke or TIA warfarin or a DOAC should be given as the anticoagulant of choice.
- If valvular AF, Warfarin must be used
- Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities
- in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
- following a stroke or TIA warfarin or a DOAC should be given as the anticoagulant of choice.
Lady with hx of AF presents to A&E with fast AF, pulmonary oedema and peripheral oedema. What do you give initially?
Options:
Furosemide and warfarin
Furosemide and Ramipril
DC cardioversion (if an option)
Cardioversion indicated in Peri-arrest rhythms: tachycardia
- shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- syncope
- myocardial ischaemia
- heart failure
Furosemide and ?warfarin
- nb.acute pulmonary edema may increase sensitivity to ACE inhibition or angiotensin blockade, including risks of hypotension and renal dysfunction*
- warfarin will initiall decrease the INR (increase risk of clotti**ng) – it is often recommended that heparin should be administered in the ED if a AF patient is going to be admitted to hospital for expedited elective cardioversion (AF duration < 48 hours, or AF duration > 48 hours with a negative TEE study)*
Management options in acute heart failure include:
- oxygen
- diuretics
- opiates
- vasodilators
- inotropic agents
- CPAP
- ultrafiltration
- mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
Drug management of heart failure:
- first-line= ACE-inhibitor + beta-blocker
- second-line= aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate
- third line= cardiac resynchronisation therapy or digoxin* or ivabradine (in pt on ACE-inhibitor, beta-blocker + aldosterone antagonist, with HR > 75/min and a left ventricular fraction < 35%)
- diuretics should be given for fluid overload
- offer annual influenza vaccine
- offer one-off** pneumococcal vaccine
30 something man with joint pain - sacroilitis and distal interphalangeal joint pain?
Options:
Ank spond
Psoriatic arthritis
Rheumatoid arthritis.
Psoriatic arthropathy
correlates poorly with cutaneous psoriasis and often precedes the development of skin lesions. Around 10-20% percent of patients with skin lesions develop an arthropathy with males and females being equally affected
Types*
- rheumatoid-like polyarthritis: (30-40%, most common type)
- asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
- sacroilitis
- DIP joint disease (10%)
- arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
Management
- treat as rheumatoid arthritis
- but better prognosis
nb ankylosing spondylitis: affects axial spine
Guy on prednisolone presents with darkened red reflex and problems with night vision. What does he have?
Cataracts
opacities in lens, cornea or vitreous results in loss of red reflex
Presentation
- Increasing myopia
- Blurred vision → gradual visual loss
- Dazzling in sunshine / bright lights
- Monocular diplopia
Cause
Majority
- age related
- UV light
Systemic
- diabetes mellitus
- steroids
- infection (congenital rubella)
- metabolic (hypocalcaemia, galactosaemia)
- myotonic dystrophy
- Down’s syndrome
Ocular
- trauma
- uveitis
- high myopia
- topical steroids
Classification
- Nuclear: change lens refractive index, common in old age
- Polar: localized, commonly inherited, lie in the visual axis
- Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
- Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
Lady from some Pakistan or somewhere with HTN controlled on amlodipine and BP of 150/90 has retinal findings: blot haemorrhages and yellow deposits (hard exudates I think) on macula. What is this?
Options:
Hypertensive retinopathy
Diabetic retinopathy
NOTE: Drusen seen in age related macular degeneration
Background diabetic retinopathy
- microaneurysms (dots)
- blot haemorrhages (<=3)
- hard exudates
Pre-proliferative retinopathy
- cotton wool spots (soft exudates; ischaemic nerve fibres)
- > 3 blot haemorrhages
- venous beading/looping
- deep/dark cluster haemorrhages
- more common in Type I DM, treat with laser photocoagulation
Proliferative retinopathy
- retinal neovascularisation - may lead to vitrous haemorrhage
- fibrous tissue forming anterior to retinal disc
- more common in Type I DM, 50% blind in 5 years
Maculopathy
- based on location rather than severity, anything is potentially serious
- hard exudates and other ‘background’ changes on macula
- check visual acuity
- more common in Type II DM
Footballer inverts his ankle and presents with foot pain, surprised he has no ankle pain. What does he have?
Options:
Fractured base of 5th metatarsal
Damaged ligaments
Fractured base of 5th metatarsal
is caused by forcible inversion of the foot in plantar flexion
Associated with Lisfranc injury
Guy jumps and lands on his knee (repeated question)
Options:
medial meniscus tear
patella fracture
damage to ACL
patella fracture
Pulmonary adenocarcinoma Ca met to liver via what route?
