Mrcs Notes

8/12/2019 Mrcs Notes

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Fluid resuscitation burns

Indication: >15% total body area burns in adults (>10% children)

The main aim of resuscitation is to prevent the burn deepening

Most fluid is lost 24h after injury

First 8-12h fluid shifts from intravascular to interstitial fluid compartments

Therefore circulatory volume can be compromised. However fluid resuscitation causes more fluid

into the interstitial compartment especially colloid (therefore avoided in first 8-24h)

Protein loss occurs

Fluid resuscitation formula

Parkland formula(Crystalloid only e.g. Hartman's solution/Ringers' lactate)

Total fluid requirement in 24 hours =

4 ml x (total burn surface area (%)) x (body weight (kg))

50% given in first 8 hours

50% given in next 16 hours

Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to

achieve this)

Points to note:

Starting point of resuscitation is time of injury

Deduct fluids already given

After 24 hours

Colloid infusion is begun at a rate of 0.5 ml x(total burn surface area (%))x(body weight (kg))

Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x(burn

area)x(body weight) Colloids used include albumin and FFP

Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to the

inflammatory cascade in burns

High tension electrical injuries and inhalation injuries require more fluid

Monitor: packed cell volume, plasma sodium, base excess, and lactate


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All local anaesthetics have a chemical bond linking an amine to either an amide oranester. Most local anaesthetics are of the amino- amide types, these have a more favorable side

effect profile and are more stable in solution. Procaine and benzocaine haveamino - ester groups, these are metabolised by pseudocholinesterases.

Ventricular tachcardia

Ventricular tachycardia (VT)is broad-complex tachycardia originating from a ventricular ectopic focus. Ithas the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

There are two main types of VT:

monomorphic VT: most commonly caused by myocardial infarction

polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by

prolongation of the QT interval. The causes of a long QT interval are listed below

Causes of a prolonged QT interval

Congenital

Jervell-Lange-Nielsen syndrome

(includes deafness and is due to

an abnormal potassium channel)

Romano-Ward syndrome (no

deafness)

Drugs

amiodarone, sotalol,

class 1a antiarrhythmic

drugs

tricyclic antidepressants,

fluoxetine

chloroquine

terfenadine*

erythromycin

Other

electrolyte: hypocalcaemia,

hypokalaemia,

hypomagnesaemia

acute myocardial infarction

myocarditis

hypothermia

subarachnoid haemorrhage

Valves of the heart

Mitral valve Aortic valve Pulmonary valve Tricuspid valve

2 cusps 3 cusps 3 cusps 3 cusps

First heart sound Second heart sound Second heart sound First heart sound

1 anterior cusp 1 anterior cusp 2 anterior cusps 2 anterior cusps

Attached to chordae tendinae No chordae No chordae Attached to chordae tendinae


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Acute intermittent porphyria

Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect inporphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxicaccumulation of delta aminolaevulinic acid and porphobilinogen. It characteristically presents with

abdominal and neuropsychiatric symptoms in 20-40 year olds. AIP is more common in females (5:1)

Features

abdominal: abdominal pain, vomiting

neurological: motor neuropathy

psychiatric: e.g. depression

hypertension and tachycardia common

Diagnosis

classically urine turns deep red on standing raised urinary porphobilinogen(elevated between attacks and to a greater extent during

acute attacks)

assay of red cells for porphobilinogen deaminase

raised serum levels of delta aminolaevulinic acid and porphobilinogen

Pagets disease

Paget's disease is a disease of increased but uncontrolled bone turnover and is characterised byarchitecturally abnormal bones. It is thought to be primarily a disorder of osteoclasts, with excessiveosteoclastic resorption followed by increased osteoblastic activity causing areas of sclerosis anddeformity. Paget's disease is common (UK prevalence 5%) but symptomatic in only 1 in 20 patients

Predisposing factors

increasing age

male sex

northern latitude

family history

Clinical features


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May induce state of dissociative anaesthesia resulting in nightmares

Etomidate Has favorable cardiac safety profile with very little haemodynamic instability

No analgesic properties

Unsuitable for maintaining sedation as prolonged (and even brief) use may result in

adrenal suppression

Post operative vomiting is common

ower limb- Muscular compartments

Anterior compartment

Muscle Nerve Action

Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot

Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint

Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot

Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment

Muscle Nerve Action

Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion

Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment


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The sino atrial node is also capable of spontaneous discharge and in the absence of background

vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate

found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is

lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at

which point an action potential is generated.

Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA

node will depolarise first. The cells have a refractory period during which they cannot be re-

stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states

this time period is overridden and inadequate ventricular filling may then occur, cardiac output

falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympatheticfibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenalinebinds to 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle

Image sourced fromWikipedia

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic

pressure is high.
http://en.wikipedia.org/wiki/Cardiac%20cyclehttp://en.wikipedia.org/wiki/Cardiac%20cyclehttp://en.wikipedia.org/wiki/Cardiac%20cycle


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Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic

volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction.

AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected.

Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular

pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and

elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the

aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml

(i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave

associated with closure of the aortic valve increases aortic pressure. The pressure dip before this

rise can be seen on arterial waveforms and is called the incisura. During systole the atrial

pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed

ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure

falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if theneck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid thisoccurrence if veins are inadvertently cut, or during CVP line insertion.

Mechanical properties

Preload = end diastolic volume

Afterload = aortic pressure

It is important to understand the principles of Laplace's lawin surgery.


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It states that for hollow organs with a circular cross section, the total circumferential wall tension

depends upon the circumference of the wall, multiplied by the thickness of the wall and on the

wall tension.

The total luminal pressure depends upon the cross sectional area of the lumen and the

transmural pressure. Transmural pressure is the internal pressure minus external pressure and at

equilibrium the total pressure must counterbalance each other.

In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs

during the ejection phase is due to physical change in heart size. It also explains why a dilated

diseased heart will have impaired systolic function.

Starlings law

Increase in end diastolic volume will produce larger stroke volume.

This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke

volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant

patients who need to increase their cardiac output.

Baroreceptor reflexes

Baroreceptors located in aortic arch and carotid sinus.

Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal

nerve.

They are stimulated by arterial stretch.

Even at normal blood pressures they are tonically active.

Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in strokevolume.*Decreased sympathetic discharge to venous system causing increased compliance.*Decreased peripheral arterial vascular resistance

Atrial stretch receptors

Located in atria at junction between pulmonary veins and vena cava.

Stimulated by atrial stretch and are thus low pressure sensors.

Increased blood volume will cause increased parasympathetic activity.

Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:

the Bainbridge reflex.


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Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal

blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by

juxtaglomerular apparatus-Increase in angiotensin II.

Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Organ Transplant

A number of different organ and tissue transplants are now available. In many cases an allograft isperformed, where an organ is transplanted from one individual to another. Allografts will elicit an immuneresponse and this is one of the main reasons for organ rejection.

Graft rejection occurs because allografts have allelic differences at genes that codeimmunohistocompatability complex genes. The main antigens that give rise to rejection are:

ABO blood group

Human leucocyte antigens (HLA)

Minor histocompatability antigens

ABO MatchingABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies toother groups. Group O donors can give organs to any type of ABO recipient whereas group AB donor canonly donate to AB recipient.

HLA SystemThe four most important HLA alleles are:

HLA A

HLA B

HLA C

HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, foureach = 8 alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLAmismatching. However, the greater the number of mismatches the worse the long term outcome will be. Tlymphocytes will recognise antigens bound to HLA molecules and then will then become activated. Clonalexpansion then occurs with a response directed against that antigen.

Types of organ rejection

Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO

incompatibility).


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Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates

and vascular lesions.

Chronic. Occurs after the first 6 months. Vascular changes predominate.

HyperacuteRenal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility and

HLA Class I incompatible transplants will all fare worse in long term.

Acute

All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of

transplanted organ are susceptible and it may occur in up to 50% cases.

Chronic

Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other

immunosensitising events all increase the risk. Vascular changes are most prominent with myointimal

proliferation leading to organ ischaemia. Organ specific changes are also seen such as loss of acinar

cells in pancreas transplants and rapidly progressive coronary artery disease in cardiac transplants.

Surgical overview-Renal transplantation

A brief overview of the steps involved in renal transplantation is given.

Patients with end stage renal failure who are dialysis dependent or likely to become so in the immediate

future are considered for transplant. Exclusion criteria include; active malignancy, old age (due to limited

organ availability). Patients are medically optimised.

