ESA 4 Clinical Conditions Flashcards
1
Q
Spread of infection within fascial planes
A
Superficial - None (simple cellulitis)
Retropharyngeal space (anterior to alar fascia) - Down to mediastinum (results from URTIs)
Danger space (posterior to alar fascia) - Down to diaphragm (results from URTIs)
Parapharyngeal space - Down to T2/3 (affecting carotid sheath structures,
Prevertebral fascia - Down to T2/3 results from bad dentition/quinsy)
2
Q
Branchial cysts/fistulae
A
Arise as a failure of the pharyngeal clefts to recede (1 st one remains and becomes the ear canal). Cysts are fluid filled pockets, whereas fistulae are openings between two epithelia. Both types are visible along the anterior border of SCM within the neck.
3
Q
Carotid atheroma formation
A
Carotid sinus is a bulge that leads to turbulent blood flow, which damages epithelia and kick-starts atheroma formation.
If an atheroma or thrombosis breaks off and travels to the brain it can result in a stroke or TIA.
4
Q
Carotid sinus hypersensitivity
A
Carotid sinus is extremely sensitive, so a small touch can be perceived as a huge rise in pressure, sending signals down CN IX (afferent) and CN X (efferent), activating the baroreceptor reflex and causing a drop in blood pressure.
More common in men, manifests as being unable to wear a tie or shave without feeling faint.
5
Q
Scalp laceration
A
Blood supply is rich so bleeds profusely. Blood vessels are embedded in dense connective tissue layer so vessels have restricted ability to constrict.
Also, lacerations to the epicranial aponeurosis cause contraction in both directions (occipital and frontal bellies) leading to a wound being held open.
6
Q
Cavernous sinus thrombosis
A
Facial veins are valveless so blood can drain both ways i.e. facial veins can drain into the cavernous sinus. An infection that tracks back causes thrombosis within the cavernous sinus which can compress CN III, CN IV, CN VI, CN V 1 or the ICA (this method of infection tracking back can also cause meningitis)
7
Q
Danger triangle of face
A
Area bound by the canthuses of the mouth and the bridge of the nose. Infection increasingly likely to track back here vs other areas of the face (see cavernous sinus thrombosis)
8
Q
Enlarged lymph node(s)
A
Generally speaking, lymph nodes are enlarged due to either or infection.
Obviously, infection is almost always the cause for enlargement. Malignant lymph nodes are hard, matted and non tender, and importantly immobile.
Lymphadenopathy secondary to infection leads to tender, firm and importantly mobile lymph nodes
9
Q
Tonsillitis
A
Refers to inflammation of the palatine tonsils usually (back of mouth). Leads to odynophagia and fever. Prone to reinfection in some people, tonsillectomy is performed in these cases
10
Q
Whiplash
A
An acute and large force applied across the C spine leads to overstretching of the tendons and ligaments of the spine, causing intense and sharp pain.
Common cause is a car crash, the seatbelt immobilises the thoracic spine but the head keeps moving, and the collision of the forces stretches the spine
11
Q
Burst/Jefferson fracture
A
Huge force applied to atlas i.e. falling on face from height. Bilateral fractures occur in the posterior portion, accompanied with avulsion of the anterior arch, so atlas bursts into pieces. As fragments travel outwards spinal cord injury may not occur
12
Q
Hangman’s fracture
A
Hyperextension of the neck (landing on chin) leads to bilateral fractures of pars interarticularis, damaging the spinal cord and leading to death
13
Q
Fractured pterion
A
Middle meningeal artery lies deep to the pterion (point on lateral side of skull where sphenoid, temporal, parietal and frontal bones fuse), thinnest portion of skull. A fracture here (the ‘temple’) leads to rupture of this artery and subsequent extradural haematoma
14
Q
Coning
A
Increased ICP forces the cerebellar tonsils through the foramen magnum of the occiput, putting pressure on the brainstem and leading to immediate death (due to cease of respiratory function)
15
Q
Consequences of Premature birth to the calvaria
A
Suture lines not completely formed at birth leading to bones having manoeuvrability to allow for manipulation (and interlocking) within the birth canal.
Bones are too far apart in premature babies so cannot fuse together, leading to brain damage. Premature babies usually delivered by C section
16
Q
Fractures of the skull
A
Depressed fracture – fracture caves inwards, pressing on the brain, common in squamous parts of the skull, especially the pterion (where temporal, sphenoid, parietal and frontal bones meet) - Pterion fractures damage the anterior branch of the middle meningeal artery and cause an
Linear fracture – lines spread out from the impact bone in several directions but bone doesn’t cave inwards - Can be seen in the frontal bone
Comminuted fracture – skull is split into several distinct pieces of bone, also usually involves a break in the skin
Countercoup fracture – force travels round skull and occurs on the opposite side to the point of impact
Basilar fracture – occurs on the back of the head (basilar part of occipital bone) extradural haematoma
17
Q
Fractures of the mandible
A
Coronoid process fracture – unusual and usually unilateral
Condylar process fracture – usually result in avulsion and/or dislocation of the TMJ
Angle of mandible fracture – can damage the 3 rd molar socket
Body of mandible fracture – tend to occur at the area of a canine tooth
18
Q
Lateral cleft lip
A
Failure of MNP and maxillary prominence to fuse leading to split in mucosa up to the nostril
19
Q
Cleft palate
A
Failure of palatal shelves to fuse in midline leading to a difficulty suckling and with speech
20
Q
Foetal alcohol syndrome
A
Results on the foetus of alcohol intake during pregnancy.
Alongside alcohol related neurodevelopmental delay (combined as foetal alcohol spectrum disorder) incidence is 1/100 births
Physical features
Short palpebral fissures (small eyes) No philtrum Small head Underdeveloped jaw Thin upper lip
Mental features
Behavioural disorders e.g. ADHD
Learning disorders e.g. thinking, speech, social skills
Hearing and sight problems
21
Q
CN I lesion
A
Usually a result of cribriform plate fracture (accompanied by CSF rhinorrhoea) or meningitis. Leads to anosmia
22
Q
CN II lesion
A
Can be due a number of things, including central retinal artery occlusion, compression by a pituitary adenoma etc. Loss of vision depends on where the lesion is along the nerve but leads to reduced visual acuity, visual fields and defective direct and consensual pupillary reflexes. Can also show a relative afferent pupillary defect (both eyes show a consensual pupillary reflex by side with damaged CN II causes both pupils to constrict less)
23
Q
Differentiating CN II lesions
A
Proximal to the optic chiasm – CN II is carrying all sensory input from one eye, so this leads to a total loss of vision in this one eye. This manifests as reduced vision on the lateral field of vision on the same side (specifically, the loss of the medial fibres of that eye – the lens flips the image before it hits the retina)
At the optic chiasm (bitemporal hemianopia) – here, the medial fibres supplying sensory information from the lateral fields of vision cross, and are both damaged. This leads to reduced vision at the peripheries, known as tunnel vision. This is most commonly caused by an enlarging pituitary adenoma
At the optic tract (homonymous hemianopia) – here, the fibres that receive information from the other side’s field of vision (e.g. left optic tract carries information from right FOV) are damaged, and so leads to loss of vision in the contralateral field of vision (not the contralateral eye, it’s slightly different). Commonly caused by a parietal lobe tumour
24
Q
CN III lesion
A
Can be a result of a number of things but a common one is cavernous sinus thrombosis. Increased ICP is also a common cause.
