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PACES > Miscellaneous > Flashcards

Miscellaneous Flashcards

1
Q

what is the diagnostic criteria for RA

A

at least 4 of:
1) morning stiffness >1 hour
2) symmetrical joint involvement
3) arthritis affecting > 3 joints
4) involvement of the small joints of the hands
5) positive RF
6) rheumatoid nodules
7) radiographical evidence

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2
Q

what are extrarticular features of RA

A

cervical- atlanto axial subluxation
eyes- scleritis/ episcleritis/ sjogrens
skin- rheumatoid nodules
lungs- lung fibrosis/ effusions
heart- pericarditis
hepatosplenomegaly
renal- nephrotic syndrome

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3
Q

what are causes of tiredness in RA

A

anaemia of chronic disease
iron deficiency- GI loss from NSAIDs use
methotrexate- folate deficiency / bone marrow suppression (also from sulfasalazine)

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4
Q

how do you differentiate episcleritis from scleritis

A

Scleritis is painful, episcleritis is painless

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5
Q

what is RF

A

an antibody found in approx 75% of patients with RA, also present in other CTDs such as SLE

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6
Q

what are poor prognostic factors in RA

A

positive RF
presence of anti- CCP
early evidence of erosive disease
functional impairement

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7
Q

what are the radiological findings of rheumatoid arthritis

A

loss of joint space
erosions
subchondral cysts
subchondral sclerosis

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8
Q

what are the radiological findings of osteoarthritis

A

Loss of joint space
osteophytes
soft tissue swelling
see-through bones (osteopaenia)

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9
Q

what monitoring is important with the following DMARDs
sulphasalazine
methotrexate
hydroxychloroquine

A

1) neutropaenia/ thrombocytopaenia/ liver impairment - 3/12 LFT + FBC
2) neutropaenia/ thrombocytopaenia/ liver impairment/ pneumonitis- baseline CXR, monthly FBC/ LFT
3) hydroxychloroquine- corneal deposits and retinopathy- annual acuity testing

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10
Q

how is systemic sclerosis classified

A

diffuse scleroderma- diffuse involvement of the skin/ trunk/ extremities. Early involvement of lung, kidney, gut and heart

limited scleroderma- skin only affected in the extremities/ face. CREST syndrome- calcinosis, raynauds phenomenon, oesophageal dysmotility, sclerodactyly, telangectasia. late involvement of other organs, renal crisis is rare.

systemic sclerosis sine scleroderma- organ involvement without skin involvement

malignant scleroderma- accelerated course of disease leading to death- often found in elderly men

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11
Q

what are the diagnostic criteria for systemic sclerosis

A

American rheumatism association has clear diagnostic criteria- 1 major or 2+ minor criteria needed

minor- sclerodactyly, finger pulp atrophy, bilateral pulmonary fibrosis
major- skin sclerosis affecting arms, face, neck

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12
Q

what is the most common cause of mortality in systemic sclerosis

A

renal failure

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13
Q

what auto antibodies are associated with systemic sclerosis

A

limited: anti-centromere antibody, ANA, Rh factor
diffuse: anti- scl70, anti- RNA polymerase

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14
Q

what is the management of systemic sclerosis

A

MDT approach
physio- exercises for contractures and deformities
general- patient education and counselling, analgesia for arthralgia
raynauds- smoking cessation, hand warmers, vasodilators (CCB, ACEi, prostacyclin analogues)
GI- prokinetics for dysmotility, PPI, nutritional support
renal- strict hypertension control and ACEi for renal crisis
respiratory- vasodilators for pulmonary hypertension

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15
Q

complications of neurofibromatosis

A

phaeochromocytoma + RAS - HYPERTENSION
acoustic neuroma
optic glioma
epilepsy
restrictive cardiomyopathy
pulmonary fibrosis
pnuemothorax

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16
Q

what are the genetics of NF

A

autosomal dominant disease
mutation on chromosome 17 (NF1) or 22 (NF2)

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17
Q

what are the diagnostic criteria of NF1

A

2 of:

> 6 cafe au lait spots
axillary freckling
2 neurofibromata
2 lisch nodules
optic glioma
first degree relative with NF
bone involvement- thinning of long bones/ sphenoid dysplasia

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18
Q

what are the diagnostic criteria for NF2

A

any of:

bilateral 8th nerve involvement
neurofibroma
meningioma/ glioma/ shwanoma
first degree relative with NF