Donor kidneys, these may be taken from live related donors and close family, members may have less

HLA mismatch than members of the general population. Laparoscopic donor nephrectomy further

minimises the operative morbidity for the donor. Other organs are typically taken from brain dead or dying

patients who have a cardiac arrest and in whom resuscitation is futile. The key event is to minimise thewarm ischaemic time in the donor phase.

The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron

immediately prior to implantation and factors such as accessory renal arteries and vessel length are

assessed and managed.

For first time recipients the operation is performed under general anaesthesia. A Rutherford-Morrison

incision is made on the preferred side. This provides excellent extraperitoneal access to the iliac vessels.

The external iliac artery and vein are dissected out and following systemic heparinisation are cross

clamped. The vein and artery are anastamosed to the iliacs and the clamps removed. The ureter is then

implanted into the bladder and a stent is usually placed to maintain patency. The wounds are then closed

and the patient recovered from surgery.

In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular necrosis

and this tends to resolve.

Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic twin

transplant (live donor) may survive as long as 25 years.


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Voice production

There are 2 main nerves involved:

Superior laryngeal nerve (SLN)

Innervates the cricothyroid muscle

Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high notes duringsinging, SLN paresis and paralysis result in:

a. Abnormalities in pitchb. Inability to sing with smooth change to each higher note (glissando or pitch glide)

Recurrent laryngeal nerve (RLN)/Inferior laryngeal nerve

Innervates intrinsic larynx muscles

a. Opening vocal folds (as in breathing, coughing)

b. Closing vocal folds for vocal fold vibration during voice use

c. Closing vocal folds during swallowing Hormonal regulation of calcium

Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and decrease phosphate levels

Increases bone resorption

Immediate action on osteoblasts to increase ca2+in

extracellular fluid

Osteoblasts produce a protein signaling molecule that activate

osteoclasts which cause bone resorption

Increases renal tubular reabsorption of calcium

Increases synthesis of 1,25(OH)2D (active form of vitamin D) in

the kidney which increases bowel absorption of Ca2+

Decreases renal phosphate reabsorption

1,25-dihydroxycholecalciferol (the

active form of vitamin D)

Increases plasma calcium and plasma phosphate

Increases renal tubular reabsorption and gut absorption of

calcium

Increases osteoclastic activity

Increases renal phosphate reabsorption

Calcitonin Secreted by C cells of thyroid

Inhibits intestinal calcium absorption


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Inhibits osteoclast activity

Inhibits renal tubular absorption of calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

Dorsal column lesion Loss vibration and proprioception

Tabes dorsalis, SACD

Spinothalamic tract lesion Loss of pain, sensation and temperature

Central cord lesion Flaccid paralysis of the upper limbs

Osteomyelitis Normally progressive

Staph aureus in IVDU, normally cervical region affected

Fungal infections in immunocompromised

Thoracic region affected in TB

Infarction spinal cord Dorsal column signs (loss of proprioception and fine discrimination

Cord compression UMN signs

Malignancy

Haematoma

Fracture

Brown-sequard syndrome Hemisection of the spinal cord

Ipsilateral paralysis

Ipsilateral loss of proprioception and fine discrimination

Contralateral loss of pain and temperature

Coagulation cascade

Two pathways lead to fibrin formation

Intrinsic pathway(components already present in the blood)

Minor role in clotting

Subendothelial damage e.g. collagen

Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK),

prekallikrein, and Factor 12


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Prekallikrein is converted to kallikrein and Factor 12 becomes activated

Factor 12 activates Factor 11

Factor 11 activates Factor 9, which with its co-factor Factor 8a form the tenase complex which

activates Factor 10

Extrinsic pathway(needs tissue factor released by damaged tissue)

Tissue damage

Factor 7 binds to Tissue factor

This complex activates Factor 9

Activated Factor 9 works with Factor 8 to activate Factor 10

Common pathway

Activated Factor 10 causes the conversion of prothrombin to thrombin

Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form

links between fibrin molecules

FibrinolysisPlasminogen is converted to plasmin to facilitate clot resorption

http://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Coagulation


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Intrinsic pathway Increased APTT Factors 8,9,11,12

