7 and 8. Lump in neck and lymphadenopathy Flashcards

1
Q

History taking neck lump/lymphadenopathy

A

Duration of onset
Any recent change in size, number of neck lumps
Associated symptoms (especially red flag symptoms, discussed below)
Relevant past medical history – smoking status, alcohol intake, previous head and neck cancers, and known radiation exposure (e.g. previous radiotherapy)
How long has the lump been present?
Is it painful?
Has it changed? If so, over what time frame?
Are there symptoms of recent infection of nearby structures (cough, cold, sore throat, earache, toothache, skin problems, head lice, bites)?
Has there been a fever?
Does eating affect the lump?
Is there pain when swallowing?
Is there any effect on voice?
Does the person smoke?
Is there a history of travel?
Is there a past history of cancer?
Are there red flag symptoms of systemic illness? For example:
Night sweats.
Weight loss.
Unexplained bruising or bleeding.
Persistent fatigue.
Breathlessness.

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2
Q

Examination neck lump and lymphadenopathy

A

Look, feel, move

LOOK:
Location (anterior triangle, posterior triangle or midline)
Size
Shape (oval, round or irregular)
Skin changes (erythema, tethering or ulceration)
Pulsatile (e.g., carotid body tumours)

FEEL
Consistency (hard, soft or rubbery)
Surface eg rough, smooth, irregular
Shape
Warmth (e.g., infection)
Tenderness (e.g., infection)
Size: use a tape measure
Compressible?
Fluctuant?
Pulsatile (high blood flow) or expansile (aneurysmal)? Is there a palpable thrill?

MOVE
● Skin tethering - attempt to pick up a fold of skin over the swelling and compare the
degree of tethering with the other side
● Tethering to deeper structures - attempt to move the swelling in different planes
relative to the surrounding tissues.
● Tethering to muscles and tendons - palpate the swelling whilst asking the patient to
use the relevant muscle.
Movement with swallowing (e.g., thyroid lumps) or sticking their tongue out (e.g., thyroglossal cysts)

Special tests:
Transilluminates with light (e.g., cystic hygroma – usually in young children)
● Auscultation for bruits or bowel sounds

ENT
- ear infections –> reactive lymphadenopathy
- nose –> h&n ca,
- throat - h&n ca,

Thyroid

Cranial nerves

Respiratory
- clubbing - lung ca

Abdo
- hepatosplenomegaly eg EBV, leukemia, lymphoma
- gastric ca

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3
Q

differentials neck lump and lymphadenopathy

A

Infectious
Reactive lymphadenopathy eg post-URTI
Skin infection such as abscess
Measles, mumps, rubella
Generalised lymphadenopathy (HIV, EBV, HSV, CMV)
Cat scratch disease
Extra-pulmonary tuberculosis
Specific risks (toxoplasmosis, lyme disease, cat scratch)

Immune
Amyloidosis
Sarcoidosis
Kawasaki

Malignant lymphadenopathy
Lymphoma
Leukaemia

Tumours
Head and neck cancer
Sarcoma
Salivary gland tumours/pathology
Metastasis - lung and gastric
Lipoma
Neural tumours
Vascular tumours such as hemangioma

Thyroid
Goitre

Congenital
Thyroglossal cyst
Cystic hygroma
Branchial cyst
Dermoid cyst

Degenerative
Pharyngeal pouch

Vascular
Carotid body tumour
Carotid aneurysm

Trauma
Haematoma

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4
Q

red flags for lump in neck ?

A

buffer

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5
Q

infectious ddx lump in neck

A

Reactive lymphadenopathy eg post-URTI
Skin infection such as abscess
Measles, mumps, rubella
Generalised lymphadenopathy (HIV, EBV, HSV, CMV)
Cat scratch disease
Extra-pulmonary tuberculosis
Specific risks (toxoplasmosis, lyme disease, cat scratch)

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6
Q

what is the most common cause of neck swellings?

A

Reactive lymphadenopathy

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7
Q

what local lesions of infection may you see on the neck

A

boils

carbuncle

abscess

pustule

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8
Q

boil vs carbuncle

A

Boil/furuncle: staphylococcal infection around or within a hair follicle.

Carbuncle: staphylococcal infection of adjacent hair follicles (i.e. multiple boils/furuncles).

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9
Q

pustule vs abscess

A

Abscess: a localised accumulation of pus.

Pustule: a pus-containing lesion less than 0.5cm in diameter.

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10
Q

most common causative organism boils/carbuncle/abscess

A

staph aureus

may be MRSA or PVL-SA

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11
Q

when should you take a swab of boils/carbuncles/abscess

A

Consider taking a swab of pus from the contents of the lesion if:

The boil or carbuncle is:
Not responding to treatment.
Persistent or recurrent, to exclude atypical mycobacteria or Panton-Valentine leukocidin Staphylococcus aureus (PVL-SA).
There are multiple lesions.
The person:
Is immunocompromised.
Is known to be colonized with MRSA.
Has diabetes.
Is a member of a household, or resides in an institutional setting, where recurrent outbreaks of skin and soft tissue infections have been reported (to exclude PVL-SA).

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12
Q

management boil/caruncle/abscess?

A
  1. urgent same-day incision and drainage if large
  2. admit for IV abx based on clinical judgement eg systemically unwell or on face or immunocompromised

if not req ref or admis
1. prescribe 7-day abx if fever, cellulitis, sev pain, co-morbidities, on face
+ advise apply moist heat tds to hasten drainage of pus and alleviate pain
+ once drained, cover with steruke dressing
+ safety net

abx
Flucloxacillin is recommended first line (erythromycin [preferred in pregnancy and breastfeeding] or clarithromycin are alternatives if the person has a true allergy to penicillin)

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13
Q

what is the most common site of s.aureus colonisation

A

nose

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14
Q

when might you consider staph aureus carriage and decolonisation?

what do you do to investigate?

A

recurrent boils/abscesses or infections caused by s.aureus

Take swabs from the contents of the boil or carbuncle.
If recurrent boils or carbuncles are localized to the facial area, swab the nasal cavity.
If the boils or carbuncles are more extensive, consider swabbing the perineum, groin, axillae, and umbilicus in addition to the nose.