Options:
Transcoelomic
Direct invasion
Haem
Lymph
Heamatogenous
Spread:
- local: to pleura, left recurrent laryngeal and phrenic nerve, pericardium, oesophagus, sympathetic chain, and brachial plexus
- Lymphatic: to mediastinal and cervical nodes. Compression of the SVC by massive mediastinal node involvement produces gross oedema and cyanosis of the face and upper limbs
- Blood: to bone, brain, liver and adrenals
- Transcoelomic: pleural seeding and effusion
Cancers which matastasise heamatogenously = Folicular, Renal Cell Ca, Hepatocellular carcinoma
- *Hematogenous–Hepatoma**
- *S**preading – Sarcoma
- *Cancers –Choriocarcinoma**
- *R**eign – Renal cell carcinoma
- *F**oolishly – Follicular carc. of the thyroid
Lady playing squash suddenly runs, hears a crack from behind ankle then pain whenever she tries to plantar flex. What happened?
options:
Ruptured Achilles
Fractured talus
Fractured calcaneus
Achilles tendon rupture
..suspected if the person describes the following whilst playing a sport or running; an audible ‘pop’ in the ankle, sudden onset significant pain in the calf or ankle or the inability to walk or continue the sport.
An examination should be conducted using Simmond’s triad, to help exclude Achilles tendon rupture. This can be performed by asking the patient to lie prone with their feet over the edge of the bed. The examiner should look for an abnormal angle of declination; Achilles tendon rupture may lead to greater dorsiflexion of the injured foot compared to the uninjured limb. They should also feel for a gap in the tendon and gently squeeze the calf muscles if there is an acute rupture of the Achilles tendon the injured foot will stay in the neutral position when the calf is squeezed.
An acute referral should be made to an orthopaedic specialist following a suspected rupture.
Middle aged lady presenting with atypical chest pain – what would be used to decide pre test probability she has ischaemic heart disease?
Options:
Epidemiological evidence of something
Case control study on atypical chest pain RFs
Clinical experience
Exercise ECG
Epidemiological evidence of something
Evidence based medicine works by deciding pre-test probability of something and then doing tests and changing the probability of that thing accordingly.
Pretest Probability
- Definition
- Pretest Probability is defined as the probability of a patient having the target disorder before a diagnostic test result is known. It represents the probability that a specific patient, say a middle-aged man, with a specific past history, say hypertension and cigarette smoking, who presents to a specific clinical setting, like Accident and Emergency, with a specific symptom complex, say retrosternal chest pressure, dyspnoea and diaphoresis, has a specific diagnosis, such as acute myocardial infarction.
- Application
- The pretest probability is especially useful for four things:
- interpreting the results of a diagnostic test,
- selecting one or more diagnostic tests
- choosing whether to start therapy:
- * a) without further testing (treatment threshold);
- * b) while awaiting further testing;
- deciding whether it’s worth testing at all (test threshold)
- Calculation
- The probability of the target disorder, usually abbreviated P(D+), can be calculated as the proportion of patients with the target disorder, out of all the patients with the symptoms(s), both those with and without the disorder:
- P(D+) = D+ / (D+ + D-)
- where D+ indicates the number of patients with target disorder, D- indicates the number of patients without target disorder, and P(D+) is the probability of the target disorder.
- The probability of the target disorder, usually abbreviated P(D+), can be calculated as the proportion of patients with the target disorder, out of all the patients with the symptoms(s), both those with and without the disorder:
- Example:
- A group of investigators in North America studied the underlying diseases found in patients presenting to a primary care setting with persistent dizziness. They studied a total of 100 dizzy patients, finding 16 had dizziness from psychiatric conditions.
- Thus, 16 / 100, or 16 per cent, is the estimate of of disease probability for psychiatric conditions from this study.
- So, if this information proves valid and applicable to your practice, if IF one of your patients presents to a primary care setting with persistent dizziness, the P(D+) of a psychiatric cause might be estimated at 16 per cent.
Person with 4cm head of pancreas ca that has invaded mesenteric vessels. How do you manage?
options
ERCP and biliary stent
PTC drainage
Whipple’s
Vit k
Abx
ERCP and biliary stent
Management
- less than 20% are suitable for surgery at diagnosis
- Resectable:
- a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas.
- Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
- adjuvant chemotherapy is usually given following surgery
- a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas.
- Palliation:
- ERCP with stenting is often used for palliation
Son of 75 year old lady requests home visit for mother who has recent behavioural changes. Sometimes gets confused and sees people in the room who aren’t there. Recent loss of appetite. Cause?
options:
Lewy body dementia
Alzheimer’s
Acute Confusional State
Depression with psychosis
Acute confusional state
is also known as delirium or acute organic brain syndrome. It affects up to 30% of elderly patients admitted to hospital.
Features - wide variety of presentations
- memory disturbances (loss of short term > long term)
- may be very agitated or withdrawn
- disorientation
- mood change
- visual hallucinations
- disturbed sleep cycle
- poor attention
(if not an option, potentially LBD)
Guy post-op with delirium and morphine epidural in situ, what is best initial management?
Options:
Put in well lit side room
Haloperidol
Discontinue morphine epidural
Put in a well lit side room
Management of Acute Confusional State
- treatment of underlying cause
- modification of environment
- haloperidol 0.5 mg as the first-line sedative or olanzapine
Guy with short history of back pain and painless black lesions on his feet appear. What ix do you do?