Displays ptosis (loss of levator palpebrae superiorus) and down and out pupil (unopposed actions of superior oblique and lateral rectus). If parasympathetic fibres are involved (they usually are) then also shows loss of accommodation reflex and a blown (dilated) pupil due to loss of constrictor pupillae
25
Horner’s syndrome
Damage to the sympathetic trunk e.g. due to a Pancoast tumour leads to ptosis (loss of superior tarsus), a constricted pupil (myadrisis due to loss of dilator pupillae) and anhydrosis (loss of sympathetically mediated sweating)
26
CN IV lesion
Can be caused by cavernous sinus thrombosis. Leads to diplopia when looking down and in (action of superior oblique lost). Can also see patient has a head tilt as they try to compensate for the loss of intortion
27
CN V lesion
Damage to fibres leads to loss of sensation. V 1 and V 2 purely cause sensory loss in their distributions, but V 3 damage leads to loss of mastication muscle bulk (e.g. masseter) as well. Sympathetic fibres that hitch hike the nerve to the relative distributions also damaged leading to vasodilation and anhydrosis
28
Harlequin syndrome
Damage to the sympathetic fibres that hitch hike CN V at the level of the sympathetic trunk/thoracic cord leading to vasodilation and anhydrosis across the entire half of the face
29
Trigeminal neuralgia
Severe sharp pain within the distribution of the trigeminal nerve that lasts for a few seconds to a few minutes. Triggered by sudden movements, wind or just idiopathic
30
CN VI lesion
Usually seen as one of the first signs of increased ICP. As such, CN VI palsy can be misdiagnosed as falsely localising whereas in fact it is due to a whole brain pathology. Paralysis of lateral rectus leads to diplopia on attempted lateral gaze in the affected eye
31
CN VII lesion (Facial nerve palsy)
A lesion to the ‘clinical’ facial nerve i.e. containing the parasympathetic fibres is much more common than one of the anatomical ‘proper’ facial nerve i.e. just the motor and sensory roots. It is at risk in a number of locations:
Parotid gland (parotitis or malignancy) – affects only motor functions
Facial canal (inflammation) – doesn’t affect the pterygopalatine ganglion but can affect stapedius (leading to hyperacusis) and submandibular ganglion (taste sensation, sublingual and submandibular glands). Also affects motor function
Forceps delivery – affects the extracranial portion only motor functions affected
As shown the damage depends on the level/structure at which CN VII is damaged. Tends to be permanent
32
Bell’s palsy
Idiopathic damage to CN VII. Tends to be motor functions only i.e. affects the nerve extracranially (but can have intracranial Bell’s palsy leading to parasympathetic and sensory damage). Many cases thought to be caused by inflammation due to Herpes zoster but this is difficult to prove. Tends to resolve spontaneously
33
Stroke (in the context of CN VII)
Lesion to one hemisphere of the brain can cause infarction of the facial motor nucleus. However, the branch of CN VII that supplies frontalis (temporal) receives fibres from both the right and the left facial motor nuclei. This is true for CN VII on both sides. This means that someone with a stroke will be unable to perform most facial actions but they will be able to wrinkle their forehead/raise their eyebrows
34
CN VIII lesion
As the vestibulocochlear nerve is comprised of the vestibular (balance) and cochlear (hearing) nerves you would expect some dysfunction in either of these. Damage to the vestibular portion leads to inability to balance and subsequent vertigo. Damage to the cochlear portion leads to sensorineural hearing loss (air conduction still > bone conduction but hearing reduced vs the contralateral side)
35
Vestibular schwannoma
Benign tumour of the Schwann cells of CN VIII. Leads to symptoms seen with a CN VIII lesion/palsy. If it grows large enough it can begin to impinge on CN VII within the facial canal, which shows both changes in hearing (hyperacusis due to paralysis of stapedius) and taste (loss of chorda tympani), alongside facial paralysis
36
CN IX lesion
Damage to CN IX leads to a loss of function in stylopharyngeus, which is a key muscle involved in elevating the larynx during swallowing, to position the epiglottis correctly. It also supplies taste to the posterior 1/3 rd of the tongue, so this could be tested with a specific kit. However, CN IX cannot be examined alone, and is instead examined alongside CN X with things such as the gag reflex or getting the patient to cough/swallow
37
CN X lesion(s)
There are two key types of CN X lesion (in the context of the head and neck i.e. not considering its distribution throughout the thorax and abdomen), but there are some features that may be common to both. Any deviation in the uvula away from the lesion may be evident, as musculus uvulae will contract to pull the uvula towards the unaffected side.
Also, any damage to the vagus nerve may damage the pharyngeal constrictors, leading to disorders of swallowing.
There are two key branches that may provide differing symptoms when considering phonation:
External/superior laryngeal nerve – solely provides innervation to cricothyroid, which tenses and elongates the vocal cords, allowing for a higher pitch and is known as the ‘singers muscle’. Damage to this nerve leads to a monotone voice and loss of strength (loudness) of phonation
Recurrent laryngeal nerve – provides innervation for the other intrinsic muscles of the larynx, the most important of which is the posterior cricoarytenoids, which abduct the vocal cords. They also innervate the lateral cricoarytenoids, which adduct the vocal cords. Total damage to the nerve less to loss of both of these muscles leading to the vocal cord being stuck between abducted and adducted. This may produce a hoarse voice
Partial paralysis adversely affects the posterior cricoarytenoids, leading to a vocal cord that is locked in the adducted position. If this occurs bilaterally, the larynx cannot open and it is a surgical emergency that requires a needle cricothyroidotomy to resolve
Can easily undergo iatrogenic damage during any thyroid surgery – care must be taken to identify and avoid these nerves
38
CN XI lesion
Lesions to CN XI lead to denervation atrophy of trapezius and SCM, along with weakness of shrugging the shoulders and rotation of the head
39
CN XII lesion
Damage leads to fasciculations of the tongue and a deviation in movement towards the affected side. This is because when sticking the tongue out, the transverse intrinsic muscle on both sides contracts to elongate/narrow the tongue. If this is paralysed on the right side, it stays short on the right side, so it will deviate towards this side.
40
Orbital (blowout) fractures
Certain walls of the orbit are much thinner than others and as such are prone to fractures when a large force is applied across the orbit. All fractures usually give some degree of diplopia, enopthalmos, lid swelling, pain, reduced vision and reduced visual fields. Common types are:
Floor (aka maxillary) – results from relatively minor trauma directly to the orbit
Leads to inferior displacement of the eye and relevant apparatus, this means the inferior rectus can get trapped and this results in inability to raise the eye (leading to diplopia on vertical gaze)
Also may lead to enopthalmos, as the eye is pushed posterior and inferior within the socket
Can be accompanied by infraorbital anaesthesia (lower eyelid and upper lip), due to damage of the infraorbital nerve (branch of CN V 2 )
Medial (aka ethmoidal) – results from relatively minor trauma directly to the orbit
Rarely isolated and usually seen in combination with other fractures
Can trap the medial rectus, leading to horizontal diplopia on medial gaze
Damage to the ethmoidal air cells within the ethmoid sinus can lead to surgical emphysema
Lateral (aka zygomatic arch) – results from major trauma due to the relative thickness of the frontozygomatic suture
Usually found alongside other facial injuries
Can trap the lateral rectus, leading to horizontal diplopia on lateral gaze
41
Retinal detachment
The retina and the choroid have different embryological origins, and as such can easily become detached from each other if force is applied to them e.g. trauma. Outer layers of the retina are supplied by the choroid, and inner ones by the central retinal artery. As such, loss of the choroid leads to avascular necrosis of the retina and subsequent loss of vision
42
Open angle glaucoma
Increased fluid formation within the anterior chamber of the eye leads to the iris being displaced anteriorly and the angle of the trabecular network getting wider i.e. more open.
This progresses gradually and increases intraocular pressure until the optic nerve is compressed, leading to a loss of vision
43
Closed angle glaucoma
Different pathology to open angle glaucoma, in this the iris is forced against the trabecular network (i.e. posteriorly), leading to acute vision loss
44
Central retinal artery occlusion
Interruption of this artery (running within CN II) leads to painless and instantaneous vision loss, very difficult to fix as the nerve begins to die shortly after. Shows on fundoscopy as a pale retina (blood supply delivered by this artery), aside from the macula/fovea which is entirely perfused by the choroid
45
Central retinal vein occlusion
Interruption of this venous drainage (running within CN II), usually due to dehydration or thrombophlebitis, leads to acute but not instantaneous vision loss due to a backup of pressure. Shows on fundoscopy as a ‘stormy sunset’ picture
46
Papilloedema
Swelling of the optic disc as a result of (usually) increased ICP, but can in rare cases be due to bad, untreated hypertension as well. On fundoscopy appears as a red, angry picture with a bulging optic disc and raised retinal arteries
47
Meibomian cyst
Blocked tarsal gland found on the eyelid. Not infected per se but may become so (so can be treated just with a hot compress)
48
Styes
Infected ciliary gland found within the margin of the eyelid. By definition are infected so require antibiotics to treat
49
Thyroid eye disease
Usually a result of poorly controlled hyperthyroidism (Grave’s disease is the usual cause). Swelling of the tissues within the orbit causes exophthalmos as they have no where else to go.
