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FRACP clinicals > Green book 1 flashcards > Flashcards

Green book 1 flashcards

1
Q

In iodine sufficient areas, is hyper or hypothyroidism from amiodarone therapy more common

A

Hypothyroidism

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2
Q

What are the types of amiodarone induced thyrotoxicosis

A

Type 1: abnormal gland w pre existing pathology (e.g. multinodular goiter or latent Graves’) increased synthesis of T3/4

Type 2: a destructive thyroiditis that results in excess release of T3/4. Due to direct toxic effect of amiodarone on thyroid follicular epithelial cells.

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3
Q

Manifestations of amiodarone induced thyrotoxicosis

A

Atrial arrythmias
Exacerbation of IHD/HF
Unexplained weight loss, restlessness, or low grade fever

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4
Q

How to distinguish between Type 1 and 2 amiodarone induced thyrotoxicosis

A

Doppler US - type I increased vascularity, II decreased

Type I have goiters

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5
Q

Treatment of type 1 amiodarone induced thyrotoxicosis

A
  1. Complex decision making re stopping amiodarone - how essential is amiodarone, long half life (100 days),
  2. Thionamides
  3. Radioiodine (but increased uptake)
  4. Surgery - thyroidectomy
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6
Q

Treatment of type 2 amiodarone induced thyrotoxicosis

A

Steroids

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7
Q

Nephrotic syndrome + RA - what systemic disease

A

Amyloidosis

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8
Q

Nephrotic syndrome and myeloma - what systemic disease

A

Amyloidosis

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9
Q

How to diagnosis amyloidosis

A

Biopsy - fat pad or rectal or involved site

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10
Q

Light chain amyloidosis - pathophysiology and organs involved

A

Primary amyloidosis from plasma cell dyscrasia w monoclonal immunoglobulin
Associated with MM or waldenstrom’s or non Hodgkin’s lymphoma

Organs involved:
Mucocutaneous - petechia/ecchymosis, raccoon eyes, allopecia, papules/nodules
Tongue - macroglossia
Heart - ischaemic, arrhythmia, orthostatic hypotension,
Other vascular: claudication
Renal-  proteinuria, nephrotic syndrome
GI - haemorrhage/malabsorption
Hepatomegaly
Neuropathies - autonomic/sensory
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11
Q

Serum amyloid A protein amyloidosis - pathophysiology and manifestations

A

Secondary amyloidosis to inflammatory/infective chronic conditions

Organs involved:

  • Kidney - 90% of patients
  • Liver and spleen (howell jolly bodies)
  • GI (rare)
  • Cardiac - AA deposites (less than AL amyloidosis)
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12
Q

What titre of ANA is more suggestive of autoimmune disorder

A

> 1:640

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13
Q

What ANA pattern is linked to limited scleroderma

A

Anti-centromere

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14
Q

What antibodies are found in primary Sjogren’s

A

Ro/La

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15
Q

What ENAs are SLE specific

A

dsDNA, anti Sm

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16
Q

What ENA is found in mixed CTD

A

U1RNP

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17
Q

What ENA is found in diffuse systemic sclerosis

A

SCL-70

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18
Q

What ENA is found in anti-synthetase syndrome

A

Jo-1

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19
Q

What ENA is associated with congenital heart block

A

anti Ro (SSA)

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20
Q

What at the antiphospholipid antibodies

A

Lupus anticoagulant
Anticardiolipin antibodies
Beta2-glycoprotein-1 antibodies

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21
Q

Most common venous thrombus site in antiphospholipid syndrome

A

Calf

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22
Q

Most common arterial thromboses site in antiphospholipid syndrome

A

Cerebral vessels

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23
Q

Diagnostic criteria for antiphospholipid syndrome

A

+ve antiphospholipid antibody (need repeat measurement 12 weeks apart)
AND
At least 1 clinical feature (venous/arterial thromboses, recurrent foetal loss, thrombocytopenia)

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24
Q

Primary thrombosis prevention in patients who have antiphospholipid antibodies

A

Not indicated if they have not had a thrombotic event or if they have only had a pregnancy morbidity
Aspirin may have a role in cardiovascular risk reduction

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25
Q

CHADS2 risk criteria score

A 
Prior stroke
Age >65 score 1 >75 score 2
HTN
DM
HF EF <40%
Valvular heart disease
Female sex
Vascular disease
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26
Q