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15
Q

process of s.aureus decolonization

A

Do not start decolonization until acute infection has resolved.

Eliminate nasal carriage by prescribing Naseptin® cream (chlorhexidine plus neomycin), four times a day for 10 days. Be aware that Naseptin® contains arachis oil (peanut oil) and should not be used by a person known to be allergic to peanuts or soya.

Use an antiseptic preparation (such as chlorhexidine 4% body wash/shampoo or Triclosan 2%) daily as liquid soap in the bath, shower, or sink for 5 days.

consider other options for sensitive skin/dermatological conditions

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16
Q

what infections should you specifically assess for in children with neck lump

A

measles
mumps
rubella
infectious mononucelosis

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17
Q

features measles

A

prodromal phase
irritable
conjunctivitis
fever
Koplik spots
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa
rash
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that typically spares the palms and soles may occur after a week
diarrhoea occurs in around 10% of patients

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18
Q

what is measles?

A

RNA paramyxovirus
one of the most infectious known viruses
spread by aerosol transmission
infective from prodrome until 4 days after rash starts
incubation period = 10-14 days

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19
Q

invetsigations measles

A

IgM antibodies can be detected within a few days of rash onset

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20
Q

management of measles

A

mainly supportive
admission may be considered in immunosuppressed or pregnant patients
notifiable disease → inform public health

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21
Q

most common complication of measles

A

otitis media

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22
Q

most common cause of death following measles

A

pneumonia

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23
Q

complications measles

A

otitis media: the most common complication

pneumonia: the most common cause of death

encephalitis: typically occurs 1-2 weeks following the onset of the illness)

subacute sclerosing panencephalitis: very rare, may present 5-10 years following the illness
febrile convulsions
keratoconjunctivitis, corneal ulceration
diarrhoea
increased incidence of appendicitis
myocarditis

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24
Q

how should you manage a contact of measles who is unvaccinated against measles

A

give MMR within 72 hours

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25
Q

what is mumps?

A

Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring

Spread
by droplets
respiratory tract epithelial cells → parotid glands → other tissues
infective 7 days before and 9 days after parotid swelling starts
incubation period = 14-21 days

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26
Q

clinical features mumps?

A

fever
malaise, muscular pain
parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

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27
Q

how effective is MMR at preventing mumps?

A

MMR vaccine: the efficacy is around 80%

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28
Q

management mumps

A

rest
paracetamol for high fever/discomfort
notifiable disease

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29
Q

complications mumps

A

orchitis - uncommon in pre-pubertal males but occurs in around 25-35% of post-pubertal males. Typically occurs four or five days after the start of parotitis

hearing loss - usually unilateral and transient

meningoencephalitis
pancreatitis

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30
Q

what is rubella?

A

Rubella is caused by the togavirus.

If contracted during pregnancy there is a risk of congenital rubella syndrome

outbreaks more common around winter and spring
the incubation period is 14-21 days
individuals are infectious from 7 days before symptoms appear to 4 days after the onset of the rash

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31
Q

features rubella

A

prodrome, e.g. low-grade fever
rash: maculopapular, initially on the face before spreading to the whole body, usually fades by the 3-5 day
lymphadenopathy: suboccipital and postauricular

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32
Q

complications rubella

A

arthritis
thrombocytopaenia
encephalitis
myocarditis

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33
Q

what is the classic triad of infectious mononucleosis

A

sore throat, pyrexia and lymphadenopathy

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34
Q

features of infectious mononucleosis

A

sore throat, pyrexia and lymphadenopathy

Other features include:
malaise, anorexia, headache
palatal petechiae
splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
hepatitis, transient rise in ALT
lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
haemolytic anaemia secondary to cold agglutins (IgM)
a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

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35
Q

diagnosis infectious mononucleosis

A

heterophil antibody test (Monospot test)
NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.

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36
Q

when do symptoms resolve infectious mononucleosis

A

Symptoms typically resolve after 2-4 weeks.

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37
Q

management infectious mononucelosis

A

rest during the early stages, drink plenty of fluid, avoid alcohol
simple analgesia for any aches or pains
consensus guidance in the UK is to avoid playing contact sports for 4 weeks after having glandular fever to reduce the risk of splenic rupture
Safety netting
If you get any severe symptoms such as difficulty breathing, severe abdominal pain then go to a&e

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38
Q

how does HIV seroconersion present?

A

glandular fever type illness

sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis

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39
Q

how does lymph node TB present?

A

A “cold abscess” is a firm painless abscess caused by TB, usually in the neck. They do not have the inflammation, redness and pain you would expect from an acutely infected abscess.

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40
Q

what is toxoplasmosis

A

Toxoplasma gondii is an obligate intracellular protozoan that infects the body via the gastrointestinal tract, lung or broken skin. It’s oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.

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41
Q

How does toxoplasmosis affect immunocompetent patients?

A

Most infections are asymptomatic. Symptomatic patients usually have a self-limiting infection, often having clinical features resembling infectious mononucleosis (fever, malaise, lymphadenopathy). Other less common manifestations include meningoencephalitis and myocarditis.

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42
Q

what causes cat scratch disease

A

Gram negative rod Bartonella Henselae

Cats become infected with Bartonella henselae from the bites of infected fleas or contact with infected blood

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43
Q

features of cat scratch disease

A

fever
History of cat scratch
Regional Lymphadenopathy
Headache, malaise

  • one or more erythematous lesions at the site of inoculation, 3-12 days after scratch from a cat - most likely a kitten with fleas
  • O/e: crusted papeles or, rarely, a pustule
  • 1-3 weeks after primary lesion, regional lymphadenopathy appears, usually next to innoculation site - painful and may suppurate
  • Systemic symptoms: fever malaise, headache, anorexia
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44
Q

complications cat scratch

A

aseptic meningitis
Encephalopathy
Prolonged fever
Myelitis, paraplegia, cerebral arthritis
Joint pain
Back pain
If innoculation directly into eye —> unilateral granulomatous conjunctivitis
Neuroretinitis
Abdominal pain (hepatitis/splenitis)

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45
Q

management cat scratch disease

A

supportive - antipyretics and analgesia

may need fluctulant tender nodes aspirated

Antibiotics are indicated in immunocompromised patients and atypical cases involving severe or systemic disease

Patients should follow up in 2-6 months for confirmation of symptom resolution.