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19
Q

how would you investigate and treat a patient with a phaeochromocytoma

A

24 hour urinary catecholamines
alpha blocker then beta blocker
surgery is definitive management

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20
Q

tests for a bitemporal hemianopia

A

full hormone panel- prolactin, IGF-1, TFT, LH/FSH, cortisol, ACTH, testosterone, short synACTHen test, GTT

brain MRI to visualise the pituatary and look for a tumour

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21
Q

how to manage a pituatary tumour

A

if there were hormone deficienicies, I woul start hormone replacement.
Offer surgery for resection of the tumour or radiotherapy if there were recurrence/ residual disease
for prolactinoma- dopamine agonists such as bromocriptine are first line

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22
Q

what are some differentials for thyroid eye disease

A

orbital mass- unilateral/ tender
orbital cellulitis- unilateral, tender, systemic symptoms
orbital fracture- trauma, enopthalmos not proptosis

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23
Q

what is the management of thyroid eye disease

A

tear film lubrication
steroids for eye disease
smoking cessation
optimise thyroid function
eyes taped at night

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24
Q

what are specific features of graves thyroid disease

A

graves opthalmopathy (proptosis, chemosis, soft tissue swelling, opthalmaplegia), thyroid acropatchy, pretibial myxoedema

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25
Q

causes of proptosis

A

graves disease
cavernous sinus thrombosis
oribital cellulitis
retroorbital tumour
trauma

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26
Q

management of graves disease

A

symptomatic- beta blocker eg propanolol for palpitations, tachycardia, anxiety
thionamides- carbimazole (preferred), PTU (for pregnancy)
radioiodine ablation- may worsen graves eye disease
thyroidectomy- rarely used unless extremely large goitre causing obstructive symptoms

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27
Q

advise for patients who recently received radio iodine

A

must avoid contact with pregnant women for 2 weeks
pregnancy contraindicated
risk of hypothyroidism is 2-3%

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28
Q

definition of ankylosing spondylitis

A

Symptomatic sacroilitis (pain and stiffness for >3 months) associated with morning stiffness and improvement on mobilising/ worsening with rest. Associated with the allele B27 which is present in up to 95% of causasian patients and implies an 80 fold risk

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29
Q

what are the systemic manifestations of ankylosing spondilitis

A

apical fibrosis
aortic regurgitation
achilles tendonitis
AVN conduction defects
amyloidosis
anterior uveitis
atlanto- axial subluxation

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30
Q

how do you diagnose ankylosing spondylitis

A

XR of the sacro-iliac joints
graded from 0 (normal) to 4 (fused)
MRI can be used to visualise further (most sensitive and specific)

31
Q

what do you understand by the term seronegative arthritis

A

It’s a subtype of inflammatory arthritis (RA) in adults that’s diagnosed when blood tests are negative for rheumatoid factor (RF) and anti-cyclic citrullinated peptides (anti-CCPs). common subtypes:
psoriatic, enteropathy- associated, ankylosing spondylitis, reactive arthritisw

32
Q

what is the management of ankylosing spondylitis

A

MDT approach
patient education and counselling
physiotherapy
occupational therapy
hydrotherapy
pharmacological- NSAIDs, analgesia,
DMARDs- methotrexate/ sulphasalazine for peripheral disease (not spine),
biologics e.g. adalimumab

33
Q

how do you explore the differentials in a patient with excessive cortisol

A

low dose dexamethasone test (1mg) resulting in an abormal cortisol >50 would confirm cortisol excess
confirming cause look at ACTH:

high dose dexamethasone test
suppressed cortisol- pituatary adenoma
elevated cortisol- ectopic ACTH/ adrenal cushing
ACTH low- adrenal cushing
ACTH high- ectopic ACTH

34
Q

management of endogenous cushings syndrome

A

management of underlying cause e.g. surgical resection
medical treatment e.g. metyrapone

35
Q

what is the difference between cushings disease and cushings syndrome

A

cushings syndrome refers to the digns and symptoms caused by elevated cortisol (most commonly exogenous). Cushings disease is caused by the hypersecretion of ACTH from a pituatary adenoma which is a cuase of cushing’s syndrome

36
Q

how would you investigate a patient with suspected addisons disease

A

I would perform a short synacthen test
In the case of addisons disease I would expect the adrenals to fail to produce an adequete cortisol response (170 at baseline, 550 at peak)