Symptoms
Ocular irritation
Red eyes
Diplopia
Symptoms
Proptosis/exophthalmos
Lid retraction
Restrictive myopathy
Lid lag
The severity can be graded by using the NOSPECS mnemonic:
No signs OR symptoms
Only signs, no symptoms
Soft tissue involvement e.g. lid oedema
Proptosis (exophthalmos)
Extraocular muscle involvement (e.g. restrictive myopathy)
Corneal abrasion (eyelids not closing properly due to lid oedema)
Sight loss
Starting with no signs or symptoms at 0, you gain a point as you head down the scale. Anything >3 needs referring for imaging and steroids to prevent permanent vision loss
50
Conjunctivitis
Inflammation of the bulbar conjunctiva giving a red appearance to the sclera of the eyeball. Usually self limiting and does not require any treatment
51
Periorbital cellulitis
Inflammation of the soft tissue structures within the orbit itself. Differentiated from simple conjunctivitis by the presence of swollen eyelids. Accompanied by visual dysfunction, relative afferent pupillary defect, fever and exophthalmos. Infection is at a high risk of tracking back into either the ocular structures themselves e.g. CN II or the brain itself e.g. leading to meningitis so needs IV antibiotics and admission
52
Orbital mass lesions
Several different types, but essentially some sort of accumulation of cells/fluid that leads to swelling in or around the orbit, pain, inflammation, diplopia, proptosis and restricted eye movements. These are just some of the types:
Mucocoele – a blocking of the sinus openings in the nose leading to back up of secretions into the area of the orbit
Dermoid cysts – congenital cysts that can be superficial or deep and are often well circumscribed, they tend not to cause pain
Wegener’s granulomatosis – these lesions are a result of necrotising vasculitis and as such are prone to infection if the necrotic tissue is not removed properly (corticosteroids may reduce the necrosis formation)
Dacryoadenitis – inflammation of the lacrimal glands, can commonly be caused by mumps or gonhorrea
Pseudotumour – idiopathic diagnosis of exclusion after the lesion has been biopsied
Capillary haemangioma – aka strawberry nevus, tend to be congenital, superficial ones are easily identified on the eyelid
Cavernous haemangioma – a benign tumour of dilated and well vascularised blood vessels (through which blood moves slowly), they tend to be found deep within the orbit (in the intraconal space, posterior to the eyeball but bound either side by the rectus muscles) and as such may caus proptosis/exophthalmos
53
Corneal abrasion
Any foreign body can scratch the cornea, the fibrous layer that overlies the pupil/iris (technically overlies the anterior chamber). This is usually mitigated by the blink reflex; cornea is supplied by CN V 1 , which when stimulated leads to contraction of orbicularis oculi, blinking out the foreign body. If this is lost e.g. the nerve is damaged, then the eye can be damaged. Abrasions usually heal on their own but antibiotic eye drops may be needed
54
Antihelix deformity
Lack of the antihelix fold of the pinna, leading to a ‘dumbo ear’ appearance
55
Pinna malform
Congenital hypoplasia or aplasia of the pinna
56
Pre-auricular pit
Small hole immediately anterior to the EAM within the pinna
57
Pre-auricular skin tag
Small swelling immediately anterior to the EAM within the pinna
58
Traumatic rupture of pinna
Pinna is ‘ripped apart’ due to trauma. Tends to look worse than it is due to the tendency of elastic cartilage to rip apart when it is damaged due to elastic fibres providing recoil, pulling the edges of the wound further apart
59
Pinna haematoma
Accumulation of blood between cartilage and perichondrium (usually secondary to trauma), which if not treated may lead to avascular necrosis of the pinna as the cartilage’s ‘blood supply’ has been stripped leading to cauliflower ear
60
Cauliflower ear
‘Collapsed down’ pinna due to avascular necrosis (usually secondary to a pinna haematoma)
61
Otitis externa
Infection of the external ear, commonly caused by Staphylococcus spp., leads to an inflamed, sore external ear, which can be accompanied by discharge and some degree of hearing loss
62
Foreign body insertion (external ear)
Small objects lodged in the ear canal lead to pain and a degree of conductive hearing loss. Can also lead to tympanic rupture if left in situ without prompt removal
63
Tympanic membrane rupture
Occurs either due to trauma (cotton buds!) or pressure difference on either side of the membrane (otitis media leading to a bulging and then ruptured membrane due to the build up of pus is common). As the membrane is now not in tact its ability to vibrate is reduced, leading to a degree of hearing loss. Tears can be minor, or central holes or subtotal perforations
64
Acute otitis media
Infection of the middle ear, almost always a result of tracking of an upper respiratory tract infection via the Eustachian tube (especially common in children due to the fact it is shorter, narrower and at a less oblique angle). Leads to pain, conductive hearing loss and retraction of tympanic membrane, however in some cases the build-up of pus can lead to bulging and subsequent rupture of the eardrum
65
Otitis media with effusion
Thick effusions develop behind the eardrum as a result of consistent negative pressure (such as a chronically collapsed Eustachian tube in children) leading to reduced ability to hear (conductive hearing loss) and a predisposition to an infection, creating a vicious cycle. Can be treated with grommet insertion into the tympanic membrane to provide an alternate route for pressure to equalise
66
Mastoiditis
Infectious spread to the air cells of the mastoid process of the temporal bone (via the epitympanic recess), leading to swelling of this bone. Can be seen externally as post-auricular inflammation, and pushes the ipsilateral pinna anteriorly, which can be spotted on examination. Spreads very easily and so can cause intracranial infection (e.g. meningitis) and death. Requires antibiotics and surgical clear-out of the mastoid air cells
67
Cholesteatoma
Retraction pockets appear (as a result of –ve pressure) and accumulate dead skin cells, forming a necrotic mass of dead cells that multiplies and spreads through adjacent structures. Acts cancerous but isn’t cancerous. The most lateral portion of a cholesteatoma can be spotted in the attic/pars flaccida of the tympanic membrane
68
Benign positional paroxysmal vertigo
Displacement of otolith (stone within the canal) that keeps moving when the fluid stops (like sediment within water), so you perceive movement when you are actually still (mismatch between vision and vestibular system is unpleasant). Only lasts a few seconds
69
Meniere’s disease
Overaccumulation of endolymph leads to vertigo, tinnitus, hearing loss and aural fullness
70
Motion sickness
Very common complaint of many people. Occurs when there is a mismatch between vestibular and visual systems, which the brain perceives as poisoning and activates the vomiting centres as a defence mechanism. Common example is seasickness; vestibular system perceives rocking of boat whereas your eyes see you’re steady (if you look within the boat/close your eyes), so can be remedied by focussing on the horizon so your eyes know you’re not steady
71
Nasal fractures
Most common fracture of the facial skeleton. Occurs when a force is applied across the nose e.g. a punch. If it heals misaligned, then the entire nose (including the cartilage) is misaligned permanently
72
Septal haematoma
Trauma to the nose can also cause a septal haematoma, which like a pinna haematoma strips the perichondrium from the cartilage, leaving the nasal septum at risk of avascular necrosis. If this happens the patient can end up with a deviated septum, leading to snoring or even sleep apnoea (temporary cessation of breathing in sleep)
73
Rhinitis
Umbrella term for any inflammation and irritation of the nasal mucosa, which manifests as the feeling of a blocked, stuffy nose, with some alteration to speech, inability to breath through the nose and discharge from the nose. Many causes/types:
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Viral/bacterial infection
Allergic rhinitis (hayfever)
Nasal polyps (benign collections of eosinophilic cells that grow close to the middle meatus)
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74
Sinusitis
Rhinitis in a different location essentially (within the paranasal sinuses). Leads to feelings of head/cheek pain, toothache (referring of pain) and halitosis (amongst other symptoms). Can be classified into different types by its longevity (>90 days leading to chronic sinusitis). Tends to be a result of secondary bacterial colonisation (e.g. H. influenzae) following a primary viral infection (e.g. Adenoviridae). Maxillary sinusitis is more likely to be chronic as they drain from their superior border, so any infection that resides in the lower portion is unlikely to be cleared
75
Epistaxis
A nosebleed. In most individuals they are self resolving (and originate from Kisselbach’s plexus on anterior portion of nasal septum) and just a nuisance, but can be life threatening with the right risk factors (old, warfarinised, underlying infection, cancer, sphenopalatine bleed etc). Stepwise treatment is as follows:
1. Adopt Hippocratic position (hunched over sitting) and pinch nasal cartilage just inferior to nasal bones for 20 mins
2. Cauterisation of bleeding vessels with diathermy or silver nitrate (if visible)
3. Anterior packing (nasal tampons e.g. Merocel)
4. Posterior packing (horizontally layered cause and Foley catheter inflated posteriorly to choana to stop blood flow down the oropharynx)
5. Ligation of vessels using a surgical or radiological approach (in order they’re tried; sphenopalatine then maxillary then ECA)
76
Gingivitis
Inflammation of the gingival mucosa, which lines the anterior surface of the bottom/root of teeth. This chronic inflammation, if left untreated, can lead to a route for bacteria to enter systemic circulation, causing bacteraemia that may progress to infective endocarditis (Viridans strep). Also, it may lead to bacteria invading the periodontium (the specialised tissue that lies between the tooth and the alveolar bone) or even the alveolar bone, which would lead to tooth loss
77
Tooth decay (dental caries)
Breakdown of tooth (particularly enamel) matter due to involvement of bacteria. Visible as defects/changes in colour of the tooth’s surface. Most commonly caused by a combination of a diet high in refined sugars and poor dental hygiene
78
Ankyloglossia
An abnormally short (or anteriorly attached) lingual frenulum restricts the movement of the tongue. In babies this may lead to problems with feeding, and in adults/younger children it may lead to speech impediments
79
Tonsillitis
(Usually viral) inflammation of the palatine tonsils, situated in the isthmus of the fauces (between the palatoglossal and palatopharyngeal arches, separating the oral cavity proper and oropharynx). This leads to odynophagia, fever etc. If tonsillitis is recurrent, then the tonsils may be surgically amputated (usually using diathermy), known as a tonsillectomy
80
Quinsy (peritonsillar abscess)
Formation of an abscess (accumulation of pus) within or on the tonsil as a result of untreated (usually bacterial) tonsillitis. It causes a huge swelling of the tonsil which may partially occlude the oropharynx, leading to stridor. When lanced, care must be taken not to lance the internal carotid artery lying just lateral to it
81
Salivary gland stone (sialolithiasis)
Stones forming within the salivary glands, usually the submandibular (Wharton’s) duct. Thought to be a result of dehydration, decreased salivary flow rate and an alteration in salivary pH due to presence/overgrowth of bacteria
82
Anaphylaxis
Activation of IgE antibodies that are bound to mast cells causes huge mast cell degranulation, releasing histamine into the circulation. This causes massive blood vessel dilation and ‘leaky capillaries’, which causes the mucosa of the airways to swell greatly (known as angioedema) and bronchial smooth muscle to contract. This may lead to occlusion of the airway. Also, as histamine is a vasodilator, it can cause a huge drop in TPR and slide the patient into anaphylactic shock (persistently low BP leading to systemic hypoperfusion). Needs adrenaline to buy you some time; acts on A1 receptors to vasoconstrict, preserving TPR, B1 to inc CO, and B2 to dilate bronchial smooth muscle. Immune system must be ‘reset’ with IV chlorphenamine and hydrocortisone
83
Dislocations of the TMJ
Can occur in a few directions
Anterior dislocation – forward dislocation is usually prevented by the articular tubercle. In a huge yawn/opening of the TMJ, the condyles are pulled too far anteriorly, causing them to override the articular tubercle. The lateral pterygoids immediately go into spasm, preventing the jaw from being relocated
Posterior dislocation – usually prevented by the postglenoid tubercle. Occurs when being punched hard anteriorly in the jaw with the mandible elevated
Superior dislocation – occurs when uppercutted when the mandible is depressed
84
Bruxism
Grinding of the teeth. Thought to have many causes, ranging from iatrogenic (drugs e.g. MDMA, citalopram) to CNS patterns of sleep. Leads to tooth attrition due to excessive contact between the teeth, and may predispose to dental caries
85
Mal-occlusion syndromes
Any situation in which the teeth do not line up properly. These include having an overbite (the maxillary teeth are anterior to the mandibular teeth), an underbite (the mandibular teeth are anterior to the maxillary teeth) or any situation where the line between the central incisors doesn’t match up superiorly and inferiorly. May be treated by an orthodontist with rubber bands attached to braces, that manipulate the position of the mandible to remove the deficit
86
First Arch syndromes
A spectrum of diseases caused by failure of neural crest cells to migrate into the first pharyngeal arch. This includes Treacher-Collins syndrome
87
Treacher-Collins syndrome
An autosomal dominant condition that is thought to be caused by a genetic mutation that causes a reduction in rRNA within neural crest cells, leading to their apoptosis and inability to colonise the pharyngeal arches. This manifests as hypoplasia of the mandible and facial bones, conductive hearing loss (due to an incorrectly formed ear canal) and disfigured or absent ears
88
Di-George syndrome
Caused by a deletion of a small section of chromosome 22. The deletion results in an abnormal growth of the neural crest. Effects can be remembered using the mnemonic CATCH22:
Cardiac abnormality (particularly Tetralogy of Fallot)
Abnormal facies
Thymic aplasia
Cleft palate
Hypoparathyroidism
89
CHARGE syndrome
Defect in a gene (CHD7) that is essential for the production of multipotent neural crest cells (that are involved with the pharyngeal arches). Effects can be remembered using the mnemonic
CHARGE:
Coloboma
Heart defects (e.g. ASD)
Choanal atresia (unable to conduct air via the nasopharynx)
Retardation (both growth and mental)
Genital hypoplasia
Ear defects
90
Adenoidal hypertrophy
The adenoid or pharyngeal tonsil is found within the posterior border of the nasopharynx, and is generally quite large in children, and then regresses throughout adulthood. It can become enlarged and lead to recurrent ear infections (blocking Eustachian tube) or obstructive sleep apnoea (anything from snoring to periods of brief respiratory arrest during sleep). This mandates removal in an adenoidectomy, which can either be done using curettage or diathermy. Complications include bleeding and atlanto-occipital joint dislocation (secondary due to infection as it sits anterior to C1)
91
Nasopharyngeal carcinoma
Relatively rare type of cancer that is common in Chinese people. Tend to be squamous cell carcinomas, and are usually treated with radiotherapy
92
Pharyngeal pouch (diverticulum of Zenker)
A diverticula of the pharyngeal mucosa that can punch through the weak area (Killian’s dehiscence) that exists between the inferior constrictor and stylopharyngeus. Food can collect in this pouch and lead to dysphagia, regurgitation or halitosis
93
Acute epiglottitis
Bacterial inflammation of the epiglottis (e.g. Haemophilus influenzae, Staph spp. etc.) that leads to acute airway obstruction due to blocking of the glottis. Patients are always paeds (2-7yrs old) and adopt a ‘tripod’ position by leaning forward and drooling. Needs a RSI to ensure airway patency, steroids and antibiotics to treat and then can be extubated when the swelling has subsided
94
Laryngotracheo-bronchitis (croup)
Common cause of paediatric stridor. Tends to have an initial viral throat infection, and gives a ‘seal bark’ subglottic cough, due to inflammatory response causing oedema that narrows the subglottis. Can be managed with antibiotics at home or intubation at hospital and everything inbetween depending on severity
95
Foreign bodies in the upper respiratory tract
Biggest cause of 1-3yr old mortality. Tends to present with a toy that’s gone missing, a coughing fit and constant choking. A lot of foreign bodies are radio-opaque e.g. coins and many can be visualised with bronchoscopy. Can give some radiological signs such as localised emphysema (due to the FB creating a valve like a pneumothorax does but with the bronchus), lobar collapse etc. Removed with a grabber like you’re at the arcades!
96
Laryngomalacia
Commonest cause of infant stridor. Epiglottis is too floppy and as a result droops and covers the glottis to a certain degree, producing stridor. Results in a characteristic high pitched ‘dog toy’ inspiratory squeak. Most cases self resolve as the child grows, some require surgery to trim the epiglottis (the vocal cords if they adduct properly work adequately as a mechanism to guard the respiratory tract)
97
Singer’s nodules
Mass of tissue that grows on the true vocal cord that typically appear in the junction between the anterior and middle third. They are a result of injury to the vocal cords caused by singing, yelling, shouting etc. Their presence impairs the ability of the vocal cord to vibrate, meaning they may have a hoarse voice, a breaking voice etc.