Consensus practice guidelines for warfarin bridging in surgery

A

No bridging for CHADS2 <4

Can bridge for CHADS2 5/6 or high bleeding risk procedures

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27
Q

How to bridge warfarin if required

A

stop warfarin 5 days before procedure and bridge w LMWH 3 days before and restart LMWH 24 hours after procedure and up to 10 days while warfarin reintroduced

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28
Q

Aims of rate control in AF

A

60-80 bpm at rest and 90 to 115 beats per minute during moderate exercise

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29
Q

How long to anticoagulate for before and after cardioversion

A

3 weeks before and 4 weeks after

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30
Q

What agents can be used in maintenance of sinus after DC cardioversion?

A

Amiodarone
Sotalol
Flecanide (<60yr and no structural heart disease)

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31
Q

Ends of DMARDs:

  • cept
  • mab
  • ximab
  • zumab
  • tinib
A 
cept - fusion
mab - mAb
ximab - chimeric mAb
zumab - humanized mAb
tinib - tyrosine kinase inhibitor
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32
Q

Secukinumab mechanism of action

A

IL 17

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33
Q

Ustekinumab mechanism of action

34
Q

Requirement for PBS biologic for RA

A

Methotrexate 20mg weekly for 6 months and additional DMARD for 3 months
Raised inflammatory markers
20 tender swollen joints or 4 major joints

35
Q

Requirements for PBS biologic for ank spond

A

Reduced ROM
Raised inflammatory markers
High BASDAI (visual analogue score of pain and stiffness)
Significant sacroiliitis proven on Xray
Failed 2 consecutive NSAIDs over 3 months with a concurrent exercise program
Raised inflammatory markers (ESR 25, CRP 10)

36
Q

What biologic DMARD exacerbates severe heart failure

A

TNF inhibitors

37
Q

Perioperative management for biologics for surgical procedures

A

Withhold treatment with etanercept for 2-4 weeks and adalimumab, certolizumab, golimumab and infliximab 4-8 weeks prior to major surgery. Treat may be started post operatively once wound healing is satisfactory and there is no evidence of infection/wound healing

38
Q

Aetiologies of HFrEF

A

Ischaemic heart disease (2/3rds of cases)
HTN
Dilated cardiomyopathy

39
Q

HFpEF aetiologies

A 
HTN 
Female
Elderly
IHD
Hypertrophic cardiomyopathy
Aortic stenosis
40
Q

Precipitants of acute exacerbation of HF

A 
Ischaemia
Non adherence
Arrythmia
AKI
SYstemic infections
Anaemia
Hyperthyroidism
NSAIDs
PE
41
Q

Aims of treatment for HFrEF

A

Manage fluid
Reduced hospital admissions/HF exacerbations
Reduced morbidity
Reduce mortality

42
Q

Primary prevention indication for implantable cardioverter-defibrillator (ICD)

A

1 month post myocardial infarction and LVEF <30%

HFrEF and ischaemic or dilated cardiomyopathy LVEF <35%

43
Q

How to present kidney staging/classification

A

Stage x kidney w norm/mic/macalbuminuria secondary to diabetic nephropathy

44
Q

What are CKD blood pressure targets

A

<140/90

w diabetes/albuminuria 130/80

45
Q

Mx of albuminuria

A

ACEi/ARB
Reduction in salt intake
Spironolactone
Glycaemic control (BGL 6-8 post prandial, HbA1C <7%)

46
Q

Relationship of CKD and dyslipidaeia

A

CKD associated with abnormalities of lipid metabolism
More severe in albuminuria - especially nephrotic syndrome
Statin for anyone >50 years w CKD or <50 years w other risk factors

47
Q

When to use calcitriol

A

suppression of secondary hyperparathyroidism - PTH >3-5 upper limit of normal

48
Q

When is cinacalcet used

A

Hyperparathyroidism in patients on dialysis

49
Q

When does anaemia develop in CKD

50
Q

When does acidosis develop in CKD

51
Q

why is acidosis in CKD bad

A

demineralisation ofbone and increased protein degradation

52
Q

Bicarb aims in CKD

53
Q

Adverse effects of sodibic

A

fluid retention, worse BP control

54
Q

Modifiable causes of depression in CKD

A

Insomnia
Medication SE
Inadequate dialysis

55
Q

Salt restriction CKD

56
Q

Treatment approach to chronic pain syndrome

A

Rehab
Physical therapy
Occupational therapy - including desensitisation techniques
Recreation therapy
Medical rapport, realistic treatment goals, psychological evaluation, involvement of family members/carers