Extrinsic pathway Increased PT Factor 7

Common pathway Increased APTT & PT Factors 2,5,10

Vitamin K dependent Factors 2,7,9,10

Upper limb fractures

Colles' fracture

Fall onto extended outstretched hands

Described as a dinner fork type deformity

Classical Colles' fractures have the following 3 features:

Features of the injury1. Transverse fracture of the radius2. 1 inch proximal to the radio-carpal joint3. Dorsal displacement and angulation

Smith's fracture (reverse Colles' fracture)

Volar angulation of distal radius fragment (Garden spade deformity)

Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed

Bennett's fracture

Intra-articular fracture of the first carpometacarpal joint

Impact on flexed metacarpal, caused by fist fights

X-ray: triangular fragment at ulnar base of metacarpal

Monteggia's fracture

Dislocation of the proximal radioulnar joint in association with an ulna fracture

Fall on outstretched hand with forced pronation

Needs prompt diagnosis to avoid disability


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Galeazzi fracture

Radial shaft fracture with associated dislocation of the distal radioulnar joint

Occur after a fall on the hand with a rotational force superimposed on it.

On examination, there is bruising, swelling and tenderness over the lower end of the forearm.

X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation

of the inferior radio-ulnar joint.

Barton's fracture

Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation

Fall onto extended and pronated wrist

Scaphoid fractures

Scaphoid fractures are the commonest carpal fractures.

Surface of scaphoid is covered by articular cartilage with small area available for blood vessels

(fracture risks blood supply)

Forms floor of anatomical snuffbox

Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal 1/3)

The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on

wrist movements and on longitudinal compression of the thumb. Ulnar deviation AP needed for visualization of scaphoid

Immobilization of scaphoid fractures difficult

Radial head fracture

Fracture of the radial head is common in young adults.

It is usually caused by a fall on the outstretched hand.

On examination, there is marked local tenderness over the head of the radius, impairedmovements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of

rotation (pronation and supination).

Benign liver lesions


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Benign liver lesions

Haemangioma Most common benign tumours of mesenchymal origin

Incidence in autopsy series is 8%

Cavernous haemangiomas may be enormous

Clinically they are reddish purple hypervascular lesions Lesions are normally separated from normal liver by ring of fibrous tissue

On ultrasound they are typically hyperechoic

Liver cell adenoma 90% develop in women in their third to fifth decade

Linked to use of oral contraceptive pill

Lesions are usually solitary

They are usually sharply demarcated from normal liver although they usually lack a

fibrous capsule

On ultrasound the appearances are of mixed echoity and heterogeneous texture. On

CT most lesions are hypodense when imaged prior to administration of IV contrast

agents

In patients with haemorrhage or symptoms removal of the adenoma may be required

Mesenchymal

hamartomas

Congential and benign, usually present in infants. May compress normal liver

Liver abscess Biliary sepsis is a major predisposing factor

Structures drained by the portal venous system form the second largest source

Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in

50%

Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in

chronic abscesses

Amoebic abscess Liver abscess is the most common extra intestinal manifestation of amoebiasis

Between 75 and 90% lesions occur in the right lobe

Presenting complaints typically include fever and right upper quadrant pain

Ultrasonography will usually show a fluid filled structure with poorly defined boundaries

Aspiration yield sterile odourless fluid which has an anchovy paste consistency

Treatment is with metronidazole

Hyatid cysts Seen in cases of Echinococcusinfection

Typically an intense fibrotic reaction occurs around sites of infection

The cyst has no epithelial lining

Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thickand has an external laminated hilar membrane and an internal enucleated germinal

layer

Typically presents with malaise and right upper quadrant pain. Secondary bacterial

infection occurs in 10%.

Liver function tests are usually abnormal and eosinophilia is present in 33% cases

Ultrasound may show septa and hyatid sand or daughter cysts.