98
Hypopharyngeal/laryngeal carcinoma
Laryngeal carcinoma is the most common:
Risk factors/aetiology
Common in Western (white) populations
5x more common in males vs females
Smoking and alcohol are major risk factors
Presentation
Sensation of a foreign body stuck in the throat
Dysphagia (and odynophagia) - Trouble with solids usually due to obstruction (liquids usually indicates achalasia
Otalgia (referred via CN X)
Hoarseness (RLN damage) and coughing
Symptoms of tumour burden e.g. cachexia, fatigue
Loss of laryngeal crepitus
Head and neck lymphadenopathy due to mets secondary to a neurological deficit)
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Treatment
Need TNM staging under the care of a MDT
Radiotherapy and chemotherapy
Surgical interventions - Laryngectomy
Palliative care
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99
Indirect inguinal hernia (in context of repro)
In males, the processus vaginalis (outcropping of peritoneum) descends down through the inguinal canal to allow for the testes to follow behind it. If this doesn’t obliterate (becoming the tunica vaginalis) then the deep inguinal ring doesn’t close fully and bowel can slip through
100
Congenital adrenal hyperplasia
Umbrella term for several autosomal recessive mutations in genes that are involved in the steroid synthesis pathway. Defect in mineralocorticoid/glucocorticoid synthesis means that excess cholesterol is funnelled through testosterone synthesis pathway, leading to ambiguous genitalia in female new-borns. Males don’t present until later in life. Main concerns are Addison’s disease/hyponatraemia/hypovolaemia from deficiency of other steroids, not the genitalia
101
Male foetus with genitalia insensitive to testosterone
Mesonephric Ducts - Regress (lack of testosterone binding)
Mullerian ducts - Regress (still producing MIH)
External genitalia - Female (lack of testosterone binding)
Ext female genitalia
Lack of internal genitalia
Short vagina
102
Female foetus with excessive androgens
Mesonephric ducts - Persist (bind testosterone)
Mullerian ducts - Persist (no MIH)
External genitalia - Ambiguous
Ambiguous ext. genitalia
Internal female genitalia with vas deferens
103
Male foetus with low MIH
Mesonephric ducts - Persist (bind testosterone)
Mullerian ducts - Persist (no MIH)
External genitalia - Male
Ext male genitalia
Internal female genitalia Testes in abdomen (caught by Fallopian tubes)
104
Female foetus with excessive MIH
Mesonephric ducts - Regress (lack of testosterone)
Mullerian ducts - Regress (MIH)
External genitalia - Female
105
Pituitary not in situ (hypothetical)
The hypothalamus secretes releasing hormones into the hypophyseal vessels which connect with the pituitary, allowing small amounts of these hormones to produce a large effect. If the pituitary were to be removed and placed somewhere else then these would be too diluted in circulation and levels of TSH, ACTH, GH, LH/FSH would drop off. However, as prolactin secretion occurs in the absence of dopamine, levels of prolactin would rise and rise
106
Prolactinoma
Tumour of the pituitary that produces large levels of prolactin. Causes hyperprolactinaemia that leads to suppression of GnRH release leading to low FSH/LH and anovulation
107
Precocious puberty
Gonadotropin dependant (central precocious puberty) – HPG axis prematurely activated (due to many things; idiopathic, pituitary tumours, trauma/meningitis, radiotherapy/chemotherapy etc) premature (<8yrs girls, <9yrs boys) development of breast buds/testicular enlargement. Progresses through normal puberty as expected unless treated with reversible chemical castration e.g. GnRH agonists. If untreated epiphyseal growth plates close prematurely short stature
Gonadotropin independent (precocious pseudopuberty) – puberty begins without involvement of HPG axis i.e. sex hormones come from another source (such as congenital adrenal hyperplasia, testotoxicosis, hCG secreting tumour, exogenous ingestion of OCP etc). Levels of GnRH, FSH/LH supressed due to –ve feedback. Can be supressed by treating the underlying cause and/or reversible chemical castration
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Delayed puberty
Gonadal failure – problem is with the gonad itself (so [GnRH] high) e.g. autoimmune syndromes, Turner’s syndrome, damage post radiotherapy
Gonadal deficiency – problem is at the level of GnRH or FSH/LH e.g. pituitary damage post radiotherapy
109
Turner’s syndrome
45X karyotype leading to problems with heart, kidneys, skeleton (including short stature). Importantly also causes gonadal dysgenesis so leads to delayed/absent puberty (hypergonadotrophic hypogonadism)
110
Testotoxicosis
Aka familial male precocious puberty. Autosomal dominant condition that causes mutation in LH receptor leading to a huge gain in function leading to rapid growth, early skeletal maturity (closing of growth plates) and sexually aggressive behaviour in first 2/3 years of life
111
Menorrhagia
Abnormally heavy menstrual bleeding. Defined by the effect on the patient (soaking through pads, messing the bed, using extra protection, symptoms of anaemia/hypovolaemia etc) not numbers, but can be said to be >80ml a cycle. Causes include:
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Clotting disorders e.g. idiopathic thrombocytopenia
Fibroids
Withdrawal of progesterone contraception
IUD – endometrial trauma on insertion
Cancer
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Treatment varies by age. <35 is treated with IUS (progesterone coil), tranexamic acid and iron tablets.
112
Primary amenorrhea
Never experienced menarche. Can be due to delayed puberty or just being too young (
113
Secondary amenorrhea
Experienced menarche but now menstrual periods have stopped. Number of different causes. Physiological include:
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Menopause
Post-surgery (hysterectomy/oophorectomy)
Low body weight
Stress
Progesterone based contraception (especially IUS)
Pregnancy
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Pathology of amenorrhea
Cryptomenorrhea – stenosed cervix inability of blood to exit vagina
Uterine/endometrial dysfunction – inability to respond to oestrogen so no proliferation
Ovarian – loss of ovulation/follicular stimulation so no oestrogen secretion
Pituitary – loss of FSH or LH secretion e.g. acquired insensitivity to GnRH
Hypothalamic – loss of pulsatile GnRH release e.g. prolactinoma
115
Abnormal uterine bleeding
Much more worrying than menorrhagia or amenorrhea. Common causes include:
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Stress
Low body weight/poor diet
Endometrial polyps
Contraception (breakthrough bleeding/’spotting’)
Endometriosis
Endometrial cancer
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116
Benign prostatic hyperplasia (BPH)
Enlargement of the transitional zone of the prostate occurs due to aging in males. This compresses the prostatic urethra and causes obstructive LUTS symptoms (nocturia, urge incontinence, feeling of incomplete emptying, increased time to urinate). Can be treated with transurethral resection of prostate but that can lead to stress incontinence and impotence
117
Carcinoma of the prostate
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Malignancy develops (usually) within the peripheral zone of the prostate. This means that a lot of growth/spread is required before it causes LUTS like BPH does. Many tumours are slow growing and as they occur in elderly men a lot of people are treated with ‘aggressive maintenance’ as they’re more likely to die from something else (MI) first. Can present with back pain first due to sacral mets that arise as the prostatic venous plexus communicates with the vertebral venous plexus. Can be examined
with DRE (digital rectal exam, not Dr Dre) to show an enlarged and craggy prostate
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118
Haematocele
Collection of blood within the scrotum. Can be due to trauma. Distinguishable from a hydrocele by transillumination (light that comes out the other side will be red if you shine a pen torch through it)
119
Varicocoele
Varicosities of the pampiniform plexus. Feels like a bag of worms on palpation. Much more common on the left side as the blood has longer to travel (left renal vein vs IVC on right) and left renal vein merges with testicular vein at a perpendicular angle. Varicocoeles on the right can be a sign of renal malignancy as their metastases tend to end up in and partially obstruct the IVC
120
Hydrocele
Accumulation of fluid within the scrotum. Can be congenital (incomplete obliteration of the processus vaginalis) or acquired e.g. trauma/infection. Transillumination shows no red pigmentation
121
Spermatocoele/epididymal cyst
benign growth found on the epididymis. Can be surgically removed but may regress on their own
122
Testicular cancer
Commonly affects men aged 15-49. Usually presents as a lump in the scrotum that’s non tender and immobile. Requires orchidectomy to remove and prevent spread. Tend to be seminomas (tumours of the germinal epithelium of the seminiferous epithelium). 5yr survival of >95% if caught early
123
Abnormal uterine position
Normally found anteverted with respect to the vagina and anteflexed with respect to the cervix (so it curves round the posterior surface of the bladder and comes to sit superior to it but parallel). Three key abnormal positions:
Excessively anteflexed – points too far inferiorly i.e. not parallel with bladder
Anteflexed and retroverted – angle between cervix and uterus normal, but angle with vagina is decreased i.e. uterus begins to point superiorly
Retroflexed and retroverted – both angles lost so the uterus is either directly superior to vagina in straight line or beginning to curve backwards
All abnormal positioning leads to an increased risk of prolapse
124
Bartholin cysts