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46
Q

prevention of cat scratch disease

A

Vigilant elimination of fleas from cats.[12]
Avoiding traumatic injury from cats, especially kittens. Cat-scratches and bites should be washed immediately and cats should not be allowed to lick open wounds

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47
Q

what are the stages of lyme disease

A

Stage 1: inoculation and localised infection
PC; erythema migrans

Stage 2: dissemination
joints, heart, nervous system
PC: flu-like illness, headache, feve, tiredness, n&v
PC: facial nerve palsy, meningitis, encephalitis, peripheral mononeuritis
PC: migratory joint pain
PC: carditis with heartblock

Stage 3: late manifestations/ dysregualted host immune response
PC: chronic arthritis, encephalopathy or peripheral neuropathy, ‘post-Lyme syndrome’

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48
Q

what is lyme disease? causative organism?

A

transmitted by bite of infected Ixodes ticks

The risk of transmission increases with the duration of tick attachment, with the highest risk occurring after 36-48 hours.

Lyme disease is caused by the spirochete bacterium Borrelia burgdorferi,

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49
Q

investigations lyme disease

A

If considering testing for Lyme disease, speak to ID

Erythema migrans and a history of tick bite or likely exposure
Treat with oral abx for 2-3 weeks. DO NOT TEST

Discuss any other cases with ID
If high clinical suspicion - investigate but start treatment before results

  1. ELIZA
  2. Immunoblot
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50
Q

management lyme disease

A

Doxycycline or amoxicillin

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51
Q

what is kawasaki disease

A

Kawasaki disease is also known as mucocutaneous lymph node syndrome. It is a systemic, medium-sized vessel vasculitis. It affects young children, typically under 5 years. There is no clear cause or trigger. It is more common in Asian children, particularly Japanese and Korean children. It is also more common in boys.

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52
Q

key complication kawasaki disease

A

A key complication is coronary artery aneurysm.

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53
Q

symptoms and criteria for diagnosis kawasaki

A

Fever of ≥5 days’ duration associated with at least four of these five changes

4 of 5 of Crash & burn

Conjunctivitis (bilateral non-purulent)

Rash (polymorphous, priamarily truncal)

Adenopathy (cervical)

Strawberry tounge (criteria is MM - throat redness, dry lips, red lips)

Hands (swelling and erythema) or arms or legs (redness, swelling, peeling)

and Burn (5 or more days of fever)

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54
Q

Invetsigations kawasaki

A

Full blood count can show anaemia, leukocytosis and thrombocytosis

Liver function tests can show hypoalbuminemia and elevated liver enzymes

Inflammatory markers (particularly ESR) are raised

Urinalysis can show raised white blood cells without infection

Echocardiogram can demonstrate coronary artery pathology

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55
Q

disease course kawasaki

A

Acute phase: The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.

Subacute phase: The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.

Convalescent stage: The remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks.

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56
Q

management kawasaki disease

A

High dose aspirin to reduce the risk of thrombosis

IV immunoglobulins to reduce the risk of coronary artery aneurysms

Patients will need close follow up with echocardiograms to monitor for evidence of coronary artery aneurysms.

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57
Q

when should you use aspirin in children

A

Kawasaki disease is one of the few scenarios where aspirin is used in children.

Aspirin is usually avoided due to the risk of Reye’s syndrome.

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58
Q

what is required urgently when leukemia is a ddx for a presentation

A

An urgent full blood count

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59
Q

what are lymphomas ? types?

A

Lymphomas are a group of cancers that affect the lymphocytes inside the lymphatic system. These cancerous cells proliferate within the lymph nodes and cause the lymph nodes to become abnormally large (lymphadenopathy).

Hodgkin’s lymphoma: caused by proliferation of lymphocytes.
Non-hodgkin’s lymphoma: encompasses all other types of lymphoma including burkitts

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60
Q

Presentation symptoms lymphoma

A

PC:
Painless lymphadenopathy

Bone marrow involvement
Anaemia
Thrombocytopenia → purpura
Infections

B symptoms:
Unintentional weight loss
Night sweats
Pyrexia

Mass effect
If mediastinal lymph nodes are involved, this can compress the airway and lead to dyspnoea, chest pain, and dry cough. It may also cause superior vena cava obstruction.
Compression of the superior vena cava: shortness of breath and facial oedema
Compression of the external biliary tree: jaundice
Compression of the ureters: hydronephrosis
Bowel obstruction: vomiting and constipation
Impaired lymph drainage: chylous pleural or peritoneal fluid, or lymphoedema of the lower limbs

Specific symptoms
Alcohol induced pain = hodgkins
Pruritus = more common in hodgkins
Burkitt’s lymphoma: large abdominal mass and symptoms of bowel obstruction

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61
Q

when should you 2ww for susepcted lymphoma? when should it be done sooner?

A
  • unexplained lymphadenopathy or splenomegaly for adults aged 25 years or more
  • within 48 hours for children and young people up to and including 24 years of age
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62
Q

Initial investigations lymphoma

A

FBC (anaemia, thrombocytopenia, neutropenia, lymphocytosis)
U&E (acute kidney injury from obstructive nephropathy)
LFTs
LDH (often elevated in high grade lymphomas, but non-specific)
Viral screening tests (hepatitis B/C, HIV, HTLV-1)

Hodgkins blood tests:
Erythrocyte sedimentation rate (ESR): Non-specific but tends to be elevated and indicates a poorer prognosis when the ESR level is >50 mm/hour in patients without B symptoms or >30 mm/hour in those with B symptoms.

