Random viva Qs Flashcards
Black hairy tongue
What/predisposing/management
Black hairy tongue is relatively common condition which results from defective desquamation of the filiform papillae. Despite the name the tongue may be brown, green, pink or another colour.
Predisposing factors:
- poor oral hygiene
- antibiotics
- head and neck radiation
- HIV
- intravenous drug use
The tongue should be swabbed to exclude Candida
Management
- tongue scraping
- topical antifungals if Candida
What is scleoderma and what are the different types?
A group of auto-immune diseases
Types
localised-morphea; patches of focal/generalised sclerotic skin
systemic, limited; distribution limited to below elbows, knees, face, slow progression (years), pulmonary HTN in 15%, involves CREST syndrome
systemic, difuse; widespread cutaneous and early visceral involvement, rapid progression (months)
What are the examination features seen in scleroderma?
hand/face/extra
Hands
- Scleroderma (Can you move skin between your fingers?/Tight skin)
- Sclerodactyly
- Calcinosis
- Raynaud’s phenomenon → ulceration
Face
- Beaked nose: “nasal skin tethering”
- Microstomia (Ask pt. to open and close mouth)
- Perioral furrowing
- Telangiectasia
- En coup de sabre: scar down central forehead
Extras
- BP: HTN
- Lungs: pulmonary fibrosis
- Cardiac: pulmonary HTN
- ↑ JVP
- Parasternal heave
- Loud P2
- Peripheral oedema and ascites
- Morphea: patches of sclerotic skin (Localised scleroderma)
What are the features of systemic scleroderma you may see on the face?
- beaked nose -due to nasal skin tethering
- microstomia-small mouth
- perioral furrowing
- alopecia
- +telangiectasia
- +en coup de sabre
What are the features of CREST syndrome
CREST
Calcinosis; Ca deposition in pulp of fingers
Raynaud’s phenomenon (+/- ulcers); ASK is the colour change observes? white (vasoconstriction) -> blue (cyanosis) -> crimson (hyperaemia). Long-lasting blanching of knuckes on clenching fist (points to raynaud’s)
Esophageal dysmotility
Sclerodactlyly (+/- ulceration); loicalised thickening of fingers and toes distal to MCP or MTP joints. ASK-can you move the skin between your fingers
Telangiectasia; dilated nail fold capillaries
Describe the anatomy of the carpal tunnel
- Formed by flexor retinaculum and carpal bones
- contains median nerve
- contains 4 tendons of FDS, 3 tendons of FDP, 1 tendon of FPL
What is the typical patterns of sensory loss seen in carpal tunnel syndrome?
median nerve supplies thenar eminence and lateral 3.5 fingers
What is the typical pattern of motor loss seen in carpal tunnel syndrome?
LlOAF
- Lateral 2 lumbricals
- Opponens pollicis
- Abductor pollicis brevis
- flexor pollicis brevis
What are the main causes of CTS?
idiopathic (commenest
water- altered fluid balance; pregnancy, menopause, hypothyroidism, obesity, amyloidosis, renal failure
radial # - colles
Inflammation - RA, gout
Soft tissue swelling; lipomas, ganglia, acromegaly, amyloidosis
toxic; DM EtOH
How can you surgically Rx carpal tunnel
Carpal tunnel decompression by division of flexor retinaculum
Can you describe the lesion? (Dx asked later)
Numerous small violaceous nodules present on the back and forearm in no particular distribution; neurofibromas
What does this image show?