Options:
Arteriogram
CT abdo
CT abdo with contrast
Abdominal aortic aneurysms occur primarily as a result of the failure of elastic proteins within the extracellular matrix. Aneurysms typically represent dilation of all layers of the arterial wall. Most aneurysms are caused by degenerative disease. After the age of 50 years the normal diameter of the infrarenal aorta is 1.5cm in females and 1.7cm in males. Diameters of 3cm and greater, are considered aneurysmal. The pathophysiology involved in the development of aneurysms is complex and the primary event is loss of the intima with loss of elastic fibres from the media. This process is associated with, and potentiated by, increased proteolytic activity and lymphocytic infiltration.
symptomatic
- pain in the abdomen, loin or lower back
- abdominal pain may spread to the back
- require urgent referral for investigation and management because they may indicate impending rupture
- patient may feel a pulsatile mass in the abdomen
- features of limb ischemia - caused by distal embolisation
- lower extremity oedema
- rarely seen caused by compression of the inferior vena cava
Investigations
- ultrasonography
- non invasive, low cost method with the sensitivity and specificity close to 100%
- measures the size of the aorta in longitudinal as well as in anteroposterior and transverse directions
- modality of choice for initial assessment, follow up, screening and surveillance
- should have a low threshold for arranging abdominal ultrasonography in patients at risk.
- CT
- can visualise
- the proximal neck (the transition between the normal and aneurysmal aorta)
- any extensions of the aneurysm (to the iliac areries)
- patency of visceral arteries
- the presence of blood within the thrombus (crescent sign) - is considered a predictive marker of imminent rupture
- helical CT and CT angiography can provide additional anatomical details - useful if an endovascular procedure is considered
- can visualise
- resonance angiography (MRA)
- safer than conventional arteriography since it does not use nephrotoxic contrast material
- plain radiography
- calcified aneurysmal wall may be seen in some cases
Guy presenting to GP with nocturia. PSA 18, urinalysis trace blood and protein, urea and cr mildly elevated. What do you do?
Options:
Refer routinely to uro
Refer urgently to uro
Refer routinely to renal
Refer urgently to renal
Refer urgently to uro
refer men using a suspected cancer pathway referral (for an appointment within 2 weeks) for prostate cancer if their PSA levels are above the age-specific reference range
Management Programme are as follows:
- aged 50-59 >= 3.0 ng/ml;
- aged 60-69 >= 4.0 ng/ml;
- aged 70 and over > 5.0 ng/ml.
- (Note that there are no age-specific reference ranges for men over 80 years. Nearly all men of this age have at least a focus of cancer in the prostate. Prostate cancer only needs to be diagnosed in this age group if it is likely to need palliative treatment.)
exclude urinary infection before PSA testing. Postpone the PSA test for at least 1 month after treatment of a proven urinary infection (indicated by nitrite and leucocyte on urine dip)
?75 year old lady with 2.5cm firm breast lump not tethered to skin and no skin changes. Daughter 40 year old just had benign breast cyst diagnosed. What does the old lady have?
Options:
Ductal carcinoma
Breast cyst
Lobular carcinoma in situ
Ductal carcinoma
- Age, solitary, firm lump – increases likelihood of cancer vs benign cyst. Ductal (70%) more common than lobullary, proliferative breast disease with atypia = risk factor
Breast cyst
- 7% of all Western females will present with a breast cyst
- Usually presents as a smooth discrete lump (may be fluctuant)
- Small increased risk of breast cancer (especially if younger)
Commonest Single Breast Lumps
- Fibroadenoma
- Cyst
- Fat necrosis
- Cancer
Features of a Malignant Lump
- Irregular, nodular surface
- Poorly defined edge
- Hard / scirrhous consistency
- Painless
- Fixation to skin or chest wall
- Nipple involvement
In this patient AGE makes Ca more likely?
45 year old lady with spontaneous dark brown nipple discharge. Examination reveals only one duct producing discharge. What does she have?
options:
Intraductal papilloma
Duct ectasia
Intraductal papilloma
- Commoner in younger patients
- May cause blood stained discharge originating from a single duct
- There is usually no palpable lump
- NO risk of malignancy
- Growth of papilloma in a single duct
Duct ectasia
- Dilatation breast ducts.
- Most common in menopausal women
- Discharge typically thick and green in colour, which may be from single or multiple ducts (usually present age >50 years)
- Most common in smokers
Tall 28 year old man with radiofemoral delay and hypertension. BP 210/110. Has rib notching. What is underlying diagnosis?
Options:
Coarctation
Marfan’s
ED
Coarctation of the aorta
…describes a congenital narrowing of the descending aorta
more common in males (despite association with Turner’s syndrome)
Features:
- infancy: heart failure
- adult: hypertension
- radio-femoral delay
- mid systolic murmur, maximal over back
- apical click from the aortic valve
- notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
Associations
- Turner’s syndrome
- bicuspid aortic valve
- berry aneurysms
- neurofibromatosis
Marfans is associated with the following cardiac abnormalities:
- Aortic aneurysm and dissection
- Aortic root dilatation → regurgitation
- MV prolapse ± regurgitation
The post MI papillary muscle rupture question (repeated again)
Revision Qs:
How will this present?
List the complications of an MI
Acute mitral regurgitation
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. An early-to-mid systolic murmur is typically heard and late systolic click. Patients are treated with vasodilator therapy but often require emergency surgical repair.
Death Passing PRAED st.