Percutaneous aspiration is contra indicated

Treatment is by sterilisation of the cyst with mebendazole and may be followed by


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surgical resection. Hypertonic swabs are packed around the cysts during surgery

Polycystic liver

disease

Usually occurs in association with polycystic kidney disease

Autosomal dominant disorder

Symptoms may occur as a result of capsular stretch

Cystadenoma Rare lesions with malignant potential

Usually solitary multiloculated lesions

Liver function tests usually normal

Ultrasonography typically shows a large anechoic, fluid filled area with irregular

margins. Internal echos may result from septa

Surgical resection is indicated in all cases

Muscle relaxants

Suxamethonium Depolarising neuromuscular blocker

Inhibits action of acetylcholine at the neuromuscular junction

Degraded by plasma cholinesterase and acetylcholinesterase

Fastest onset and shortest duration of action of all muscle relaxants

Produces generalised muscular contraction prior to paralysis

Adverse effects include hyperkalaemia, malignant hyperthermia and lack of

acetylcholinesterase

Atracurium Non depolarising neuromuscular blocking drug

Duration of action usually 30-45 minutes

Generalised histamine release on administration may produce facial flushing,

tachycardia and hypotension

Not excreted by liver or kidney, broken down in tissues by hydrolysis

Reversed by neostigmine

Vecuronium Non depolarising neuromuscular blocking drug

Duration of action approximately 30 - 40 minutes

Degraded by liver and kidney and effects prolonged in organ dysfunction

Effects may be reversed by neostigmine

Pancuronium Non depolarising neuromuscular blocker

Onset of action approximately 2-3 minutes

Duration of action up to 2 hours

Effects may be partially reversed with drugs such as neostigmine


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Renal stones

Type of

stones

Features Percentage of all

calculi

Calcium

oxalate

Hypercalciuria is a major risk factor (various causes)

Hyperoxaluria may also increase risk

Hypocitraturia increases risk because citrate forms complexes with calcium

making it more soluble

Stones are radio-opaque (though less than calcium phosphate stones)

Hyperuricosuria may cause uric acid stones to which calcium oxalate binds

85%

Cystine Inherited recessive disorder of transmembrane cystine transport leading to

decreased absorption of cystine from intestine and renal tubule

Multiple stones may form

Relatively radiodense because they contain sulphur

1%

Uric acid Uric acid is a product of purine metabolism

May precipitate when urinary pH low

May be caused by diseases with extensive tissue breakdown e.g. malignancy

More common in children with inborn errors of metabolism

5-10%
http://en.wikipedia.org/wiki/Adductor%20longus%20musclehttp://en.wikipedia.org/wiki/Adductor%20longus%20musclehttp://en.wikipedia.org/wiki/Adductor%20longus%20muscle


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Radiolucent

Calcium

phosphate

May occur in renal tubular acidosis, high urinary pH increases supersaturation

of urine with calcium and phosphate

Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2

and 4 do not)

Radio-opaque stones (composition similar to bone)

10%

Struvite Stones formed from magnesium, ammonium and phosphate

Occur as a result of urease producing bacteria (and are thus associated with

chronic infections)

Under the alkaline conditions produced, the crystals can precipitate

Slightly radio-opaque

2-20%

Laxatives

Bulk forming laxatives

Bran

Psyllium

Methylcellulose

Osmotic laxatives

Magnesium sulphate

Magnesium citrate

Sodium phosphate

Sodium sulphate

Potassium sodium tatrate

Polyethylene glycol

Stimulant laxatives

Docusates

Bisacodyl

Sodium picosulphate

Senna

Ricinoleic acid

Diseases affecting the vertebral column

Ankylosing

spondylitis

Chronic inflammatory disorder affecting the axial skeleton

Sacro-ilitis is a usually visible in plain films

Up to 20% of those who are HLA B27 positive will develop the condition

Affected articulations develop bony or fibrous changes

Typical spinal features include loss of the lumbar lordosis and progressive kyphosis


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of the cervico-thoracic spine

Scheuermann's

disease

Epiphysitis of the vertebral joints is the main pathological process

Predominantly affects adolescents

Symptoms include back pain and stiffness

X-ray changes include epiphyseal plate disturbance and anterior wedging Clinical features include progressive kyphosis (at least 3 vertebrae must be involved)

Minor cases may be managed with physiotherapy and analgesia, more severe cases

may require bracing or surgical stabilisation

Scoliosis Consists of curvature of the spine in the coronal plane

Divisible into structural and non structural, the latter being commonest in adolescent

females who develop minor postural changes only. Postural scoliosis will typically

disappear on manoeuvres such as bending forwards

Structural scoliosis affects > 1 vertebral body and is divisible into idiopathic,

congential and neuromuscular in origin. It is not correctable by alterations in posture