57
Q

Analgesia in chronic pain syndrome

A

Simple analgesia
Avoid opioids
Amitriptyline/pregabalin/gabapentin
SSRI or duloxetine

58
Q

Organs that cystic fibrosis affect

A 
Lungs
Sinuses
Pancreas
Reproductive system
Liver
Intestine - meconium ileus
59
Q

CF complications in the respiratory system

A 
Bronchiectasis
Recurrent infections
Sinusitis
Pulmonary haemorrhage
Pulmonary HTN
Spontaneous pneumothorax
60
Q

Pancreatic complications of Cystic Fibrosis

A

exocrine - malabsorption

endocrine - diabetes

61
Q

What diagnoses CF

A

Sweat chloride value greater than 60 mEq/L

62
Q

Names of CFTR modulators

A

Ivacaftor
Lumancaftor/Ivacaftor
Tezacaftor/lumacaftor

63
Q

Indication for transplant in cystic fibrosis

A

FEV1 <30%
Severe hypoxaemia or hypercapnia after recovery from an acute illness
Increasing functional impairment
Life threatening pulmonary complication - recurrent massive haemoptysis

64
Q

What is the major risk factor for microvascular disease in diabetes

A

hyperglycaemia

65
Q

What type of diabetes is associated with microvascular and macrovascular

A

T1DM - microvascular

T2DM - macrovascular

66
Q

Most important RF for diabetic retinopathy

A

hyperglycaemia and hypertension

67
Q

How to treat diabetic retinopathy

A

Laser photocoagulation

68
Q

What DOAC is sensitive to coagulation tests

A

Dabigatran to APTT/TT/TCT

69
Q

Dose reduction for dabigatran

A 
Age >75 or CrCl 30-50mL
110mg bd (normally 150mg bd)
70
Q

What is granulomatosis with polyangiitis?

A

Systemic vasculitis of the medium and small arteries, as well as the venules, arterioles and occasionally large arteries

71
Q

What to classify granulomatosis with polyangiitis?

A

Classic GPA
- Upper and lower respiratory tract + kidneys
Limited GPA
- Upper respiratory tract with majority progressing to GN
- less likely to be ANCA positive

72
Q

Organ involvement in granulomatosis with polyangiitis

A

Lungs

  • nodules
  • alveolar/pleural opacities
  • haemorrhage

Kidneys

  • renal impairment
  • GN

Upper and lower airways

Joints

Eyes
- conjunctivitis, corneal ulceration, episcleritis, optic neuropathy, nasolacrimal duct obstruction

Skin

Nervous system
- CNS, eye, Cranial nerves, mononeuritis multiplex

73
Q

Granulomatosis with polyangiitis diagnostic criteria

A

2 or more of:

  • Nasal/oral inflammation
  • Radiographic chest changes (nodules/infiltrates/cavities)
  • Abnormal urinary sediment
  • Granulomatous inflammation on biopsy of an artery or perivascular area
74
Q

How proportion of people with granulomatosis with polyangiitis are ANCA positive

75
Q

Treatment of GPA

A

Induction
- Cyclophosphomide, steroids, rituximab

Maintenance of remission
- methotrexate, azathioprine

Plasma exchange

76
Q

Indications for plasma exchange in granulomatosis with polyangiitis

A

anti-GBM antibodies as well as ANCA
severe pulmonary haemorrhage on presentation
advanced renal dysfunction

77
Q

haemachromatosis mutation gene

78
Q

Haemachromatosis inheritance

A

autosomal recessive

79
Q

Most common manifestations of haemachromatosis

A 
Liver function abnormalities
Systemic - weakness/lethargy
Skin hyperpigmentation
Diabetes
Arthralgia
Impotence
ECG abnormalities
80
Q

What manifestations of haemachromatosis doesn’t respond to Fe removal?

A

Arthritis

Diabetes (partial)

81
Q

Diagnosis of haemachromatosis

A

Organ involvement
Ferritin >1000, transferritin >50%
C282y mutation

82
Q

Preventative measures in haemachromatosis

A

Avoid ETOH

Monitor for HCC

FRACP clinicals (24 decks)

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