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63
Q

what imaging might you organise ?lymphoma

A

Chest x-ray
mediastinal adenopathy, pleural or pericardial effusions and parenchymal involvement

CT-PETchest abdo pelvis for staging

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64
Q

Diagnostic tests lymphoma

A

BIOPSY
1. excisional biopsy

Hodgkins = Reed-Sternberg cells (owl’s eye appearance), or other distinctive Hodgkin’s cells such as lacunar cells or popcorn cells.
If the lesion is in the lung or abdomen, a core needle biopsy is preferred

IMMUNOPHENOTYPING FOR NHL
FISH (fluorescence in situ hybridisation) is used to identify a MYC rearrangement (Burkitt’s lymphoma) in all people newly presenting with histologically high-grade B-cell lymphoma
If a MYC rearrangement is found, FISH is then used to identify the immunoglobulin partner and the presence of BCL2 and BCL6 rearrangements

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65
Q

what is a CT vs PET scan

A

The CT scan takes a series of x-rays from all around your body and puts them together to create a 3 dimensional (3D) picture.

The PET scan uses a mildly radioactive drug to show up areas of your body where cells are more active than normal.

therefore called PET-CT

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66
Q

staging imaging lymphoma?

A

CT chest abdomen pelvis or PET/CT
FDG-PET-CT imaging to confirm staging should be offered to people diagnosed with:

Stage I diffuse large B-cell lymphoma by clinical and CT criteria
Stage I or localised stage II follicular lymphoma if disease is thought to be encompassable within a radiotherapy field
Stage I or II Burkitt lymphoma with other low-risk features

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67
Q

what staging system is used to stage lymphoma? explain it.

A

Ann-Arbor

Stage 1: Confined to one region of lymph nodes.
Stage 2: In more than one region but on the same side of the diaphragm (either above or below).
Stage 3: Affects lymph nodes both above and below the diaphragm.
Stage 4: Widespread involvement including non-lymphatic organs such as the lungs or liver.

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68
Q

HL vs NHL- which is more common?

A

Non-hodgkins is more common

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69
Q

HL vs NHL - which has alcohol induced pain?

A

hodgkins

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70
Q

HL vs NHL which is associated with pruritis

A

HL

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71
Q

HL vs NHL - which is associated with extra-nodal disease? what does extra-nodal dsease mea?

A

Extra-Nodal disease more common in non-hodgkins

N!!!

gastric (dyspepsia, dysphagia, weight loss, abdominal pain)

bone marrow (pancytopenia, bone pain)

lungs

skin

central nervous system (nerve palsies)

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72
Q

HL vs NHL reed sternberg cells?

A

hodgkins

Mature B cells - Reed Sternberg cells

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73
Q

which lymphoma associated w increasing age?

A

non-hodgkins

hodgkins has bimodal age distribution

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74
Q

HL vs NHL which has continguous spread lymph nodes

A

hodgkins

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75
Q

lymphoma large abdominal mass and symptoms of bowel obstruction

A

burkitts

a type of NHL

76
Q

what is mass effect lymphoma? what can it cause?

A

If mediastinal lymph nodes are involved, this can compress the airway and lead to dyspnoea, chest pain, and dry cough. It may also cause superior vena cava obstruction.

Compression of the superior vena cava: shortness of breath and facial oedema

Compression of the external biliary tree: jaundice

Compression of the ureters: hydronephrosis

Bowel obstruction: vomiting and constipation

Impaired lymph drainage: chylous pleural or peritoneal fluid, or lymphoedema of the lower limbs

77
Q

management lymphoma

A

chemo and radiation

78
Q

what type of cancer are head and neck cancers usually - histology

A

squamous cell carcinomas arising from the squamous cells of the mucosa.

79
Q

what areas of the head and neck may head and neck cancers arise

A

The potential areas of head and neck cancers are:
Nasal cavity
Paranasal sinuses
Mouth
Salivary glands
Pharynx (throat)
Larynx (epiglottis, supraglottis, vocal cords, glottis and subglottis)

80
Q

why is lymphadenopathy sometimes important in head and neck ca diagnosis

A

Head and neck cancers usually spread to the lymph nodes first. Squamous cell carcinoma cells may be found in an enlarged, abnormal lymph node (lymphadenopathy), and the original tumour cannot be found. This is called cancer of unknown primary.

81
Q

risk fatcors ehad and neck ca

A

Smoking
Chewing tobacco
Chewing betel quid (a habit in south-east Asia)
Alcohol
Human papillomavirus (HPV), particularly strain 16
Epstein–Barr virus (EBV) infection

82
Q

what vaccine can help prevent head and neck ca

A

The HPV vaccine (Gardasil) protects against strains 6, 11, 16 and 18.

83
Q

what strain of HPV is ass with head and neck ca

A

Human papillomavirus (HPV), particularly strain 16

84
Q

Presenting symptoms and signs that may indicate head and neck cancer?

A

persistent sore throat, difficulty swallowing, hoarseness, or a lump in the neck. Other common symptoms include ear pain, facial pain, and changes in vision or hearing.

Red flags:
Lump in the mouth or on the lip
Unexplained ulceration in the mouth lasting more than 3 weeks
Erythroplakia
Erythroleukoplakia
Persistent neck lump
Unexplained hoarseness of voice
Unexplained thyroid lump

85
Q

what is erythroplaki and erythroleukoplakia?

A

Erythroplakia = red patch on oral mucous membranes, including your tongue, inner cheeks or floor of your mouth

Erythroleukoplakia = Erythroplakia affects the mucous membranes of your mouth. It causes red lesions (spots) that may appear in combination with white patches (leukoplakia). Erythroplakia may be cancerous or noncancerous. Smoking and chewing tobacco use are the leading causes of erythroplakia.

86
Q

rf criteria laryngeal cancer

A

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for laryngeal cancer in people aged 45 and over with:
persistent unexplained hoarseness or
an unexplained lump in the neck.

87
Q

rf criteria oral cancer

A
  • unexplained ulceration in the oral cavity lasting for more than 3 weeks
  • a persistent and unexplained lump in the neck.
  • a lump on the lip or in the oral cavity
  • a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia.
88
Q

what are sarcomas?

A

Sarcomas are a diverse group of malignant tumours originating from mesenchymal tissue.