37
Q

management of addisons disease

A

mainstay of treatment would be steroid replacement- glucocorticoid and mineralocorticoid
in the instance of an adrenal crisis- rapis steroid and fluid replacement with correction of any electrolyte derangements would be crucial
advise patient to wear a medic alert bracelet
educate patient e.g. sick day rules

37
Q

what are the causes of primary adrenal failure

A

autoimmune (70-90%)
TB (10-20%)

38
Q

what other autoimmune conditions are associated with addisons disease

A

polyglandular autoimmune syndrome
- diabetes, thyroid, vitiligo, RA, SLE, alopecia

39
Q

what autoantibodies are present in addisons disease

A

antibodies to 21-hydroxylase is the most common and specific
also can have antibodies to 17-hydroxylase

40
Q

why does pigment change in addisons disease

A

ACTH is synthesised from POMC which is also the precursor to MSH. These biproducts are structurally similar therefore high ACTH can activate melanocyte receptors and cause melanin deposition.

41
Q

types of meningitis

A

viral meningitis
lyme meningitis
fungal meningitis
protozoa meningitis
paraneoplastic/ malignant causes

42
Q

what are the complications of bacterial meningitis

A

can be fatal
permanent neurological sequela
cognitive problems
vascular complications- amputations from sepsis

43
Q

management of acromegaly

A

surgery may be considered for a pituitary tumour as the first line mangement

If it is inoperable or surgery unsuccessful then medication may be indicated:

somatostatin analogue e.g. octreotide
directly inhibits the release of growth hormone
effective in 50-70% of patients

pegvisomant. GH receptor antagonist. once daily s/c administration. very effective - decreases IGF-1 levels in 90% of patients to normal. doesn’t reduce tumour volume therefore surgery still needed if mass effect

dopamine agonists, for example bromocriptine.
the first effective medical treatment for acromegaly, however now superseded by somatostatin analogues
effective only in a minority of patients.

External irradiation is sometimes used for older patients or following failed surgical/medical treatment

44
Q

what other organs can be affected in acromegaly

A

cardiac- cardiomyopathy, diabetes, hypertension
visual consequences

45
Q

possible complications of transphenoidal pituatary resection

A

panhypopituatarism

46
Q

obstructive sleep apnoea scoring

A

epworth sleep score
stop bang score

47
Q

osteogenesis imperfecta - cardiac signs

A

association with bicuspid aortic valve- can lead to aortic regurgitation

48
Q

osteogenesis imperfecta inheritence and associated features

A

autosomal dominant
8 different variations
abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides

discoloured translucent teeth
hearing impairement- middle ear bone
spinal scoliosis
bowing of long bone
short stature

49
Q

bisphosphonates side effects

A

gastroc irritation
osteonecrosis of the jaw (teeth check)

50
Q

CHADsVASc score

A

Age

Sex

CHF history

Hypertension history

Stroke/TIA/thromboembolism history

Vascular disease history (prior MI, peripheral artery disease, or aortic plaque)

Diabetes history

51
Q

complications of ehlers danlos syndrome

A

elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks, glaucoma
haemorrhage- GI

52
Q

what is ehlers danlos

A

autosomal dominant connective tissue disorder that mostly affects type III collagen

53
Q

antiphospholipid syndrome investigations

A

antibodies
- anticardiolipin antibodies
- anti-beta2 glycoprotein I (anti-beta2GPI) antibodies
- lupus anticoagulant
thrombocytopenia
prolonged APTT

54
Q

marfans syndrome cardiac features

A

aortic dilatation
aortic regurgitation
mitral valve proplapse

55
Q

indications for aortic root surgery

A

dilatation ?50mm at root or 45mm if family history of aoritc dissection
or rate expanding >3mm a year

56
Q

what are the secondary causes of HTN

A

endocrinological causes- Conn’s, Cushings, thyroid, acromegaly
phaeochromocytoma
renal causes- chronic renal disease of any cause, renovascular disease
cardio-respiratory- obstructive sleep apnoea, coarctation of aorta

57
Q

how is cardiovascular risk assessed in hypertensive patients

A

10 year CHD risk is calculated. Scoring system based on the Faringham heart study. Looks at age, gender, systolic blood pressure, smoking status, cholesterol. Used only in patients for primary prevention.