Within structural scoliosis, idiopathic is the most common type

Severe, or progressive structural disease is often managed surgically with bilateral

rod stabilisation of the spine

Spina bifida Non fusion of the vertebral arches during embryonic development

Three categories; myelomeningocele, spina bifida occulta and meningocele

Myelomeningocele is the most severe type with associated neurological defects that

may persist in spite of anatomical closure of the defect

Up to 10% of the population may have spina bifida occulta, in this condition the skin

and tissues (but not not bones) may develop over the distal cord. The site may be

identifiable by a birth mark or hair patch

The incidence of the condition is reduced by use of folic acid supplements during

pregnancy

Spondylolysis Congenital or acquired deficiency of the pars interarticularis of the neural arch of a

particular vertebral body, usually affects L4/ L5

May be asymptomatic and affects up to 5% of the population

Spondylolysis is the commonest cause of spondylolisthesis in children

Asymptomatic cases do not require treatment

Spondylolisthesis This occurs when one vertebra is displaced relative to its immediate inferior vertebral

body

May occur as a result of stress fracture or spondylolysis

Traumatic cases may show the classic "Scotty Dog" appearance on plain films Treatment depends upon the extent of deformity and associated neurological

symptoms, minor cases may be actively monitored. Individuals with radicular

symptoms or signs will usually require spinal decompression and stabilisation

Branches of the trigeminal nerve


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Ophthalmic nerve Sensory only

Maxillary nerve Sensory only

Mandibular nerve Sensory and motor

SensoryOphthalmic Exits skull via the superior orbital fissure

Sensation of: scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose

(including the tip of the nose, except alae nasi), the nasal mucosa, the frontal sinuses, and parts of

the meninges (the dura and blood vessels).

Maxillary

nerve

Exit skull via the foramen rotundum

Sensation: lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal

mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses, and parts

of the meninges.

Mandibular

nerve

Exit skull via the foramen ovale

Sensation: lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw), parts

of the external ear, and parts of the meninges.

MotorDistributed via the mandibular nerve.The following muscles of mastication are innervated:

Masseter

Temporalis

Medial pterygoid

Lateral pterygoid

Other muscles innervated include:

Tensor veli palatini

Mylohyoid

Anterior belly of digastric

Tensor tympani

Neo-intimal hyperplasia in distal arterial anastamoses may be reduced by use of a Miller Cuff

when PTFE is the bypass conduit.

PTFE may induce neo-intimal hyperplasia with subsequent occlusion of the distal anastomosis. In more

proximal arterial bypass surgery the process of neo-intimal hyperplasia is not sufficient to cause

anastomotic occlusion. However, distal bypasses are at greater risk and if vein cannot be used as a


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conduit then the distal end of the PTFE should anastomosed to a vein cuff to minimise the risk of neo-

intimal hyperplasia.

'Machine' - Causes of Increased Serum K

+

M - Medications - ACE inhibitors, NSAIDS

A - Acidosis - Metabolic and respiratory

C - Cellular destruction - Burns, traumatic injury

H - Hypoaldosteronism, haemolysis

I - Intake - Excessive

N - Nephrons, renal failure

E - Excretion - Impaired

Familial periodic paralysis has subtypes associated with hyper and hypokalaemia.Lower limb- Muscular compartments

Anterior compartment

Muscle Nerve Action

Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot

Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint

Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot

Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment

Muscle Nerve Action

Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion

Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment


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Flexor hallucis longus Tibial Flexes the great toe

Tibialis posterior Tibial Plantar flexor, inverts the foot

Type of Murmur Conditions

Ejection systolic Aortic stenosis

Pulmonary stenosis, HOCM

ASD, Fallot's

Pan-systolic Mitral regurgitation

Tricuspid regurgitation

VSD

Late systolic Mitral valve prolapse

Coarctation of aorta

Early diastolic Aortic regurgitation

Graham-Steel murmur (pulmonary regurgitation)

Mid diastolic Mitral stenosis

Austin-Flint murmur (severe aortic regurgitation)

Causes of decreased compliance:

pulmonary oedema

pulmonary fibrosis

pneumonectomy

kyphosis

Causes of increased compliance age

emphysema - this is due to loss alveolar walls and associated elastic tissue

A unilateral dilated pupil is a classic sign of transtentorial herniation.

The subclavian artery passes anterior to the middle scalene.

Mrcs Notes

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