Blockage of the Bartholin glands (found inferolateral to the vaginal opening, secrete small amount of lubricating fluid). Can become infected and then need treating
125
Endometriosis
Ectopic growth of endometrium in the Fallopian tubes, or on the ovaries/in the peritoneum. Damage leading to adhesions and infertility and chronic pelvic pain. The tissue responds to oestrogen/progesterone normally so breaks down leading to inc pressure from fluid thus pain is worse preceding/at the start of menses. Treated with an IUS first line, and can also undergo surgery to remove ectopic growths
126
Pelvic prolapse
Weakening in the pelvic diaphragm and/or perineum leads to a reduced ability to support the pelvic viscera, which can lead to bulging of any of the pelvic viscera through their respective hiatuses (‘pelvic organ prolapse’ usually refers to bulging of organs around the vagina, leading a palpable lump in the vagina). Some times a complete prolapse can occur, where the vagina inverts and the cervix is pushed outside the body. Risk factors include obesity, chronic cough (both due to inc intra-abdominal pressure being a risk factor), menopause (lack of oestrogen leading to atrophy), connective tissue laxity etc. Treated with conservative management (pelvic floor exercises, weight loss), vaginal pessaries (push the organ back) or surgery to remove the prolapsed organs/restore collective tissue function
127
Incontinence (in context of childbirth)
weakening of the perineum (or damage to the pudendal nerve) in childbirth leads to reduced function of the external urethral sphincter (due to the bladder neck descending, meaning the sphincter is out of place), leading to inability to resist increases in pressure, which can be caused by coughing, sneezing etc. Treated conservatively with pelvic floor exercises, or with minimally invasive surgery like tension free vaginal tapes etc (aiming to reposition bladder neck so that the sphincter is in the right place to compress the proximal urethra)
128
Human papilloma virus
Several different strains/types, HPV 16 + 18 are oncogenic and are implicated in cervical cancer
Symptoms – benign, painless cutaneous warts that can appear on any genital structure
Diagnosis – usually clinical
Can take a biopsy and do a genome analysis
Treatment – rarely treated as many spontaneously regress on their own
Can use local cryotherapy or topical podophyllotoxin
129
Chlamydia (C. trachomatis)
Most common STI in the UK (1/10
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Genital herpes (Herpes zoster virus)
Relatively common STD
Symptoms – painful genital ulceration, dysuria, inguinal lymphadenopathy with fever
Can have recurrent bouts due to reactivation of dormant virus in the dorsal root ganglion (just like chickenpox)
Diagnosis – usually clinical
Treatment – acyclovir
131
Gonorrhoea (N. gonorrhoeae)
Disease primarily found in MSM populations but heterosexual cases on the rise
Symptoms
Male – urethritis with purulent discharge, epididymitis, prostatitis and proctitis and pharyngitis (MSM only)
Female – a lot of cases asymptomatic, endocervicitis, urethritis with purulent discharge
May progress to PID in females
Diagnosis – endocervical/urethral swabs or urine sample used to culture diagnosis
Can gram stain pus whilst patient waits to aid diagnosis (Gneg diplococci supports diagnosis)
Treatment – IM ceftriaxone
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Syphilis (Treponema pallidum)
Relatively rare disease seen primarily in MSM populations. Can progress onto systemic disease if not treated adequately
Stages of disease
Primary – chancre (painless genital ulcer)
Secondary (6-8 wks. after infection) – fever, rash, lymphadenopathy and mucosal lesions
Tertiary (several years later) – destruction of dorsal nerve roots (neurosyphilis), cardiovascular syphilis and gummas (local destruction of face)
Diagnosis – can’t be cultured but detected via dark field microscopy and serological tests (EIA antibodies)
Clinical – painless ulcer relatively specific to syphilis
Treatment – penicillin, then watch and wait to see whether that treated it or not
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Lymphogranuloma venerum (LGV)
Specific serotypes (1-3) of C. trachomatis. Initial papule that heals then subsequent appearance of an inguinal bubo
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Chancroid (Haemophilus ducreyi)
I.e. chancre like – same appearance as primary syphilis but painful
135
Donovanosis/granuloma inguinale
Klebsiella granulomatis – genital ulcers nodules
136
Trichomonas vaginitis (T. vaginalis)
Characterised by thin, frothy, offensive discharge accompanied by irritation, dysuria and vaginal inflammation. Can be diagnosed with a vaginal wet preparation and treated with metronidazole (as it’s a microscopic parasite)
137
Vulvovaginal candidiasis/thrush (Candida albicans)
Not an STD! Overgrowth of naturally occurring vaginal yeast. Several risk factors that include OCP, antibiotics, pregnancy, obesity, steroids and diabetes. Characterised by white, frothy curd like discharge and treated with topical nystatin or oral fluconazole
138
Scabes/pubic lice (Phthirus pubis)
‘Crabs’, cause irritation and itching sensation
139
Bacterial vaginosis (Gardnerella vaginalis)
Disturbed normal flora of vagina. Characterised by scant, offensive ‘fishy’ discharge with vaginal pH disturbance (>;5) that is made worse when exposed to KOH (whiff test). Laboratory diagnosis can be made with a gram stain showing epithelial cells studded with gram variable coccobacilli and reduced numbers of lactobacilli. Treated with metronidazole (targets anaerobes)
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Pelvic inflammatory disease
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Aetiology
Signs/symptoms
differentials
investigations
management
complicaitons
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(huge card)
an umbrella term for inflammation of the internal female genitalia (endometritis, parametritis, salpingitis, oophoritis, tubo-ovarian abscess, pelvic peritonitis)
Aetiology/pathophysiology
Usually a result of untreated chlamydia or gonorrhoea
Inflammation leading to pain
Immune response leading to tissue damage and scar tissue formation (adhesions) leads to infertility/chronic pain
Symptoms/signs
Fever with rigors Pyrexia
Abnormal vaginal discharge Adnexal tenderness
Sexual history with prior STI Purulent cervical discharge with cervicitis
IUD Bilateral lower abdominal tenderness
Deep dyspareunia with suprapubic pain Cervical motion tenderness
Irregular menstrual bleeding
Differentials
GI diseases – IBS, appendicitis, mesenteric adenitis
UTI
Gynae – endometriosis, ectopic pregnancy, ruptured/tortuous ovarian cyst
Functional/idiopathic pain
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Investigations
Urine/serum BhCG
Endocervical/high vaginal swabs – positive results support diagnosis but negative results don’t exclude it
FBC, U+E and CRP
Full STI screen
```
Management
```
Antibiotics
Outpatient (14 days) – IM ceftriaxone 500mg, PO doxycycline 100mg bds, PO
Inpatient (14 days) – same as above but all IV, then down to just PO doxycycline and metronidazole 400mg bds PO metronidazole when improving
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Surgery – only indicated with no response to therapy/suspected tubo-ovarian abscess
Exploratory laparoscopy is the gold standard
Admission – indicated when patient is query appendicitis, pregnant or has signs of pelvic peritonitis/tubo-ovarian abscess
Complications
Infertility – sperm can’t get past adhesions
Ectopic pregnancy – zygote can’t get past adhesions in Fallopian tubes
Chronic pelvic pain
Fitz-Hugh- Curtis syndrome – 10% of chlamydial PID - Can’t see, pee or bend at the knee, Conjunctivitis, urethritis and reactive arthritis, Also accompanied by RUQ pain and peri-hepatitis
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Sexual dysfunction
An umbrella for two entirely different processes
Loss of desire – nothing is ‘normal’ per se, it’s what is normal for a couple and whether they have deviated from that norm. Spans a whole spectrum from hypoactive, aversion (e.g. vagina dentata) to hyperactive/nymphomania (e.g. caused by Kluver-Bucci syndrome, bilateral temporal lobe lesions leading tonymphomania and other things)
Inability of arousal – male – inability to maintain an erection. Likely cause varies by age, in young males it’s almost always nerves/stress (so psychological). As age increases other things like fibrous tears to corpus cavernosa and vascular disease can cause impotency. Drugs (alcohol, beta blockers, diuretics) can also cause it
o Treated with Viagra, which inhibits cGMP breakdown leading to inc [NO] and thus vasodilation and an erection
Inability of arousal – female – lack of vaginal lubrication. Common post menopause
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ADD CONTRACEPTIVE TABLE
x
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Female subfertility
Lack of conception >1 year after couple first started trying. Experienced by 1/7 couples. Female causes account for >50% of infertility, and are subdivided into two common types
Anovulation – can be at the level of the ovary (ovarian failure), pituitary (tumours) or hypothalamus (stress, weight loss, exercise etc)
Different causes are differentiated by checking hormone levels to check if they’re decreased
FSH taken early in cycle, progesterone taken at ~21 days and LH taken at ~14 days i.e. when they’re at their respective peaks (obviously these are adjusted if the length of the cycle is known to be atypical)
Tubal occlusion – two key causes are endometriosis and PID (see both above). Diagnosed with a hysterosalpingogram and treated with reanastamosis or IVF (as ovaries are still functioning)
144
Polycystic ovarian syndrome (PCOS)