Sarcomas can be classified based on their tissue of origin:
Bone Sarcomas
Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma
Soft Tissue Sarcomas
Liposarcoma
Rhabdomyosarcoma (striated muscle origin)
Synovial sarcoma
Fibrosarcoma
Angiosarcoma
Leiomyosarcoma (smooth muscle origin))

89
Q

presentation sarcomas?

A

Pain: Often a presenting symptom in bone sarcomas and occasionally in soft tissue sarcomas.

Swelling or a palpable mass: More common in soft tissue sarcomas.

Impaired function: Depending on the location, sarcomas may cause limitations in motion, difficulty breathing, or other functional impairments.

Pathologic fractures: Bone sarcomas can weaken the bone, leading to fractures.

Systemic symptoms: Fatigue, weight loss, and fever may be present, particularly in advanced cases.

90
Q

features of a mass/lump that should raise suspicion for sarcoma?

A

Large >5cm soft tissue mass
Deep tissue location or intramuscular location
Rapid growth
Painful lump

91
Q

when should you refer ?bone sarcoma

A

2ww adult where x-ray suggests bone sarcoma

48hr children and young ppl unexplained bone swelling or pain OR where x-ray suggests bone sarcoma

92
Q

when should you refer ?soft tissue sarcoma?

A

Consider an urgent direct access ultrasound scan (to be performed within 2 weeks) to assess for soft tissue sarcoma in adults with an unexplained lump that is increasing in size.

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for adults if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists.

Consider a very urgent direct access ultrasound scan (to be performed within 48 hours) to assess for soft tissue sarcoma in children and young people an unexplained lump that is increasing in size.

Consider a very urgent referral (for an appointment within 48 hours) for children and young people if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists.

93
Q

management sarcomas

A

Surgery: The primary treatment for most sarcomas, aiming for complete resection with negative margins to reduce the risk of local recurrence. In some cases, limb-sparing surgery can be performed to preserve function, while amputation may be necessary for more advanced or aggressive tumours.

+/- radiation, chemo, targeted therapies

94
Q

what are the three salivary glands? what are the three pathologies that can affect the salivary glands?

A

The three salivary gland locations are the:
Parotid glands
Submandibular glands
Sublingual glands

Stones blocking the drainage of the glands through the ducts (sialolithiasis)
Infection
Tumours (benign or malignant) part of head and neck cancer

95
Q

which salivary gland is most likely to be affected by stones?

A

submandibular glands

96
Q

contributing factors salivary gland stones?

A

Calcium metabolism may play a role but this is not certain
History of renal stones is associated with increased risk
The only systemic disease associated with stone formation is gout, in which case stones will be formed of uric acid rather than calcium.
Multiple medications are associated with higher risk:
Diuretics
Anticholinergic medications
Other risk factors include smoking, trauma and hypovolaemia

97
Q

presentation saliavry gland stones

A

Pain and swelling triggered when salivary flow is stimulated

Patients may present with a hard, palpable lump within the salivary duct or orifice.

Secondary infection is suggested by persistent pain and swelling, sometimes with fever and systemic upset. Sometimes these infections can lead to spreading cellulitis with deep neck infection and airway compromise.

98
Q

investigations salivary gland stones

A

Salivary gland stones are usually diagnosed clinically based upon history and examination alone. Sometimes a stone may be seen at the opening of the salivary duct into the oral cavity.

Imaging can be used if there is diagnostic doubt or there is suspicion of secondary infection/abscess formation. Both CT and ultrasound are highly sensitive for detection of stones.

99
Q

management salivary gland stone?

A

Conservative
- hydration
- encourage saliva flow - sucking sweets
- nsaids

Assess for complications
- infection
?tracking ?sepsis –> ENT urgent assessment

100
Q

how does saliavry gland malognancy present?

A

persistent/painless unilateral salivary gland mass.

most common - parotid gland tumour - can cause facial nerve palsy

101
Q

what cancers commonly metastasie to cervical lymph nodes

A

lung cancer, gastric cancer

102
Q

histological types of lung cancers? how common?

A

The histological types of lung cancer can be broadly divided into:
Small cell lung cancer (SCLC) (around 20%)
Non-small cell lung cancer (around 80%)

Non-small cell lung cancer can be further divided into:
Adenocarcinoma (around 40% of total lung cancers)
Squamous cell carcinoma (around 20% of total lung cancers)
Large-cell carcinoma (around 10% of total lung cancers)
Other types (around 10% of total lung cancers)

103
Q

whata re small cell lung cancers

A

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

104
Q

is mesothelioma a type of lung cancer?

A

Mesothelioma is not a form of lung cancer. Mesothelioma develops in the lining around the lungs (the pleura). Lung cancer develops inside the lungs.

105
Q

Presentatuon lung cancers?

A

Shortness of breath
Cough
Haemoptysis (coughing up blood)
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination

106
Q

association mesothelioma?

A

asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival, but it is essentially palliative.

107
Q

what is a paraneoplastic syndrome?

A

A paraneoplastic syndrome is a set of signs and symptoms that can occur when you have cancer. The symptoms develop when a malignant tumor causes changes in your body that aren’t directly caused by the cancer itself. The tumor may secrete a hormone or protein that affects a particular body system.

108
Q

pt lung cancer w hoarse voice? what is the paraneoplastic syndrome?

A

Recurrent laryngeal nerve palsy presents with a hoarse voice. It is caused by a tumour pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.

109
Q

pt lung cancer w diaphragm wekaness and SOB? what is the paraneoplastic syndrome?

A

Phrenic nerve palsy, due to nerve compression, causes diaphragm weakness and presents with shortness of breath.

110
Q

pt lung cancer w facial swelling, difficulty breathing ? what is the paraneoplastic syndrome?

A

Superior vena cava obstruction is a complication of lung cancer. It is caused by direct compression of the tumour on the superior vena cava. It presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.

111
Q

pt lung cancer partial ptosis, anhidrosis and miosis

A

Horner’s syndrome is a triad of partial ptosis, anhidrosis and miosis. It can be caused by a Pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion. Pancoast tumours are cancers that start in the top part of the lung (the apex).usually adenocarcinoma

112
Q

pt with lung cancer and hyponautraemia? what paraneoplastic syndrome?