axillary freckling
What does this image show (describe what you see)
Extensive flat, coffee-coloured macules; cafe au lait spots
How many cafe au lait spots are clinically relevant
6 or more
diameter >5mm in child, >15mm adults
neurofibromas (more than 2 therefore neurofibromatosis)
+
Axillary freckling
+
Cafe au lait sports (6 or more, diameter >5mm in child, >15mm adults)
=Diagnosis
Neurofibromatosis
What do you know about neurofibromatosis
NF is a conditions where tumours grow in the nervous system
there are 3 types NF1, NF2 and schwannomatosis
NF1 is the most common type and involved AD inheretance
It occues due to a defect in the NF1 gene on chromosome 17 leading to a loss of neurofibromi - a TS gene
What are the complications associated with NF1
Mild learning disability
local effects of neurofibromas; nerve root compression (weakness, pain, paraesthesia), GI (bleeds, obstruction) bone (scoliosis, cystic lesion)
High BP; from RAS/phaeochromocytoma
Malignancy; optic glioma, sarcomatous change in neurofibroma
Increased epilepsy risk
How would you manage NF
Conservative; MDT (neurologist, geneticist, surgeon, physiotherapist), genetic counselling (AD!), review for complications (yearly BP and cutaneous review and epilepsy Rx)
Surgical; excision of some neurofibromas (unsightly.catch on clothing)
Describe what you see in this image, and give the most likely Diagnosis
incisional hernia from midline laparotomy
An abdominal mass is present above the umbilicus
There is a well healed scar overlying it from a surgical incision- a midline laparotomy
it is an incisional hernia
‘an incisional hernia in the RLQ of the abdomen with a scar consitent with a rutherford morrison scar following a renal transplant
What are the risk factors for Generally developing incisional hernias?
Pre-operative: increasing age, abdominal distension (obesity, ascites), co-morbidity (DM, renal failure, malignancy), drugs (steroids, chemotherapy, radiotherapy)
Intra-operative: surgical technique/skill (major factor), incision type (e.g. midline lap has highest reported incidence) and placing drains through wounds
Post Op: increased abdominal pressure (chronic cough, strain, post op ileus), wound complications (e.g. infection, haematoma) and impaired wound healing (as per pre-op comorbidities)
What do you see?
What is this called?
What is it used to treat?
Pan photocoagulation seen as yellow-white spots across the entire fundus
Photocoagulation involves full thickness of the retina and choroid
These burns are used in proliferative retinopathy and maculopathy in patients with advanced diabetic retinopathy
What do you see
(pt presents with blurry vision and diplopia)
Left eye is ptosis
Left eye is deviated inferolaterally (not lay language ‘down and out’)
Pupil is NOT involved, it is the same size as the right pupil
suggesting
a medical third nerve palsy with pupillary sparing - suggesting a medical cause, most likely diabteres mellitys
What are some causes of a medical third nerve palsy?
mononeuritis multiplex DIABETES MELLITUS
Multiple sclerosis
Midbrain infarction (weber’s syndrome= CN3 palsy + contralateral hemiplegia)
What are some causes of surgical third nerve palsy?
posterior communicating artery aneurysm
cavernous sinus pathology thrombosis, tumour, fistula
Cerebral uncus herniation (raised ICP)
Spot Dx
describe what you see and state the diagnosis?
What other deformities might you look for in the hands?
symmetrical deforming polyarthropathy
ulnar deviation at the MCPs
Z thumb bilaterally
MCP volar subluxation
These features are in keeping with RA involving the hands
look for; boutonniere’s deformity, swan neck deformity, rheumatoid nodules
What is boutonniere’s deformity and from where does the name originate?
PIP flexion, DIP hyperextension
button hole deformity as there is a pipj prolapse through a ‘button hole’ created by 2 lateral slips
Name the extra-articular features of RA
acronym=aNTI CCP OR RF
Nodules
Tenosynovitis: de Quervains and atlanto-axial subluxation
Immune: vasculitis, amyloidosis
Cardiac: pericarditis ± effusion
Carpal tunnel
Pulmonary: fibrosis, effusions
Ophthalmic: episcleritis, scleritis, Sjogren’s
Raynaud’s
Felty’s: RA + ↓PMN + splenomegaly
What are the 4 classic features of RA on X-ray
Loss of joint space
Periarticular Erosions
Soft tissue Swellings
Soft bones i.e. periarticular osteopenia
How would you manage RA
Conservative: MDT approach, physiotherapy + OT (aids and splints) monitor disease + annual review (DAS 28)
Medical:
- analgesia; paracetamol or NSAIDs (+PPI) -> codeine -> opiods (non-pharma TENS & behavioural approaches
- Steroids: IM, PO (short term treatment) or intra-articular
- DMARDs: methotrexate + sulfasalazine 1st line (DM suppression therefore SE and monitoring)
- Biologicals: anti TNF e.g. infliximab, etanercept, adalimumab
- Biological: anti CD20 e.g. rituximab (failure of anti TNF treatment)
Surgical:
CT decompression, tendon repairs and transfers, ulna stylectomy and arthroplasty
Example presentation of lobectomy scar
Closer inspection of the chest and back revealed a left sided well healed scar starting laterally at the 5th/6th ICS which curves posteriorly and upwards, ending midway between the spine of the scapula and the thoracic vertebral spaces/ This is in keeping with a lobectomy scar
What is a lobectomy?
a surgical procedure where a lobe of lung is removed
What are the indications for a lobectomy?
