ESA3 revision session 2 Flashcards
What can cause a lump in the neck?
Vascular
Inflammatory
Traumatic
Autoimmune
Metabolic
Infection
Neoplastic
Degenerative
Idiopathic
Congenital
vascular cause of neck lump
carotid artery aneurysm
infection
cervical lymphadenopathy
congenital
- Thyroglossal cyst- midline
- Branchial cyst- SCM
- Cervical rib
- Neoplastic cause
Apical lung cancer- Pancoast tumour (left)
Thryoglossal duct cyst
- midline lump
- thyroid gland dvewlops int he floor of the pharnx, in the foramen cecum
- it descends down necks as it develops
- remains connected to tongue by thyroglossal duct
- if patency not resolved, a cyst develops

branchial cysts
lump on SCM
- incomplete fusion of the second arch over the other clefts
- fluid can fill in this space leading to a soft non-tender mass ont he anterior border of SCM
- can arise after infection/trauma causing cyst to swell and become apparent

A non-tender left supraclavicular node is a associated with what type of malignancy?
- GI metastases- gastric malignancy
- Virchow node
what does this chest x ray confirm

pancoast tumour
pancoast tumours can cause disruption of the
brachial pleuxs- lower routes C8/T1 (Klumpke)
- apex of lung in close proximity to lower nerve root of the rbachial plexus*
- pancoast tumour causes it to impingle on C8 and T1 roots*
- sensory innervation of medial hand and forearm
- intrinsic muscles of the hand
- muscles of the forearm
klumpkes palsy
C8-T1- upper brachial plexus injury
Erbs palsy-
C5 C6—shoulder dystocia (lower brachial plexus injury)
what other structures can be affecred by a pancoast tumour
- Recurrent laryngeal nerve
- Reduced ability to cough
- hoarseness
- Sympathetic trunk/chain
- Horners syndrome
- Subclavian artery and vein

horners syndrome
impingment of sympathetic chain by pancoast tumour
Symptoms:
- partial ptosis
- miosis- constircted pupil as dilatore pupillae not innervated
- anhydrosis- lack of sweating due to denervated sweat glands
What does the sympathetic nervous system do in the eye
- eyelid- helps raise it
- pipil- dilates it
- sweat glands- stimulated production

Eyelid muscle innervation
- Levator palpebrae superioris (CN III- oculomotor)
- Superior tarsal plate (sympathetic innervation)
partial psosis
- sympathetic innervation to the taral muscle of the eyelid is lost
- leads to drooping of eyelid
- innervation to levator palpebrae suprioris (LPS) is still in tact
- can partially raise eyelid

complete ptosis
- paralysis of levatoe palpebrae superioris (LPS) due to CN III lesion (compression of parasympathetic fibres)
- tarsal muscle inenrvation is intact (however too weak to riase eyelid alone)

parasympathetic fibres which hitch-hike on the ocuclomotor nerve run on the
periphery

parasympathetic fibres which hitch-hike on the ocuclomotor nerve innervates the
sphincrer pupillae muscle to constrict the pupil
pathology of CN III will causes a
dilated pupil (SNS domiantes)

Compressive vs vascular CN III lesion: Compressive
Compressive –e.g. aneurysm/tumour will compress the outside of the nerve= loss of Parasympathetic fibres first- lose pupil innervation first (pupil dilation)- motor signs will be later
Compressive vs vascular CN III lesion: Vascular
Vascular- loss of blood supply= loss of motor function CN III first (full ptosis)
- Parasympathetic is peripheral therefore can get blood supply from close structures- pupils spared
Effect of CN III lesion on eye movent?
- oculomotor (CN III) supplies 4 out of 6 muscles
- trochlear (lateral rectus) and abducens nerve (superior oblique) preserved
- unopposed action of LR and SO = down and out position

why can facial oedema and venous distention occur in patients with pancoast tumours
- pancoast tumours can compress the superior vena cava
- svc responsible for draining the upper limb, head and neck of blood
- compressur ewill cause back log of blood icnreased venous pressur
- eincreased hydrostatic pressure can cuase fluid to move out of the facial veins and into the tissue causing oedema

horners vs CN III palsy

how is venous jugular pressure
- place at 45 degrees
- turn the head towards the left
- measure the height from the sternal angle + 5cm
- >5 cm indicates raised JVP