A

Syndrome of inappropriate ADH (SIADH) can be caused by ectopic ADH secreted by a small cell lung cancer. It presents with hyponatraemia.

113
Q

pt with lung cancer and cushings syndrome? what apraneoplastic

A

Cushing’s syndrome can be caused by ectopic ACTH secretion by a small cell lung cancer.

114
Q

pt with lung cancer and hypercalcaemia

A

Hypercalcaemia can be caused by ectopic parathyroid hormone secreted by a squamous cell carcinoma.

115
Q

pt with lung cancer and symptoms such as short term memory impairment, hallucinations, confusion and seizures.

A

Limbic encephalitis is a paraneoplastic syndrome where small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.

116
Q

pt with lung cancer and weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

A

Lambert-Eaton myasthenic syndrome can be caused by antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

117
Q

referral criteria for cxr lung ca

A

patients over 40 with:
Clubbing
Lymphadenopathy (supraclavicular or persistent abnormal cervical nodes)
Recurrent or persistent chest infections
Raised platelet count (thrombocytosis)
Chest signs of lung cancer

consider in patients over 40 years old who have:
Two or more unexplained symptoms in patients that have never smoked
One or more unexplained symptoms in patients that have ever smoked

The unexplained symptoms that the NICE guidelines list are:
Cough
Shortness of breath
Fatigue
Chest pain
Weight loss
Loss of appetite

118
Q

first invetsigation ?lung ca? findings?

A

Chest x-ray is the first-line investigation in suspected lung cancer.

Findings suggesting cancer include:
Hilar enlargement
Peripheral opacity – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse

119
Q

staging scan lung ca

A

contrast enhanced CT scan of chest, abdomen and pelvis

PET-CT (positron emission tomography) scans involve injecting a radioactive tracer (usually attached to glucose molecules) and taking images using a combination of a CT scanner and a gamma-ray detector to visualise how metabolically active various tissues are. They are useful in identifying areas that cancer has spread to by showing areas of increased metabolic activity.

120
Q

maanagment of lung ca

A

surgery

chemo, radio

121
Q

options for removing lung ca

A

Segmentectomy or wedge resection involves taking a segment or wedge of lung (a portion of one lobe)

Lobectomy involves removing the entire lung lobe containing the tumour (the most common method)

Pneumonectomy involves removing an entire lung

The types of surgery that can be used are:
Thoracotomy – open surgery with an incision and separation of the rib to access the thoracic cavity
Video-assisted thoracoscopic surgery (VATS) – minimally invasive “keyhole” surgery
Robotic surgery

122
Q

whata re the type of thoracotomy incisions

A

Anterolateral thoracotomy with an incision around the front and side
Axillary thoracotomy with an incision in the axilla (armpit)
Posterolateral thoracotomy with an incision around the back and side (the most common approach to the thorax)

123
Q

what things o/e indicate prev lung ca surgery?

A

If you see a patient with a thoracotomy scar in your OSCEs, they are likely to have had a lobectomy, pneumonectomy or lung volume reduction surgery for COPD. If they have no breath sound on that side, this indicates a pneumonectomy rather than lobectomy. If they have absent breath sound in a specific area on the affected side (e.g., the upper zone), but breath sounds are present in other areas, this indicates a lobectomy. Lobectomies and pneumonectomies are usually used to treat lung cancer. In the past, they were often used to treat tuberculosis, so keep this in mind in older patients. If it is a cardiology examination and they have a right-sided mini-thoracotomy incision, this is more likely to indicate previous minimally invasive mitral valve surgery.

124
Q

Risk factors gastric cancer

A

PRIAMRY - h.pylori

Additional:
Dietary factors: High salt intake, consumption of smoked or preserved foods, and low intake of fruits and vegetables
Smoking
Alcohol consumption
Pernicious anaemia and atrophic gastritis
Family history of gastric cancer
Genetic syndromes (e.g., hereditary diffuse gastric cancer, Lynch syndrome)

125
Q

Presentation gastric cancer

A

PC:
Symptoms of gastric cancer are often nonspecific, especially in the early stages. Common clinical features include:
Dyspepsia or indigestion
Epigastric pain
Early satiety or postprandial fullness
Weight loss
Anaemia
Nausea and vomiting
Gastrointestinal bleeding (e.g., melena, haematemesis)

Advanced disease may present with additional signs, such as palpable abdominal mass, ascites, and supraclavicular lymphadenopathy (Virchow’s node).

126
Q

Examination findings gastric cancer

A

Advanced disease may present with additional signs, such as palpable abdominal mass, ascites, and supraclavicular lymphadenopathy (Virchow’s node).

127
Q

Platelet count cancer

A

High

Cancer is believed to induce platelet formation through the release of interleukin 6, a proinflammatory cytokine that stimulates the production of thrombopoietin hormone.

128
Q

Investigations gastric cancer

A

diagnosis: endoscopy with biopsy
staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT

CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in most centres.
Laparoscopy to identify occult peritoneal disease
PET CT (particularly for junctional tumours)

129
Q

Management gastric cancer

A

Chemo
Radiation
Surgery

130
Q

goitre vs thyroid lump? causes of each?

A

A goitre refers to generalised swelling of the thyroid gland. A goitre can be caused by:
Graves disease (hyperthyroidism)
Toxic multinodular goitre (hyperthyroidism)
Hashimoto’s thyroiditis (hypothyroidism)
Iodine deficiency
Lithium

Individual lumps can occur in the thyroid due to:
Benign hyperplastic nodules
Thyroid cysts
Thyroid adenomas (benign tumours the can release excessive thyroid hormone)
Thyroid cancer (papillary or follicular)
Parathyroid tumour

131
Q

primary vs secondary hyperthyroidism

A

primary = thyroid is the problem
high T3/T4, low TSH

secondary = pituitary is the problem
high T3/T4, high TSH

132
Q

priamary vs secondary hypothyroidism

A

primary = thyroid is the problem
low T3/T4, high TSH

secondary = pituitary is the problem
low T3/T4, low TSH

133
Q

what tests help you ddx between different thyroid pathology

A

TFTs:
- T3
- T4

Hormone tests:
- TSH

Antibodies:
- anti-TPO : Anti-thyroid peroxidase
- TSHr AB : TSH receptor antibodies
- anti-Tg : Anti-thyroglobulin

Imaging:
- USS
- Radioisotope scans are used to investigate hyperthyroidism and thyroid cancers.