90% are for non-disseminated lung cancers (NSCLC)
Others:
- bronchiectasis with uncontrolled symptoms
- lung abscess
- COPD- lung reduction surgery
- Historically TB pre ABx (usually upper lobe)
What are the 2 major types of lung cancer? which is more common?
classified histologically in order to determine management and prognosis
Non-small cell lung cancer (85%)
Small cell lung cancer (15%)
Tell me more about the 3 different types of NSCLC
Squamous cell carcinoma - highly related to smoking, centrally located, often secrete PTHrP leading to high calcium levels
adenocarcinomas- femal non-smokers, peripherally located, 80% present with extrathoracic metastases
Large cell carcinoma
Tell me more about small cell lung cancer?
highly related to smoking
central location
80% present with advanced disease
often associated with ectopic hormone secretion -> endocrine/paraneoplastic syndrome associaton as cells contain neurosecretory cells
What is the difference between a group and save and a crossmatch?
Group and save (G&S) – this simply means the patient’s blood is typed and tested for antibodies, then saved in the lab in case it is required; it DOES NOT get you blood products for transfusion. If you need blood products you have to request a crossmatch.
Crossmatch (XM) – this means that the patient’s blood is typed and tested as above, then matched to specific units of blood, platelets or other products for transfusion. You need to specify on the form how many units you need, why you need them and when they are required. A full crossmatch takes about 45-60 minutes in the lab – if you have an unstable bleeding patient and think you’ll need blood products sooner than this, you still need to send a crossmatch sample, but you can ask the lab for units of type-specific blood (which take 10-20 minutes), or in a genuine emergency you can use their stocks of O negative blood from the fridge.
Dextrocardia
How can you easily confirm this pt has dextrocardia
2x (not clinical exam)
CXR- heart located on RHS
ECG- electrodes placed on RHS
What is dextrocardia?
a rare congenital defect in which the apex of the heart is located on the R side of the body
What are the 2 types of dextrocardia
- Isolated D;* dextrocardia of embryonic arrest where the heart is simply placed further right in the thorax then normal- it is commonly associated with severe defects of the heart and related abnormalities including pulmonary hypoplasia
- dextrocardia situs inversus totalis* all the visceral organs are mirrored
patients with dextrocardia situs inversus are often more prone to developing some CVS disorders e.g. PS. What murmur and HS might you expect from Pulmonary valve stenosis
Ejection systolic murmur
best heard in the left parasternal 2nd ICS
increased splitting of the second HS
HOCM with murmur and heave;
what is hypertrophic obstructive cardiomyopathy?
A condition in which a portion of the heart becomes thickened, hypertrophies, without an obvious cause
Obstructive variant is where the distortion of the normal heart anatomy causes an obstruction of blood from the left ventricle of the heart
How may patients present with HOCM
some asymptomatic with no clinically detectable disease
some present with AS like sympotoms due to outflow obstruction e.g. dyspnoesa, angina and palpitations, syncopal episodes
sudden cardiac death
How would you investigate for HOCM
Hx- especially FHx of HOCM or unexplained sudden death in otherwise healthy individuals
genetic testing- although not primarily used for Dx
ECG- = LA enlargement gives P mitrale, LV enlargement gives large R waves (Sokolov-Lyon criteria greater than 35mm total R in V5 + S in V1)
Echocardiography, Cardiac catheterisation, Cardiac MRI
What pulse sign would you see in pt with HOCM?
Pulsus bisferiens - biphasic pulse, is a cardiac cycle with two peaks, a small one followed by a strong and broad one. It is a sign of problems with the aortic valve, including aortic stenosis and aortic regurgitation, as well as hypertrophic cardiomyopathy causing subaortic stenosis.
AS
What are the causes of AS
Aqcuired; age related calcification is the commonest cause, rheumatic heart disease
Congenital bicuspid aortic valve, williams syndrome
What are the 3 sx of severe AS?