A complex syndrome characterised by infertility, amenorrhea and hyperandrogenism (secondary male sex characteristics e.g. excess hair growth). Dysfunctional (workbook says lack of but Wikipedia says increased) pulsatile GnRH release inc LH/FSH ratio at baseline (this inc [LH] causes androgenism) lack of sufficient FSH levels lots of follicular development but no selection of a dominant one and subsequent atresia of others polycystic appearence of ovaries
Also characterised by insulin resistance (leading to diabetes)
145
Male subfertility
Decrease in sperm production and/or quality. Causes include hormonal dysfunction and epididymitis. Semen sample can be used to confirm or refute diagnosis
146
Ectopic pregnancy
Occurs when the blastocyst implants somewhere other than the endometrium (either the fallopian tube or the peritoneum). Lack of decidua cells means invasion from the trophoblast goes unchecked and it will eventually erode through the surrounding arterial supply. Leads to haemorrhage and potentially death. Presents with lower abdominal pain that also leads to shoulder irritation when laying down (blood irritates diaphragm and pain refers via the phrenic nerve to C3-5 dermatomes)
147
Placenta accreta
Inappropriate and excessive invasion of the trophoblast into the myometrium of the uterus (normally stopped at the endometrium by the decidual cells), which can lead to haemorrhage at delivery
148
Pre-eclampsia
Hypertension and proteinuria during pregnancy. Thought to occur as a result of insufficient of remodelling of spiral arteries into low resistance capillary bed leading to release of unknown circulating factor that induces widespread endothelial dysfunction throughout the mother’s body leading to raised BP. Risk factors include family history, diabetes, existing hypertension, multiple babies and obesity. Only drug licensed for treatment of hypertension in pregnancy is labetalol, which is a non-specific alpha/beta adrenoceptor antagonist. Also, labour may be induced prematurely (37-38wks) as removal of the placenta generally corrects BP
149
Morning sicknes
Sickness associated with early pregnancy, especially in the first trimester. Cause unknown (speculated to be inc [oestrogen]) but increased vomiting before and up to 3 months is thought to be adaptive as the foetus is most sensitive to toxins in this time period, and so vomiting may stop ingestion of teratogens
150
Gestational diabetes
A result of imbalance between the roles of hPL (human placental lactogen) and maternal insulin. hPL increases insulin resistance within the mother to ensure she uses less glucose and subsequently more is available for the growing foetus. Mother is meant to compensate by producing more insulin but if this doesn’t happen hyperglycaemia results. Can lead to congenital defects, a macrosomic foetus or stillbirth. Tends to resolve after birth as the supply of hPL ceases with loss of placenta. Risk factors include obesity and family history of diabetes
151
Rhesus disease/haemolytic disease of the newborn
Red blood cells either do or don’t express the Rh antigen. Human bodies don’t naturally express an IgG antibody to this (unlike the naturally expressed IgM antibodies to ABO antigens, which don’t cross the placenta), they must be exposed and sensitised first. If the mother is Rh- and exposed to Rh+ blood (either through a transfusion or childbirth or some red blood cells leaking across the placenta), then she will manufacture antibodies. If the foetus is Rh+, these will cross the placenta and destroy the foetal erythrocytes. Sensitisation can be prevented by giving RHOgam (Rh antibody) that destroys foetal RBCs in maternal circulation before they are recognised by the immune system
152
Anaemia in pregnancy
As the placenta and foetus develop the mother has to respond with a greater plasma volume to supply everything. The mother is able to do this but inc in erythrocyte number may not keep up with this (insufficient levels of EPO) leading to anaemia. Can also have iron or folate deficiency anaemia as these are utilised by the foetus as well
153
Thrombosis in pregnancy
Decreased fibrinolysis, increased fibrinogen and clotting factors (along with high oestrogen levels) lead to a pro-thrombotic state. Also, mobility is decreased in later pregnancy, especially if the vena cava is compressed by the expanding uterus. Cannot be treated with warfarin as it is a teratogen that freely diffuses across the placenta
154
Changes in amniotic fluid volume
Normal route for amniotic fluid is it is initially formed by the meta/mesonephros and excreted into the amniotic cavity, where it is then swallowed or aspirated (mostly swallowed). Can either have more or less:
Polyhydraminos – too much amniotic fluid. Usually indicates a problem with swallowing e.g. oesophageal atresia
Oligohydramnios – not enough amniotic fluid. Usually indicates a problem with production e.g. multicystic kidneys or renal aplasia
155
Infant respiratory distress syndrome
Normal respiration relies on Lapalce’s law equalising pressure within different sized alveoli (). At a small radius, surfactant disrupts hydrogen bonding and therefore reduces surface tension. At a large radius, surfactant is spread thinner so is less effective, meaning that surface tension remains relatively high. This means pressure is equal across different sized alveoli. Without this, alveoli would collapse into each other (as pressure goes high to low). This is why children will die if they can’t produce surfactant.
Also, terminal sacs haven’t developed <26wks, without which surface area is too low for efficient gaseous exchange
Can give mother IM steroids to induce surfactant production in the foetus if a premature birth is suspected/likely
156
Post-partum haemorrhage
>500ml blood lost in
157
Acute mastitis
A disease of lactation (unheard of without lactation). Usually results from colonisation by Staph. aureus as a result of cracks and fissures in the nipple secondary to breastfeeding. Painful, swollen, red breast that may progress to a breast abscess. Needs treating with antibiotics and expressing milk (as milk will contain the bacteria)
158
Fat necrosis
Usually presents as a mass, skin changes or mammographic abnormality (not usually painful). Quite often secondary to trauma or surgery, but trauma that causes it can easily be missed/forgotten by the patient. Clinically (and mammographically) similar to breast cancer, so needs investigating by biopsy under 2 week wait pathway
159
Fibrocystic change
The commonest type of breast abnormality/lesion. Can be comprised of either fibrous (thickening) or cystic (fluid filled pockets) changes, and commonly presents as a breast abnormality. Can often disappear after fine needle aspiration biopsy (as you’ve punctured the cyst membrane) but do tend to refill. Histology includes cyst formation, fibrosis and apocrine metaplasia
160
Fibroadenoma
Commonest growth, but not cancerous. Not a true neoplasm, more like localised hyperplasia. Known as a ‘breast mouse’ as they are very mobile and tend to slip under fingers when you try and examine them. They have several important characteristics:
Macroscopic – well circumscribed, rubbery, greyish white
Microscopic – mixture of stromal and epithelial elements
161
Gynaecomastia
Excessive growth of breast tissue in males. Some breast tissue in men due to existence in asexual phase of early development. Results from increased oestrogen:androgen ratio, which has several causes:
Transient increase in oestrogen in neonates due to placental transfer
Puberty, due to oestrogen peaking before testosterone
Oestrogen excess secondary to reduced ability to metabolise it e.g. cirrhosis
Gonadotropin excess e.g. functioning testicular cell tumours
Iatrogenic (drug-related) e.g. spironolactone, alcohol, heroin etc
162
Breast cancer - Risk factors
The commonest cancer in females:
Risk factors – mostly related to hormone exposure
Gender (obvious but still)
OCP/HRT
Early menarche and last menopause
Late first parity
Obesity (aromatase found in adipocytes converts androgens oestrogens)
Geographical location (Western world esp. Europe and USA suffer more)
Previous breast cancer/radiation/abnormality
BRCA (and other hereditary factors)
10% of all breast cancer
Dysfunctional tumour suppressor genes one hit out of two-hit hypothesis already
Can have a prophylactic bilateral mastectomy to reduce chance drastically (85% without prophylaxis)
163
Breast cancer - In situ vs invasive
In situ – BM maintained, malignant neoplasm has not yet metastasised. Ductal carcinoma in situ (DCIS) usually presents as a mammographical calcification, with central necrosis. Doesn’t always progress to invasive carcinoma but is a required precursor
Paget’s disease (of the breast) – cancer has spread to skin of the nipple but not yet
metastasised. Unilateral red and crusted nipple
Invasive – has invaded through the basement membrane and so has contact with the blood and lymphatics. Usually presents as a lump, with 50% of patients with a lump having axillary lymphatic mets
Can present as peau-d’orange – blocked lymphatic drainage induces lymphedema of the breast excluding the hair follicles (as they are anchored to the dermis)
Can present as peau-d’orange – blocked lymphatic drainage induces lymphedema of
Can also present as inverted nipple – disrupted connective tissue due to invasion
164
Breast cancer - Ductal vs lobular carcinoma
Invasive ductal carcinoma, no special type (IDC-NST) – two types exist:
Well differentiated – tubules lined by sheets of atypical cells
Poorly differentiated – sheets of pleomorphic cells
Invasive lobular carcinoma – cells infiltrate in single file (sometimes called Indian file), and lack cohesion due to loss of E-cadherin
165
Breast cancer - Metastasis
Commonly metastasises to the axillary lymph nodes, but can also metastasise via haematogenous spread:
Mets through blood – everyone’s favourite things:
Boning – bones
Thinking – brain
Drinking – liver
Breathing – lungs
166
Breast cancer - Influences on prognosis
In situ vs invasive, IDC NST vs other histological subtypes etc.