134
Q

interpretation radioisotope scans

A

Diffuse high uptake is found in Grave’s Disease

Focal high uptake is found in toxic multinodular goitre and adenomas

“Cold” areas (abnormally low uptake) can indicate thyroid cancer

( Reduced uptake/none could indicate thyroiditis )

135
Q

pathophysiology graves

A

Graves’ disease is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

136
Q

pathophysiology toxic multinodular goitre

A

Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

137
Q

Features specific to graves disease

A

exopthalmos (bulging of the eyes - caused by Graves’ disease. Inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.

Pretibial myxoedema is a skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area). It gives the skin a discoloured, waxy, oedematous appearance over this area. It is specific to Grave’s disease and is a reaction to TSH receptor antibodies.

138
Q

causes of thyroiditis

A

acute phase of:
- subacute (de Quervain’s) thyroiditis
- post-partum thyroiditis
- Hashimoto’s thyroiditis (later results in hypothyroidism)

  • amiodarone therapy
  • contrast
139
Q

causes of hyperthyroid

A

The causes of hyperthyroidism can be remembered with the “GIST” mnemonic:
G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

140
Q

features universal to hyperthyroidism

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination
Tremor

141
Q

what is De Quervain’s thyroiditis ? how does it present?

A

De Quervain’s thyroiditis, also known as subacute thyroiditis, is a condition causing temporary inflammation of the thyroid gland. There are three phases:
Thyrotoxicosis
Hypothyroidism
Return to normal

The initial thyrotoxic phase involves:
Excessive thyroid hormones
Thyroid swelling and tenderness
Flu-like illness (fever, aches and fatigue)
Raised inflammatory markers (CRP and ESR)

142
Q

management De Quervain’s thyroiditis

A

Arrange referral or discuss with an endocrinologist

It is a self-limiting condition, and supportive treatment is usually all that is necessary.

This may involve:
NSAIDs for symptoms of pain and inflammation
Beta blockers for the symptoms of hyperthyroidism
Levothyroxine for the symptoms of hypothyroidism

A small number (under 10%) remain hypothyroid long-term.

143
Q

How to manage a pt with ?hyperthyroidism in primary care?

A

If a person has a confirmed diagnosis of overt hyperthyroidism following TFTs

Admission/rf
1. arrange emergency admission if features of thyroid storm
1. Arrange urgent rf to endocrine if pituitary/hypothalamic disorder suspected
1. Arrange referral or discuss with an endocrinologist if they have a goitre, nodule, or structural change in the thyroid gland, or if malignancy is suspected

While awaiting endocrine:
1. Consider prescribing a beta-blocker and titrating the dose depending on clinical response, to provide relief of adrenergic symptoms (such as palpitations, tremor, tachycardia, or anxiety).

+ Consider seeking specialist advice about starting antithyroid drugs such as carbimazole in primary care for people

144
Q

what auto-antibodies are seen in graves?

A

TSH receptor antibodies
are present in around 90-100% of patients with Graves’ disease

there is overlap in the antibodies seen eg anti-TPO and anti-Tg can be seen in graves as well as hashimotos

145
Q

what autoantibodies are seen in hashimotos

A

Anti-thyroid peroxidase (anti-TPO) antibodies
are seen in around 90% of patients with Hashimoto’s thyroiditis.

there is overlap in the antibodies seen eg anti-TPO and anti-Tg can be seen in graves as well as hashimotos

146
Q

How to manage a pt with ?hypothyroidism in primary care

A

If a person has confirmed overt hypothyroidism

Admission/rf
1. Arrange emergency admission if a serious complication such as myxoedema coma is suspected.
1. Arrange urgent referral to an endocrinologist if secondary hypothyroidism is suspected.
1.Arrange referral or discuss with an endocrinologist if they have a goitre, nodule, or structural change in the thyroid gland, or if malignancy is suspected
1. Arrange referral or discuss with an endocrinologist if suspected/associated endocrine disease, such as Addison’s disease

If specialist referral is not needed:
1. treat overt primary hypothyroidism with levothyroxine (LT4) monotherapy.
Advise the person to take LT4 medication on an empty stomach in the morning before other food or medication.

Review the person and recheck TSH levels every 3 months after initiation of LT4 therapy and adjust the dose according to symptoms and TFT results. Consider checking FT4 in addition if the person has ongoing symptoms on treatment.

147
Q

After starting levothyroxine, when should you review the pt

A

Review the person and recheck TSH levels every 3 months after initiation of LT4 therapy and adjust the dose according to symptoms and TFT results.

148
Q

what is hashimotos?

A

It is an autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.

149
Q

what is the most common cuase of hypothyroidism in developing world?

A

Iodine deficiency is the most common cause of hypothyroidism in the developing world. In the UK,

iodine is particularly found in dairy products and may be added to non-dairy milk alternatives (e.g., soya milk).

150
Q

what drugs can cause hypothyroidism

A

Lithium inhibits the production of thyroid hormones in the thyroid gland and can cause a goitre and hypothyroidism.

Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis.

151
Q

causes of secondary hypothyroism

A

Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma

152
Q

features of hypothyroidism

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

153
Q

key complication of carbimazole?

A

pancreatitis

154
Q

How is carbimazole titrated?

A

Carbimazole is the first-line anti-thyroid drug, usually taken for 12 to 18 months.

Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), they continue on maintenance carbimazole and either:

The carbimazole dose is titrated to maintain normal levels (known as titration-block)
A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)

155
Q

what is the second-line anti-thyroid drug? why is it second-line?

A

Propylthiouracil is the second-line anti-thyroid drug. It is used in a similar way to carbimazole.

There is a small risk of severe liver reactions, including death, which is why carbimazole is preferred.

156
Q

what is a complication of both carbimazole and proylthiouracil?

A

agranulocytosis

Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

157
Q

pt with hyperthyroid and a sore throat?