Angina
Syncope
dyspnoea
AS
if this pt were to have an aortic valve replacement what complications would you warn them about?
Gen comp; anaesthetic SE, damage to structures, NAVY, infection (wound), DVT, post op pneumonia
COmplications of open heart surgery; 5% operative mortality
Complications of the valve:
- acute failure of the bvalve e.g. dehiscence, breakage
- chronic failue of the valce e.g. stenosis, incompetence
- Infective endocarditis e.g. early (<2/12 post op) likely staph epidermis/late likely strep viridans
- bleeding
- anaemia (haemolysis, warfarin and endocarditis)
- arrhythmia (AF)
- Thromboembolism (1-2% risk per annum, despite warfarin therapy)
AS
If pt presented with GI bleeding and you heard an Ejection systolic murmur, what syndrome would you be considering in your list of differentials?
Heyde’s syndrome - GI bleed angiodysplasia in the presence of AS
occurs due to depletion of vWF flowing through narrowed valvular stenosis
What are your differentials for mercedes benz scar?
Hepatobiliary surgery
such as liver transplant/gall bladder
other; segmental resection, whipple’s procedure (pancreaticoduodenectomy)
What are the commonest indications for a liver transplant?
Cirrhosis
acute liver failure (hepatitis A + B, paracetamol OD)
Malignancy (Hepatocellular carcinoma)
What are some absolute contraindications against liver transplant?
Severe infection/sepsis
Extra-hepatic malignancy
severe cardio-respiratory disease
ongoing alcohol or drug abuse
AIDS
Non-complicance with drug therapy
Cirrhosis
What is chronic liver disease ?
progressive destruction and degreneration of liver parenchyma leading to cirrhosis…
…which lasts over a period of 6 months
What is cirrhosis
Defined histologically
as a diffuse heatic process characterised by fibrosis and
conversion of normal liver architecture into structurally abnormal nodules
What are some causes of chronic liver disease?
alcohol excess
chronic hepatitis C and hepatitis B
Non-alcoholic fatte liver disease
AI e.g. hepatitis, PBC, PSC
drugs; methotrexate, amiodarone
neoplastic e.g. HCC metastases
congenital e.g. haemochromatosis, wilsons and cystic fibrosis
What blood tests would you include in a liver screen?
- LFTs e.g. AST/ALT ration (>2) + raised GGT (EtOH excess acutely)
- FBC e.g. MCV (EtOH excess)
- Clotting e.g. raised INR
- Bone profile e.g. albumin
- Us&Es e..g. hepatorenal syndrome
- ESR/CRP e.g inflammatory process
- Viral serology e.g. hep B and C
- Metabolic profile e.g. lipids and glucose
- AI screen SMA LKM1 + ANA (AIH) AMA (PBC) ANA + SMA PSC)
- Genetic e.g. caeruloplasmin, ferritin + TIBC, alpha1 AT
- Cancer- AFP Ca19-9
Ascites
commonest 3 causes of ascites
cirrhosis
CCF
carcinomatosis
How is ascites classified as a transudate and an exudate
according to Serum ascites albumin gradient (SAAG)
SAAG= serum albumin - ascites albumin
SAAG > 1.1g/dL (due to portal hypertension) = transudate e.g. cirrhosis, cardiac, renal
SAAG < 1.1 (not due to portal hypertension,) = exudate e.g. cancer, venous obstruction e.g. budd-chiari, infection TB/SBP, nephrotic syndrome
nb vise versa to fluid protein/
serum protein in assessment of pleural effusion!!
How would you manage a pt with ascites
MDT approach
fluid restriction <1.5 L/day and daily weights
low Na diet
diuretics e.g. spironolactone and furosemine (if poor response)
EtOH liason team (if relevant)
REMEMBER TO ASK Pt in social Hx if surgery is in the management options
Is there anyone available to look after you post surgery?
Polio
What is Polio?
- RNA virus
- Affects anterior horn cells
- Fever, sore throat, myalgia
- 0.1% develop paralytic polio
- Asymmetric LMN paralysis
- No sensory involvement
- May be confined to upper or lower limbs or both
- Respiratory muscle paralysis can → death
- Polio was eradicated by the 1988 WHO global polio eradication initiative; 37 cases in 2016, VACCINATION PROGRAM -> Herd immunity