- Death: VF, LVF, CVA
- Pump Failure
- Pericarditis
- Rupture: myomalacia cordis
- Cardiac tamponade
- Papillary muscle / chordae → MR
- Septum
- Arrhythmias
- Tachycardias
- SVT
- Ventricular T/F
- Bradycardia
- sinus brady
- AV block
- Ventricular brady
- Tachycardias
- Aneurysm: ventricular
- Dressler’s Syndrome: pleuro-pericarditis
Young guy vomiting after a night out presents with chest and epigastric pain, left sided pleural effusion, subcutaneous emphysema. What happened?
Oesophageal rupture
Boerhaave syndrome: Severe vomiting → oesophageal rupture
Defined as: Complete disruption of the oesophageal wall in absence of per-existing pathology. Left postero-lateral oesophageal is commonest site (2-3cm from OG junction). Suspect in patients with severe chest pain without cardiac diagnosis and signs suggestive of pneumonia without convincing history, where there is history of vomiting. Erect CXR shows infiltrate or effusion in 90% of cases
- Other:*
- Mallory-Weiss syndrome: Severe vomiting → painful mucousal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics*
- Plummer-Vinson syndrome: Triad of: dysphagia (secondary to oesophageal webs) + glossitis + iron-deficiency anaemia. Treatment includes iron supplementation and dilation of the webs*
Sickle cell girl with severe back pain (?) What do you do first?
Options:
Exchange transfusion
Epidural anaesthesia
Paracetamol/ibuprofen
Fluid bolus
Fluid bolus
Sickle cell anaemia is characterised by periods of good health with intervening crises
Four main types of crises are recognised:
- Thrombotic crises/Vaso-occlusive ‘painful’ crisis:
- precipitated by infection, dehydration, deoxygenation
- infarcts occur in various organs including the bones (e.g. avascular necrosis of hip, hand-foot syndrome in children, lungs, spleen and brain
- may cause mesenteric ischaemia, mimicking an acute abdomen
- Sequestration crises
- sickling within organs such as the spleen or lungs causes pooling of blood with worsening of the anaemia
- acute chest syndrome: dyspnoea, chest pain, pulmonary infiltrates, low pO2 - the most common cause of death after childhood
- Aplastic crises
- caused by infection with parvovirus
- sudden fall in haemoglobin
- Haemolytic crises
- rare
- fall in haemoglobin due an increased rate of haemolysis
Give prompt, generous analgesia, eg IV opiates (see p576).
• Crossmatch blood. FBC, reticulocytes, blood cultures, MSU ± CXR if T° or chest signs.
• Rehydrate with IVI and keep warm. Give O2 by mask if Pa O2 or O2 sats <95%.
• ‘Blind’ antibiotics (eg cephalosporin, p382) if T° >38°, unwell, or chest signs.
• Measure PCV, reticulocytes, liver, and spleen size twice daily.
• Give blood transfusion if Hb or reticulocytes fall sharply. Match blood for the blood group antigens Rh(C, D, E) and Kell, to prevent alloantibody formation. This helps oxygenation, and is as good as exchange transfusion (reserved for those who are rapidly worsening: it is a process where blood is removed and donor blood is given in stages). 40 Indications: severe chest crisis, suspected CNS event or multiorgan failure—when the proportion of HbS should be reduced to <30%.
Mx Acute Crises
- General
- Analgesia: opioids IV
- Good hydration
- O2
- Keep warm
- Ix
- FBC, U+E, reticulocytes, cultures
- Urine dip
- CXR
- Rx
- Blind Abx: e.g. ceftriaxone
- Transfusion: exchange if severe
Old man with smear cells. Cause?
Options
CLL
Hodgkin’s
NHL
CLL
Chronic lymphocytic leukaemia is caused by a monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells (99%)
Features
- often none
- constitutional: anorexia, weight loss
- bleeding, infections
- lymphadenopathy more marked than CML
Complications
- hypogammaglobulinaemia leading to recurrent infections
- warm autoimmune haemolytic anaemia in 10-15% of patients
- transformation to high-grade lymphoma (Richter’s transformation)
Investigations
- blood film: smudge cells (also known as smear cells)
- immunophenotyping
Guy on ibuprofen started recently for some pain. Comes in with two episodes of vomiting bright red blood. No further episodes. Stable obs, low Hb. What do you do?
Options
Observe for 24 hours and discharge with omeprazole
OGD within 2 hours
OGD on next endoscopy list
OGD on next endoscopy list (<24hrs)
Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI endoscopy within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist present.
Management of GI bleed
ABCDE: CIRCULATION!
- Resuscitate:
- Head down
- Airway: Early control of airway is vital (e.g. Drowsy patient with liver failure) -> protect the airway
- Breathing: 100% O2
-
C 2x 14G cannulae:
- Bloods: cross match blood, check FBC, LFTs (ETOH abuse), U+E (protein meal) and Clotting and ABG (lactate + Hb) and glucose
- IV crystalloid infusion up to 1L (avoid dilution)
- D: blood glucose, GCS, Temperature, expose (PR; maleana)
- Major H’gge protocol: on-going bleeding and haemodynamic instability are likely to require O negative blood pending cross matched blood
- keep Hb >10
- Upper GI endoscopy (scoring systems)
- all within 24 hours of admission.