A

agranulocytosis

Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

158
Q

pt with hyperthyroid and abdominal pain?

A

acute pancreatitis

The MHRA issued a warning in 2019 about the risk of acute pancreatitis in patients taking carbimazole.

159
Q

What is myxedema coma? presetation?

A

Life threatening hypothyroidism
Myxoedema coma typically presents with confusion and hypothermia.

Myxedema coma
Hypoxia
Decreased CO
Bradycardia
Hypothermia
Hypotension

causes:
- undiagnosed hypothyroid
- ill-managed hypothyroid
- trigger event such as an infection

160
Q

management myxedema coma?

A

IV thyroid replacement
IV fluid
IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
electrolyte imbalance correction
sometimes rewarming

161
Q

What is a thyroid storm? other name? how does it present? how is it managed?

A

thyrotoxic crisis

fever, tachycardia and delirium. It can be life-threatening and requires admission for monitoring.

beta-blockers: typically IV propranolol
anti-thyroid drugs(thionamides): e.g. methimazole or propylthiouracil then.. Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

It is treated the same way as any other presentation of thyrotoxicosis, although they may need additional supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers.

162
Q

first line invgn any thyroid nodule!!!

A

USS

163
Q

most common and second most common malignant cause of thyroid cancer

A

Papillary carcinoma 70%
Often young females - excellent prognosis

Follicular carcinoma 20%

164
Q

management of papillary adn follicualr thyroid cancer?

A

total thyroidectomy

followed by radioiodine (I-131) to kill residual cells

yearly thyroglobulin levels to detect early recurrent disease

165
Q

what are the names of some congenital neck lumps

A

thyroglossal cyst
cystic hygroma
branchial cyst
dermoid cyst

166
Q

features of thyroglossal cyst

A

glossal = tounge - moves up and down with protrusion of the tounge

Mobile
Non-tender
Soft
Fluctuant

167
Q

complication of thyroglossal cyst

A

The main complication is infection of the cyst, causing a hot, tender and painful lump.

168
Q

invgn and management thyroglossal cyst

A

Ultrasound or CT scan can confirm the diagnosis.

Management
Thyroglossal cysts are usually surgically removed to provide confirmation of the diagnosis on histology and prevent infections. The cyst can reoccur after surgery unless the full thyroglossal duct is removed

169
Q

when do branchial cysts often present?

A

Branchial cysts tend to present after the age of 10 years, most commonly in young adulthood when the cyst becomes noticeable or infected.

170
Q

features of branchial cysts?

A

Branchial cysts present as a round, soft, cystic swelling between the angle of the jaw and the sternocleidomastoid muscle in the anterior triangle of the neck.

171
Q

where does a branchial cyst originate from?

A

second branchial cleft

172
Q

complications of branchial cysts

A

Sinuses and Fistulas

A sinus is a blind ending pouches. A fistula is an abnormal connection between two epithelial surfaces.

Sinuses and fistula pose an increased risk of infections in the branchial cyst, as they are a way for pathogens to get in.

173
Q

management branchial cyst

A

Where the branchial cleft is not causing any functional or cosmetic issues, conservative management may be appropriate.

Where recurrent infections are occurring, there is diagnostic doubt about the cause of the neck lump or it is causing other functional or cosmetic issues, surgical excision may be appropriate.

174
Q

when do cystic hygromas present?

A

Cystic hygromas typically present at birth or within a few years following, with 90% being diagnosed before the age of 2 years.

175
Q

associations cystic hygromas?

A

Turner syndrome and environmental factors such as alcohol abuse and viral illness during pregnancy.

176
Q

presentation cystic hygroma?

A

occur anywhere within lymphatic system, but most common in the posterior triangle of the neck
cystic hygromas are more common on the left-side
soft and compressible
typically not painful
no movement on swallowing
transillumination is detected
may interfere with respiration or compromise the airway

177
Q

which neck lump transilluminates?

A

cystic hygroma

178
Q

plan ?cystic hygroma

A

Diagnosis and investigations:
consider and exclude other malignancy
ultrasound, CT or MR imaging
Management:
Observation (some tumours are small, static or slowly regress)
Surgical excision

179
Q

what are dermoid cysts? where may they be found on the neck?

A

A cutaneous dermoid cyst may develop at sites of embryonic developmental fusion. They are most common in the midline of the neck, external angle of the eye and posterior to the pinna of the ear. They typically have multiple inclusions such as hair follicles that bud out from its walls. They may develop at other sites such as the ovary and in these sites are synonymous with teratomas.

180
Q

how do carotid body tumours present?

A

In the upper anterior triangle of the neck (near the angle of the mandible)
Painless
Pulsatile
Associated with a bruit on auscultation
Mobile side-to-side but not up and down

181
Q

what are carotid body tumours?

A

Carotid body tumours are formed by excessive growth of the glomus cells. They are also called paragangliomas. Most are benign

The carotid body is a structure located just above the carotid bifurcation (where the common carotid splits into the internal and external carotids). It contains glomus cells, which are chemoreceptors that detect the blood’s oxygen, carbon dioxide, and pH. Groups of these glomus cells are called paraganglia.

182
Q

complication of carotid body tumours?

A

Carotid body tumours may compress the glossopharyngeal (IX), vagus (X), accessory (XI) or hypoglossal (XII) nerves. Pressure on the sympathetic nerves may result in Horner syndrome, with a triad of:
Ptosis
Miosis
Anhidrosis (loss of sweating)

183
Q

plan ?carotid body tumour

A

imaging
A characteristic finding on imaging investigations is splaying (separating) of the internal and external carotid arteries (lyre sign).

They are mostly treated with surgical removal.

184
Q

how does a carotid aneyrysm present?

A

Pulsatile lateral neck mass which doesn’t move on swallowingf

185
Q

ddx bilateral hilar lymphadenopathy

A

tb or sarcoidosis

186
Q

complications of thyroidectomy

A
  • damage to recurrent laryngeal nerve
  • damage to parathyroid glands resulting in hypocalcaemia
  • bleeding –> respiratory compromise/laryngeal oedema
187
Q

which duct drains the submandu=ibular gland

A

Whartons duct