58
Q

what are major risk factors for gastric cancer

A

family history
increased age
smoking
H.pylori infection
long term gastric reflux

59
Q

how to manage malnutrition

A

1) exclude sepsis- nutritional support is often less effective when patients have an infection + may not present typically with infection
2) rehydration
3) micronutrient deficiency replacement
4) enteral feeding with dietician support
5) Paraenteral feeding if needed
6) refeeding bloods

60
Q

causes of weight loss in elderly

A

cognition
mood
systemic causes- malignancy, malabsortion, thyroid disease
reduced intake- oral soreness, ill fitting dentures, dysphagia
medication side effects
social problems- isolation, shopping

61
Q

what do you know about hereditary colorectal cancer syndromes

A

Lynch syndrome (HNPCC)- autosomal dominanat. most common. Increased risk of CRC, gynae esp endometrial. Amsterdam criteria

FAP- also autosomal dominant. 100s of polyps. mutation in APC gene.

Peutz-Jehger sundrome- autosomal dominant. pigmented lesions and GI haemartomous polyps.

62
Q

pathophysiology of jaundice

A

jaundice can be pre-hepatic, hepatic or post-hepatic. In pre-hepatic jaundice, the breakdown of red cells results in the formation of unconjugated bilirubin. In the liver, this is then conjugated and released into the GI tract via the bile. In the colon it is metabolised to urobilinogen to stercobilinogen and then stercobilin which is what gives the faeces its brown colour. Some urobilinogen is released in the urine.

In prehepatic jaundice, you will see largely a unconjugated bilirubin.
In hepatic disease it will be likely a mixed picture due to impaired conjugation but also cholestasis.
In post hepatic jaundice you will see high levels of conjugated bilirubin

63
Q

how to diagnose and manage alcohol hepatitis

A

Blood tests characteristic- AST: ALT ratio >2
other classic liver derangement- increased clotting, decreased albumin.

severity is calculated using the Glasglow alcoholic hepatitis score/ Maddreys score. Both will indicate severity of disease. Mainstay of treatment is alcohol cessation, steroids/ pentoxyfylline may be trialed.

64
Q

liver abnormalities in pregnancy

A

HELLP syndrome- haemolytic anaemia, elevated liver enzymes and low platelets

obstetric cholestasis- usually in 2nd/ 3rd trimester characterised by pruritis and raised bile acids

acute farrty liver of pregnancy- is associated with pre-eclampsia

65
Q

how does one diagnose IBS

A

may use the Rome III criteria to aid a diagnosis. It is important to look out for any red flag features in the history which would need colonic investigations. These include: bleeding rectally, weight loss, IDA, age over 65, family history.

Rome criteria- patients should have pain 3 days per month for 3 days which is : relieved on defecation, change in stool frequency, change in stool form. Associations- mucous PR, bloating, straining/ urgency

66
Q

associations with HIV and abdominal pain

A

more susseptible to infections
HIV associated malignancy e.g. lymphoma/ Kaposi sarcoma
HIV medication related pancreatitis

67
Q

other rarer causes of abdominal pain

A

acute intermittent porphyria
vasculitis particularly polyarteritis nodosa
familial mediteranean fever- fever+ abdominal pain
adrenal insufficiency

68
Q

management of acute coronary syndrome

A

morphine and metoclopramide
oxygen- if hypoxic, is normal o2 can increase rate of ischaemia
nitrates- GTN spray
aspirine 300mg
clopidogrel 300mg

STEMI- PCI/ thrombolysis

69
Q

DVLA guidelines

A
70
Q

what is the management of CCF

A

diuretics are useful in controlling congestive symptoms
all patients should be on an
ACEi unless contraindications. Can see a rise in serum creatinine up to 20% which is expected- if more, then rule out renovascular disease.
BB
spironolactone
digoxin- if heart failure and AF

71
Q

what are the common causes of AF

A

cardiac- IHD, mitral valve disease, CCF
non-cardiac- thyrotoxicosis, acute illness, alcohol, idiopathic

72
Q

conditions associated with retinitis pigmentosa

A

Refsum syndrome- peripheral neuropathy, cerebellar ataxia, deafness, muscle wasting
Alports syndrome
Usher syndrome- sensorineural deafness

73
Q

bilateral visual disturbance

A

night time- cataract, vitamin A deficiency (CF?)
diabetes
glaucoma

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