- If unstable = immediately after resuscitation or in tandem with it.
Lady collapses on hospital ward. Had co-amox in A&E earlier and reports feeling breathless before collapse, 2 hours later is slightly tachy, slightly hypotensive, resp rate 34, sats 94% on 10L o2. What do you give first?
Options:
Adrenaline
Chlorephenamine
Steroids
IV fluid bolus
Adrenaline IM 500 micrograms (0.5ml 1 in 1,000)
hydrocortisone (200mg)
Chlorphenamine (10mg)
Salbutamol (5mg)
PBC question: antibody test for PBC
anti-mitochondrial antibodies (AMA) M2
subtype are present in 98% of patients and are highly specific
Primary biliary cirrhosis (now increasingly referred to as primary biliary cholangitis) is a chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman
Associations:
- Sjogren’s syndrome (seen in up to 80% of patients)
- rheumatoid arthritis
- systemic sclerosis
- thyroid disease
Diagnosis
- anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
- smooth muscle antibodies in 30% of patients
- raised serum IgM
Management
- pruritus: cholestyramine
- fat-soluble vitamin supplementation
- ursodeoxycholic acid
- liver transplantation e.g. if bilirubin > 100 (PBC is a major indication) - recurrence in graft can occur but is not usually a problem
PBC questions: histology showing classic PBC
Granulomatous
- PBC: intrahepatic destruction by chronic granulomatous inflammation results in cirrhosis*
- PSC: inflammation, fibrosis and strictures and intra and extrahepatic ducts*
Primary biliary cirrhosis (now increasingly referred to as primary biliary cholangitis) is a chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis, which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman
Clinical features
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
Complications
malabsorption: osteomalacia, coagulopathy
sicca syndrome occurs in 70% of cases
portal hypertension: ascites, variceal haemorrhage
hepatocellular cancer (20-fold increased risk)
Guy with metastatic renal cancer has severe pain. is/has vomited 4 times or something. Currently on oral morphine solution prn and helps for about 2 hours. What pain therapy should he be on?
Options:
Fentanyl transdermal
Morphine sub cut infusion
Morphine subcut prn
Oral morph slow release tablets
Oral morph solution prn
absence of Renal failure => Morphine sub cut infusion
Fentanyl transdermal Opioids should be used with caution in patients with chronic kidney disease. Alfentanil, buprenorphine and fentanyl are preferred
Vominting, therefore not:
Morphine subcut prn
Oral morph slow release tablets
Oral morph solution prn
Someone with previous TKR, now tender, febrile, hot, swollen. No evidence of crystals on microscopy. Aspirate showed turbid fluid.
Options:
Septic arthritis
Reactive arthritis
Gout
Septic Arthrisis
Symptoms
- Acutely inflamed tender, swollen joint.
- ↓ROM
- Systemically unwell
Investigations
- Joint aspiration for MCS
- ↑↑ WCC (e.g. >50,000/mm3) : mostly PMN
- ↑ESR/CRP, ↑WCC, Blood cultures
- X-ray
Management
- IV Abx: vanc + cefotaxime
- Consider joint washout under GA
- Splint joint
- Physiotherapy after infection resolved
Nutrient deficiency in coeliacs
Folate deficiency
Complications of coeliac disease
- anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
- hyposplenism
- osteoporosis, osteomalacia (vit D)
- lactose intolerance
- enteropathy-associated T-cell lymphoma of small intestine
- subfertility, unfavourable pregnancy outcomes
- rare: oesophageal cancer, other malignancies
Coeliac disease is an autoimmune condition caused by sensitivity to the protein gluten. It is thought to affect around 1% of the UK population. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
Signs and symptoms: (indications for coeliac disease screening)
- Chronic or intermittent diarrhoea
- Failure to thrive or faltering growth (in children)
- Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
- Prolonged fatigue (‘tired all the time’)
- Recurrent abdominal pain, cramping or distension
- Sudden or unexpected weight loss
- Unexplained iron-deficiency anaemia, or other unspecified anaemia
associated condictions: (indications for coeliac disease screening)
- Autoimmune thyroid disease
- Dermatitis herpetiformis
- Irritable bowel syndrome
- Type 1 diabetes
- First-degree relatives (parents, siblings or children) with coeliac disease
Guy who smokes and keeps pigeons, progressive shortness of breath on climbing hills. CXR shows reticulonodular shadowing.
Options
EAA
IPF
Pneumonia
Extrinsic allergic alveolitis (EAA, also known as hypersensitivity pneumonitis)
…is a condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. It is thought to be largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.
Examples
- bird fanciers’ lung: avian proteins
- farmers lung: spores of Saccharopolyspora rectivirgula (formerly Micropolyspora faeni)
- malt workers’ lung: Aspergillus clavatus
- mushroom workers’ lung: thermophilic actinomycetes*
Presentation
- acute: occur 4-8 hrs after exposure, SOB, dry cough, fever
- chronic
Investigation
- chest x-ray: upper/mid-zone fibrosis
- bronchoalveolar lavage: lymphocytosis
- blood: NO eosinophilia
Acute presentation of gout. PMH Heart failure, on ramipril. 3rd recurrence. What do you give?