Tumour grade (Bloom-Richardson scale, see MOD)
TNM stage (size, nodal involvement and distant mets)
Gene profile
Oestrogen receptor +ve – tumour is oestrogen fed and can be treated with Tamoxifen
Her2 receptor +ve – tumour is fed by human epidermal growth factor and can be treated with Herceptin
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Breast cancer - Treatment
MDT (multi disciplinary team)
Surgery
Breast surgery – mastectomy or breast conserving surgery (potentially with
Axillary surgery – axillary lymph node clearance, sentinel node is tested and if that is simultaneous reconstruction) negative complete dissection can be avoided
Long thoracic nerve damage leading to winged scapula
Chemotherapy
Traditional chemo – can be given neo-adjuvant
Tamoxifen – oestrogen antagonist in breast receptors, can shrink tumours (80%
Herceptin – Her2 receptor antagonist, can shrink tumours (20% express Her2 express oestrogen receptors) receptors)
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Cervical cancer/CIN - Pathogenesis
Almost always related to the prevalence of HPV (particularly 16 and 18)
Viral proteins E6 and E7 interfere with the activity of tumour suppressor genes one hit of two hit hypothesis
Also inhibit apoptosis and cause increased cell proliferation as a result of the inflammatory response
However, many infections are eliminated by the immune system
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Cervical cancer/CIN - Risk factors
Sexual intercourse (esp. promiscuity, promiscuous partner etc.)
Multiparous, early pregnancy
Long term use of OCP
Smoking
Immunosuppression
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CIN (cervial interepethelial neoplasia)
Dysplasia of squamous epithelia of cervix due to infection with high risk strains of HPV e.g. 16 and 18 Classified subjectively by the histologist into CIN I-III
CIN I leading to most regress spontaneously, but can be treated with cryotherapy
Progression from I to III is on average 7 years (so catchable on screening)
CIN III is carcinoma in situ, so must be treated as you don’t know if it will progress to invasive carcinoma or not
Requires cone excision
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Invasive carcinoma Cervical cancer/CIN
Average age is 45 years
Most are squamous cell but can have adenocarcinomas
May be exophytic (grow towards the surface) or infiltrative (grow deep into tissue)
Spreads either locally to other pelvic viscera or by lymphatics
Usually caught on screening, but can present with menstrual irregularities
Treatment
Microinvasive (1mm) – hysterectomy, lymph node dissection etc.
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Endometrial adenocarcinoma
Most common invasive cancer of the female reproductive tract, usually a result of endometrial hyperplasia
Endometrial hyperplasia
Increased gland:stroma ratio, associated with prolonged oestrogenic stimulation e.g. HRT, adipose etc.
Can be simple, atypical or complex
Presents with post-menopausal or irregular bleeding
Types - Both types can be exophytic or infiltrative
Endometroid – more common
Mimics glands, arises a result of endometrial hyperplasia
Spreads via myometrium, local lymph nodes etc.
Serous – less common
Poorly differentiated and aggressive
Exfoliates easily mets easily form
Travels through Fallopian tubes, and implants onto peritoneal surfaces
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Leiomyoma (fibroids)
Most common tumour in women. Benign growths of the myometrium
Tend to have a few, can be tiny or huge, symptoms arise from the mass effect (menorrhagia, bladder dysfunction, pelvic pain etc.)
Well circumscribed, round, firm and whiteish
Histologically indistinguishable from normal myometrium
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Leiomyosarcoma (myometrial cancer)
Uncommon but deadly. Highly malignant, metastasise to lungs but do not arise from fibroids
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Ovarian tumours
Generally (80%) benign, but those that are malignant (common in older women) have usually metastasised by the time of presentation and so have a poor prognosis. Usually non-functional so present as a result of mass effect (pain, distension, urinary/GI symptoms etc.) or mets. Hormonal tumours can present with menstrual disturbances. Classification is very confusing, but can be organised by where they arise from Mullerian Epethelia, Germ Cells, Sex Cords/Stromal Cells, Metastases
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Mullerian epithelia Ovarian Cancer
All epithelia of the female tract that is embryologically derived from the Mullerian/paramesonephric ducts (this includes endometriosis)
Serous – exfoliate easily, so metastasise easily into peritoneum and so have a poor prognosis
Mucinous – large cystic mass filled with sticky, thick fluid. Usually benign, can cause pseudomyxoma peritonei
Extensive mucinous ascites as a result of epithelial implantation on peritoneal surfaces
However, in this case the tumour has likely originated from the appendix and spread to the ovaries!
Endometroid – contain tubular glands that resemble endometrium. Can arise from endometriosis, and up to 1/3 rd of cases show a concurrent unrelated endometrial adenocarcinoma
All three of these types can be classified as benign, borderline or malignant (serous are most likely to be malignant)
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Germ Cell Ovarian Cancer
Non-gestational choriocarcinoma – produces BhCG, usually aggressive and fatal
Yolk sac tumour – produces a-fetoprotein
Teratoma
Mature (benign) – most common. Can contain skin cells (why they’re called dermoid cysts), hair, sebaceous material, teeth, thyroid etc.
Immature (malignant) – rare, comprised of tissues that resemble immature foetal tissue
Monodermal (highly specialised) -Struma ovarii – benign, contain thyroid tissue and so can cause hyperthyroidism or Carcinoid – malignant, can produce 5HT (serotonin) and therefore cause carcinoid syndrome (serotonin overdose, leads to flushing, diarrhoea etc.)
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Sex cord/stromal cells overain Cancer
Sex cords produce Sertoli and Leydig cells in men and granulosa and theca cells in women. Tumours are functional so can be androgenising or feminising
Granulosa tumours – found in post-menopausal women
Associated with precocious pseudopuberty in girls and endometrial hyperplasia/carcinoma and breast cancer in women
Ovarian Sertoli-Leydig cell tumours – usually functional with an androgenising effect
Blocks normal female sexual development in girls
Can cause secondary sexual characteristics in women
Breast atrophy, amenorrhea, hirsutism, clitoromegaly, hair loss, voice changes etc.
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Ovarian Cancer from Metastases
Commonly other Mullerian tumours e.g. uterus, fallopian tubes, but can be GI and breast tumours
Krukenberg tumour – metastatic GI tumour in the ovary (bilateral from stomach)
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Vulval cancer
Uncommon, and a disease of elderly women. Can have other cancers of skin (BCC and malignant melanoma) but usually squamous cell carcinoma. Also, can have extramammary Paget’s disease.
Risk factors include HPV 16 and chronic inflammation e.g. Lichen sclerosis
VIN – in situ precursor (same principle as CIN), no invasion but can be detected as brown or white patches
Vulval squamous cell carcinoma – spreads via lymph to inguinal nodes, but can also spread via blood to lungs and liver
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Tumours of gestation
Proliferation of placental tissue (either maternal or foetal). Note mole in this context just means clump of cells
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Hydatidiform mole
Cystic swelling of chorionic villi and trophoblastic proliferation. Usually present on ultrasound but can just miscarry
Look like a bunch of grapes (swollen, oedematous villi)
Treated with curettage and HCG monitoring (doesn’t fall then may be cancerous mole)
Can be classified into complete and partial
Complete – egg has lost DNA and is instead fertilised by two sperm. Higher risk of developing a choriocarcinoma
Partial – triploid or tetraploid. Low risk of developing a choriocarcinoma
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Invasive mole (cancerous molar pregnancy)
A mole that invades the uterine wall. Can cause uterine rupture and therefore haemorrhage
Produces vaginal bleeding and uterine enlargement
Persistently elevated HCG
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Choriocarcinoma
Malignant neoplasm of trophoblastic cells that comes from a previous normal or abnormal pregnancy (no villi present)
Rapidly invasive and metastasises widely, but responsive to chemotherapy
Usually in association with complete moles
Present with vaginal spotting post delivery, shows high HCG levels
Requires uterine evacuation and chemotherapy, but shows good prognosis if caught early
