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PACES Hawthorne > Random viva Qs > Flashcards

Random viva Qs Flashcards

1
Q

Black hairy tongue

What/predisposing/management

A

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
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2
Q

What is scleoderma and what are the different types?

A

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)

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3
Q

What are the examination features seen in scleroderma?

hand/face/extra

A

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)
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4
Q

What are the features of systemic scleroderma you may see on the face?

A
  • beaked nose -due to nasal skin tethering
  • microstomia-small mouth
  • perioral furrowing
  • alopecia
  • +telangiectasia
  • +en coup de sabre
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5
Q

What are the features of CREST syndrome

A

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

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6
Q

Describe the anatomy of the carpal tunnel

A
  • Formed by flexor retinaculum and carpal bones
  • contains median nerve
  • contains 4 tendons of FDS, 3 tendons of FDP, 1 tendon of FPL
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7
Q

What is the typical patterns of sensory loss seen in carpal tunnel syndrome?

A

median nerve supplies thenar eminence and lateral 3.5 fingers

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8
Q

What is the typical pattern of motor loss seen in carpal tunnel syndrome?

A

LlOAF

  1. Lateral 2 lumbricals
  2. Opponens pollicis
  3. Abductor pollicis brevis
  4. flexor pollicis brevis
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9
Q

What are the main causes of CTS?

A

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

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10
Q

How can you surgically Rx carpal tunnel

A

Carpal tunnel decompression by division of flexor retinaculum

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11
Q

Can you describe the lesion? (Dx asked later)

A

Numerous small violaceous nodules present on the back and forearm in no particular distribution; neurofibromas

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12
Q

What does this image show?

A

axillary freckling

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13
Q

What does this image show (describe what you see)

A

Extensive flat, coffee-coloured macules; cafe au lait spots

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14
Q

How many cafe au lait spots are clinically relevant

A

6 or more

diameter >5mm in child, >15mm adults

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15
Q

neurofibromas (more than 2 therefore neurofibromatosis)

+

Axillary freckling

+

Cafe au lait sports (6 or more, diameter >5mm in child, >15mm adults)

=Diagnosis

A

Neurofibromatosis

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16
Q

What do you know about neurofibromatosis

A

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

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17
Q

What are the complications associated with NF1

A

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

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18
Q

How would you manage NF

A

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)

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19
Q

Describe what you see in this image, and give the most likely Diagnosis

A

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

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20
Q

‘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?

A

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)

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21
Q

What do you see?

What is this called?

What is it used to treat?

A

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

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22
Q

What do you see

(pt presents with blurry vision and diplopia)

A

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

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23
Q

What are some causes of a medical third nerve palsy?

A

mononeuritis multiplex DIABETES MELLITUS

Multiple sclerosis

Midbrain infarction (weber’s syndrome= CN3 palsy + contralateral hemiplegia)

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24
Q

What are some causes of surgical third nerve palsy?

A

posterior communicating artery aneurysm

cavernous sinus pathology thrombosis, tumour, fistula

Cerebral uncus herniation (raised ICP)

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25
Q

Spot Dx

describe what you see and state the diagnosis?

What other deformities might you look for in the hands?

A

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

26
Q

What is boutonniere’s deformity and from where does the name originate?

A

PIP flexion, DIP hyperextension

button hole deformity as there is a pipj prolapse through a ‘button hole’ created by 2 lateral slips

27
Q

Name the extra-articular features of RA

acronym=aNTI CCP OR RF

A

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

28
Q

What are the 4 classic features of RA on X-ray

A

Loss of joint space

Periarticular Erosions

Soft tissue Swellings

Soft bones i.e. periarticular osteopenia

29
Q

How would you manage RA

A

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

30
Q

Example presentation of lobectomy scar

A

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

31
Q

What is a lobectomy?

A

a surgical procedure where a lobe of lung is removed

32
Q

What are the indications for a lobectomy?

A

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)
33
Q

What are the 2 major types of lung cancer? which is more common?

A

classified histologically in order to determine management and prognosis

Non-small cell lung cancer (85%)

Small cell lung cancer (15%)

34
Q

Tell me more about the 3 different types of NSCLC

A

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

35
Q

Tell me more about small cell lung cancer?

A

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

36
Q

What is the difference between a group and save and a crossmatch?

A

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.

37
Q

Dextrocardia

How can you easily confirm this pt has dextrocardia

2x (not clinical exam)

A

CXR- heart located on RHS

ECG- electrodes placed on RHS

38
Q

What is dextrocardia?

A

a rare congenital defect in which the apex of the heart is located on the R side of the body

39
Q

What are the 2 types of dextrocardia

A
  • 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
40
Q

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

A

Ejection systolic murmur

best heard in the left parasternal 2nd ICS

increased splitting of the second HS

41
Q

HOCM with murmur and heave;

what is hypertrophic obstructive cardiomyopathy?

A

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

42
Q

How may patients present with HOCM

A

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

43
Q

How would you investigate for HOCM

A

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

44
Q

What pulse sign would you see in pt with HOCM?

A

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.

45
Q

AS

What are the causes of AS

A

Aqcuired; age related calcification is the commonest cause, rheumatic heart disease

Congenital bicuspid aortic valve, williams syndrome

46
Q

What are the 3 sx of severe AS?

A

Angina

Syncope

dyspnoea

47
Q

AS

if this pt were to have an aortic valve replacement what complications would you warn them about?

A

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)
48
Q

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?

A

Heyde’s syndrome - GI bleed angiodysplasia in the presence of AS

occurs due to depletion of vWF flowing through narrowed valvular stenosis

49
Q

What are your differentials for mercedes benz scar?

A

Hepatobiliary surgery

such as liver transplant/gall bladder

other; segmental resection, whipple’s procedure (pancreaticoduodenectomy)

50
Q

What are the commonest indications for a liver transplant?

A

Cirrhosis

acute liver failure (hepatitis A + B, paracetamol OD)

Malignancy (Hepatocellular carcinoma)

51
Q

What are some absolute contraindications against liver transplant?

A

Severe infection/sepsis

Extra-hepatic malignancy

severe cardio-respiratory disease

ongoing alcohol or drug abuse

AIDS

Non-complicance with drug therapy

52
Q

Cirrhosis

What is chronic liver disease ?

A

progressive destruction and degreneration of liver parenchyma leading to cirrhosis…

…which lasts over a period of 6 months

53
Q

What is cirrhosis

A

Defined histologically

as a diffuse heatic process characterised by fibrosis and

conversion of normal liver architecture into structurally abnormal nodules

54
Q

What are some causes of chronic liver disease?

A

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

55
Q

What blood tests would you include in a liver screen?

A
  • 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
56
Q

Ascites

commonest 3 causes of ascites

A

cirrhosis

CCF

carcinomatosis

57
Q

How is ascites classified as a transudate and an exudate

A

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!!

58
Q

How would you manage a pt with ascites

A

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)

59
Q

REMEMBER TO ASK Pt in social Hx if surgery is in the management options

A

Is there anyone available to look after you post surgery?

60
Q
A
61
Q

Polio

What is Polio?

A
  • 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

PACES Hawthorne (18 decks)

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