Options:
Naproxen
Colchicine
Allopurinol
Colchicine
BNF: Colchicine is an alternative in patients in whom NSAIDs are contra-indicated. Aspirin is not indicated in gout. Allopurinol, febuxostat, and uricosurics are not effective in treating an acute attack and may prolong it indefinitely if started during the acute episode.
The use of colchicine is limited by the development of toxicity at higher doses, but it is of value in patients with heart failure since, unlike NSAIDs, it does not induce fluid retention; moreover, it can be given to patients receiving anticoagulants.
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)
Acute management
- NSAIDs
- intra-articular steroid injection
- colchicine* has a slower onset of action. The main side-effect is diarrhoea
- oral steroids may be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
- if the patient is already taking allopurinol it should be continued
Chronic Management Allopurinol prophylaxis
- allopurinol should not be started until 2 weeks after an acute attack has settled as it may precipitate a further attack if started too early
- initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l
- NSAID or colchicine cover should be used when starting allopurinol
- Indications
- recurrent attacks - ‘if a second attack, or further attacks occur within 1 year’
- tophi
- renal disease
- uric acid renal stones
- prophylaxis if on cytotoxics or diuretics
Lifestyle modifications
- reduce alcohol intake and avoid during an acute attack
- lose weight if obese
- avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
Other points
- losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistant hypertension
- calcium channel blockers also decrease uric acid levels, possibly by a renal vasodilatory effect
- increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
Caucasian lady with hands that change from White → blue → red
Raynaud’s phenomena
…may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon)
Raynaud’s disease typically presents in young women (e.g. 30 years old) with symmetrical attacks
Factors suggesting underlying connective tissue disease
- onset after 40 years
- unilateral symptoms
- rashes
- presence of autoantibodies
- features which may suggest rheumatoid arthritis or SLE, for example arthritis or recurrent miscarriages
- digital ulcers, calcinosis
- very rarely: chilblains
Secondary causes
- connective tissue disorders: scleroderma (most common), rheumatoid arthritis, SLE
- leukaemia
- type I cryoglobulinaemia, cold agglutinins
- use of vibrating tools
- drugs: oral contraceptive pill, ergot
- cervical rib
Management
- first-line: calcium channel blockers e.g. nifedipine
- IV prostacyclin infusions: effects may last several weeks/months
Post transplant patient has dry cough and SOB. Desaturates from 90+ to 83% on exercising. What does he have?
Options:
PCP
TB
PCP
…Whilst the organism Pneumocystis carinii is now referred to as Pneumocystis jiroveci, the term Pneumocystis carinii pneumonia (PCP) is still in common use
- Pneumocystis jiroveci is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
- PCP is the most common opportunistic infection in AIDS
- all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis
Features
- dyspnoea
- dry cough
- fever
- very few chest signs
Pneumothorax is a common complication of PCP.
Extrapulmonary manifestations are rare (1-2% of cases), may cause
- hepatosplenomegaly
- lymphadenopathy
- choroid lesions
Investigation
- CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal
- exercise-induced desaturation
- sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
Management
- co-trimoxazole
- IV pentamidine in severe cases
- steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)
Bilateral conductive hearing loss in old lady (Had to interpret Rinne Webers to work it out). Cause?
Options:
Otosclerosis
Meniere’s
Presbyacusis
Otosclerosis
Rinne’s test
- tuning fork is placed over the mastoid process until the sound is no longer heard, followed by repositioning just over external acoustic meatus
- air conduction (AC) is normally better than bone conduction (BC)
- if BC > AC then conductive deafness
Otosclerosis describes the replacement of normal bone by vascular spongy bone. It causes a progressive conductive deafness due to fixation of the stapes at the oval window. Otosclerosis is autosomal dominant and typically affects young adults
Onset is usually at 20-40 years - features include:
- conductive deafness
- tinnitus
- normal tympanic membrane*
- positive family history
Management
- hearing aid
- stapedectomy
*10% of patients may have a ‘flamingo tinge’, caused by hyperaemia
Conductive: Impaired conduction anywhere between auricle and
round window.
Canal obstruction: wax, FB
TM perforation: trauma, infection
Ossicle defects: otosclerosis, infection
Fluid in middle ear
SNHL: Defects of cochlea, cohlear N. or brain
Congenital
- Alports: SNHL + haematuria
- Jewell-Lange-Nielsen: SNHL + long QT
Acquired
- Presbyacussis
- Drugs: gentamicin, vancomycin
- Infection: meningitis, measles
- Tumour: vestibular schwannoma
Other: Meniere’s, MS, CPA lesion (e.g. acoustic neuroma), ↓B12
Someone with URTI symptoms has purple nodules on shins. What does she have?
Erythema nodosum
Erythema multiforme
Erythema nodosum
Overview
- inflammation of subcutaneous fat
- typically causes tender, erythematous, nodular lesions
- usually occurs over shins, may also occur elsewhere (e.g. forearms, thighs)
- usually resolves within 6 weeks
- lesions heal without scarring
Causes
- infection: streptococci, TB, brucellosis
- systemic disease: sarcoidosis, inflammatory bowel disease, Behcet’s
- malignancy/lymphoma
- drugs: penicillins, sulphonamides, combined oral contraceptive pill
- pregnancy
Commonest cause of corneal ulceration (branching)?