What lung conditions can cause heart failure?
What lung conditions can cause heart failure?
- Cor pulmonale (right heart failure on its own because of lung condition)
- Pulmonary hypertension increases the afterload of the right heart
- RV hypertrophies to accommodate then dilatation
- Reduced RV cardiac output- reduced LV filling
- CO unable to meet demand of the body
- Causes of Cor pulmonale
- PE
- COPD
hypoxia pulmonary vasoconstriction
30 cigs a day for 24 year. what is the pack year history
1 pack = 20 cigarettes
30 cigarettes= 1.5 packs
1.5 x 24= 36
36 pack-years
describe 2 appaoraches a health promotion campaign cna take to reduce smoking incidence
medical prevention- encourage smokers to opt into early detection to prevent smoking related disease
- behaviour change- psychological health behaviorus theories in campagins
- educational- dissemintate info
Sepsis six
*
- B- blood cultures
- U- urine outputs
- F0- fluids
- A- Ax
- L- lactate
- O- oxygen
Give 3
Take 3
- Septic shock is
- Sepsis in combination with either a lactate >2 mmol/l despite adequate fluid resus or the patient is requiring vasopressors to maintain MAP >65 mmHg
- Basically sustained low BP
- Sepsis in combination with either a lactate >2 mmol/l despite adequate fluid resus or the patient is requiring vasopressors to maintain MAP >65 mmHg
How to look at acid-base balances?
- pH- are they normal, acidotic or alkalotic
- pCO2- is the change in keep with pH
- yes- resp cause
- no - change or opposite
- HCO3- abnormal? Change in keeping with pH?
- if yes- metabolic cause
- if no- compensatory cause
acid base

- Low pH- acidic
- pCO2 low
- HCO3- low
What is this ? partially compensated metabolic acidosis
- resp is trying to compensate for low HCO3
The anion gap
An elevated anion gap means there are unmeasured cations in the blood-these unmeasured cations are acids. Hence, a high anion gap suggest a metabolic acidosis

interpret this CXR

- Emphysema- lots of ribs can be seen due to hyperinflation
- Flattened hemi diaphragm
- Very dark lung fields- lots of air
summary of how to review a CXR

What do we need to think about with COPD patients and oxygen?
*
- CO2 retainers – blue bloater (chronic bronchitis)
- Need to aim sats for 88-92%
- If they are not retainers- pinker puffer (emphysema)
- 94%
COPD and oxygen
- need controlled oxyegn therapy i.e. you know exactly how much oxygen you are giving threm
- if they are in CO2 retention, aim sat 88-92%
- regular ABGs
if we give oxygen, redue hypoxic drive, patient will hypoventilate, hypoventilation decreases CO2 removal therefore pts will end up hypercapnic

Type 1 – low pO2 <8kPa
- pCO2 normal or low
- ventilation perfusion mismatch
- solubility of O2 and CO2 (CO2 is much more soluble)
- CO2 not as badly affected as O2
- solubility of O2 and CO2 (CO2 is much more soluble)
- Type 2- low PO2 <8kPa
- pCO2 higher- retaining CO2 >6.7 kPa
- hypoventilation problem
respiratory acidosis can call
hyperkalaemia
hyperkalemia on ECG
- tall tended T wave
- flattened or absent P-waves
- PR interval prolongation
- prolonged QRS
- can become brady cardic

how to red an ECG

Why does acidosis cause hyperkalaemia?
H+ moves into cells
K+ moves out of cells

What drugs might you give to the pt to reverse the hyperkalaemia?
- IV insulin (drives K+ into cells)
- IV dextrose to avoid hypoglycaemia
what would you give to stabilise the cardiac membrane?
- calcium gluconates
- later give furosemid to removed K+ from body
calcium gluconates
to stabilise cardiac membrane