HSV
VZV
HIV
HSV
- Causes: bacterial, herpetic, fungal, protozoa, vasculitic (RA)
- Dendritic ulcer = Herpes simplex
- Acanthamoeba: protazoal infection affecting contact lens wearers swimming in pools.
Presentation
- Pain, photophobia
- Conjunctival hyperaemia
- ↓ acuity
- White corneal opacity
Risk factors: contact lens wearers
Ix: green c¯ fluorescein on slit lamp
Rx: refer immediately to specialist who will
- Take smears and cultures
- Abx drops, oral/topical aciclovir
- Cycloplegics/mydriatics ease photophobia
- Steroids may worsen symptoms: professionals only
Complications: Scarring and visual loss
Ophthalmic Shingles
Zoster of CNV1
20% of all Shingles (only commoner in thoracic dermatomes)
Presentation
- Pain in CNV1 dermatome precedes blistering rash
- 40% → keratitis, iritis
-
Hutchinson’s sign
- Nose-tip zoster due to involvement of nasociliary branch.
- ↑ chance of globe involvement as nasociliarry nerve also supplies globe
-
Ophthalmic involvement
- Keratitis + corneal ulceration (fluorescein stains)
- ± iritis
Painful vesicular derm lesion on one side of face around forehead, eye and cheek. Cause?
Options:
VZV
Herpes simplex
VZV (or Herpes Zoster)
Shingles is an acute, unilateral, painful blistering rash caused by reactivation of the Varicella Zoster Virus (VZV).
- Reactivation is due to ↓ immunity/stress
- Lifetime prevalence = 20%
- Painful vesicular rash in dermatomal distribution
- Thoracic and ophthalmic most commonly
- Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.
- Multidermatomal / disseminated in immunocomp
- Ramsay Hunt = ear zoster, facial palsy, ↓ taste, ↓ hearing
- Thoracic and ophthalmic most commonly
- Rx may ↓ progression to post-herpetic neuralgia <72hrs:
- Aciclovir PO/IV
- Famciclovir
- Valaciclovir
- Post-Herpetic neuralgia = severe dermatomal pain
*
65 yo guy comes to GP with new onset dyspepsia. No weight loss or dysphagia. What do you do first?
- Options:*
- H.pylori stool antigen test*
Refer routinely
Refer 2 weeks
OGD.
H.pylori stool antigen testing
urgent specialist referral for endoscopic investigation (i.e. seen within 2 weeks) is indicated for patients of any age with dyspepsia when presenting with any of the following:
- chronic gastrointestinal bleeding
- progressive unintentional weight loss
- progressive difficulty swallowing
- persistent vomiting
- iron deficiency anaemia
- epigastric mass or suspicious barium meal
- nb. also indicated if recent onset rapidly progressive symptoms
Routine endoscopic investigation of patients of any age, presenting with dyspepsia and without alarm signs, is not necessary
- however, for patients over 55 years old, consider endoscopy when symptoms persist despite Helicobacter pylori (H. pylori) testing and acid suppression therapy, and when patients have one or more of the following: previous gastric ulcer or surgery, continuing need for NSAID treatment or raised risk of gastric cancer or anxiety about cancerReference:
30+ year old lady with fever and fits. Scan shows temporal lobe necrosis. Cause?
Options:
HSV
Rabies
HSV
From the meninges, the virus extends to the adjacent brain where it affects the temporal and inferior frontal lobes first and more severely, and then spreads to the rest of the brain. Adult HSV encephalitis is limited to the brain. Its symptoms are fever, confusion, coma, and seizures. In addition, because of the involvement of the frontal and temporal lobes, patients often display bizarre behaviour, personality changes, anosmia, and gustatory hallucinations. Survivors may have Korsakoff’s amnesia, because of bilateral damage of the hippocampus, dementia, and seizures.
The brain in advanced HSV encephalitis shows diffuse softening and edema, accentuated by hemorrhagic necrosis of the i_nferior frontal and temporal lobes_.
Ring enhancing lesions on ct brain with HIV?
Toxoplasmosis
Toxoplasma gondii is a protozoa which infects the body via the GI tract, lung or broken skin. It’s oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.
Toxoplasmosis
- accounts for around 50% of cerebral lesions in patients with HIV
- constitutional symptoms, headache, confusion, drowsiness
- CT: usually single or multiple ring enhancing lesions, mass effect may be seen
- management: sulfadiazine and pyrimethamin
Blood transfusion, starts second unit, immediately has chest pain, SOB, dark urine. What happened?
Options:
ABO incompatibility
Immediate haemolytic transfusion reaction
Transfusion associated circulatory overload
Haemolytic transfusion reaction
ABO incompatibility
Febrile non-haemolytic transfusion reaction
- Signs and symptoms: Fever, chills, headache, malaise, flushing
- Mechanism: host abs vs donor MHC antigens or due to cytokines from leukocytes in donor blood
- Treatment: discontinue transfusion, fever resolves in 15-30 mins without specific treatment. Paracetamol may be used
- Other: most common transusion reaction, can be prevented with leukocyte filters or irradiation
Haemolytic transfusion reaction
- Signs and symptoms: Fever, chills, pain at the infusion site, dark urine, nausea, shock
- Mechanism: ABO incompatibility with host abs vs antigens on donor RBCs
- Treatment: discontinue transfusion, administer fluids
- Other: most SEVERE reaction
Allergic transfusion reaction
- Signs and symptoms: Uritcaria, pruritus
- Mechanism: allergic reaction to plasma proteins in transfused blood
- Treatment: DOES NOT require discontinuing transfusion, symptomatic treatment with antihistamines
- Other: can be prevented with anti-histamine pre-treatment
Anaphylactic transfusion reaction
- Signs and symptoms: Uritcaria, angioedema, wheezing, laryngeal oedema, abdo pain, hypotension, shock
- Mechanism: Host abs vs IgA antibodies in the donor plasma
- Treatment: discontinue transfusion, administer adrenaline
- Other: Seen in pts with IgA deficiency, can be prevented by administering washed IgA decifient products
Transfusion relatied acute lung injury (TRALI)
- Signs and symptoms: dyspnoea, hypoxaemia, bilateral chest infiltrates
- Mechanism: donor Abs to MHC class I/II/Human neutrophil antigens. Activated neutrophils cause endothelial damage
- Treatment: discontinue transfusion, provide airway support
- Other: most common cause of transfusion related DEATH
Transfusion associated circulatory overload
- Signs and symptoms: dyspnoea, pulmonary oedema, HTN, peripheral oedema
- Mechanism: rapid volume expansion.
- Treatment: supportive, diuretics can be used
- Other: seen in elderly pts with HF/anaemia, can be prevented with slower transfusions and diuretics
Patent ductus arteriosus murmur. What is it?
Options:
Machinery murmur
Diastolic murmur
Venous hum
Machinery murmur
Patent Ductus Arteriosis
- a form of congenital heart defect
- generally classed as ‘acyanotic’. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cynaosis.
- connection between the pulmonary trunk and descending aorta
- more common in premature babies, born at high altitude or maternal rubella infection in the first trimester
Features
- left subclavicular thrill
- continuous ‘machinery’ murmur
- large volume, bounding, collapsing pulse
- wide pulse pressure
- heaving apex beat
Management
- indomethacin closes the connection in the majority of cases
- if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
Old person with painful swollen knee and now has swollen dip.?
Options:
Osteoarthritis
Rheumatoid arthritis
Osteoarthritis
Bouchards nodes: Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular cartilage. (NB: RA is a disease of the synovium, DIPs are not synovial!)
Heberdens nodes: Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways.
Patient has dislocated shoulder. What nerve should we watch out for?
options:
Axillary
Radial
Ulnar
Axillary nerve
- Axillary nerve* (C5,C6): Motor=Shoulder abductions (deltoid) I Sensory=Inferior region of the Deltoid muscle I Injured=humeral neck #/dislocation, Result=deltoid wasting
- Radial nerve* (C5-C8): Motor=Extension (forearm, wrist, fingers, thumb) I Sensory= Small area between the dorsal aspect of the 1st and 2nd metacarpals I Injured=Humeral midshaft fracture, Result=Palsy results in wrist drop
- Median nerve* (C6, C8, T1): Motor=LOAF* muscles, @wrist=paralysis of thenar muscle, opponens pollicis, @elbow=loss of pronation of forearem and weak wrist flexion I Sensory=Palmar aspect of lat 3.1/2 fingers I Injured=wrist lesion (CTS)
- Ulnar nerve* (C8, T1): Motor=Intrinsic hand muscles except LOAF* and wrist flexion I Sensory=Medial 1.1/2 fingers. I Injured= medial epicondyle #, damage may result in claw hand
- Musculocutaneous nerve* (C5-C7): Motor=Elbow flexion (supplies biceps brachii) and supination I Sensory=Lateral part of the forearm I Injured=Isolated injury rare - usually injured as part of brachial plexus injury
- Long thoracic nerve* (C5-C7): Motor=Serratus anterior I Injured=Often during sport e.g. following a blow to the ribs. Also possible complication of mastectomy. Result= in a winged scapula
Guy with pulseless electrical activity, given one dose of adrenaline/epinephrine. Still no carotid pulse. What now?
Options:
Another dose of adrenaline
Shock
Pericardiocentiesis
Another dose of adrenaline
Guidance for a non-shockable rhythm: Give adrenaline every 3-5minutes
Pericardiocentiesis: only if indicated (US)
Man newly diagnosed with DM found to have glucose+++ in urine, BMI 32, random blood glucose 14. First line?
Options:
Diet and exercise
Metformin
Gliclazide
Dietary advice
- encourage high fibre, low glycaemic index sources of carbohydrates
- include low-fat dairy products and oily fish
- control the intake of foods containing saturated fats and trans fatty acids
- limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
- discourage use of foods marketed specifically at people with diabetes
- initial target weight loss in an overweight person is 5-10%
Next=Metformin
