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FRACP clinicals > Green book 2 flashcards > Flashcards

Green book 2 flashcards

1
Q

Inheritance of haemophilia A and B

A

X-linked

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2
Q

Joint most affected in haemophilia

A

Knee > elbows >ankles > shoulder/wrists

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3
Q

How to manage intramuscular bleeds in haemophiliacs

A

Intramuscular generally needs no treatment (except psoas)

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4
Q

Types of factor VIII replacement

A

Biostate
- plasma derived - factor VIII and vWF

Recombinant factor VIII
- extended half life or short acting

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5
Q

Side effects of DDVAP

A

Hyponatraemia
Fluid retention/weight gain
Tachyphylaxia
AMI/CVA in elderly patients

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6
Q

MOA of tranexamic acid

A

inhibits lysis by plasmin

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7
Q

Complications of haemophilia

A 
Joint
Disability / obesity
Development of inhibitor antibodies
Chronic pain
Complications of blood products - infections
Psychosocial issues
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8
Q

Haemophilia arthropathy management

A

Non pharmacological

  • weight loss
  • exercise

Pharmacological
- Prophylaxis 3-4x/week

Surgical

  • Synovectomy
  • Joint replacement
  • Joint fusion
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9
Q

Perioperative management for haemophiliacs

A

Infusion/bolus of factor

No VTE prophylaxis

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10
Q

Haemophiliac not responding to factor

A

inhibitor

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11
Q

treatment for people with inhibitors

A

Novoseven (recombinant factor VII)

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12
Q

How often to monitor bloods for HIV

A

every 3-6 months:

  • CD4
  • HIV RNA
  • UEC, LFT, FBE

Every 6 months
- Lipids, fasting glucose

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13
Q

Opportunistic infections in HIV based on CD4 count

A

200-500
- Herpes, Pneumococcal, TB, lymphoma

50-200

  • TB, PJP, toxo
  • Cancers: Kaposi’s sarcoma, non hodgkin’s lymphoma

<50
- MAC,,CMV, cryptosporidosis

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14
Q

What HIV antiviral drug has higher potency

A

Integrase inhibitor

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15
Q

RF for virologic failure

A

High baseline HIV/low baseline CD4
Slow viral load reduction in response to treatment
Poor adhere/psychosocial barriers

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16
Q

What to ask about HIV progress in treatment experienced person

A 
When diagnosed
Currently CD4 count/HIV load
CD4 nadir
Opportunistic infections
Treatment history and reasons for change
Current Mx
Monitoring/co infection
Co-morbidities
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17
Q

HIV exam

A

BP, BMI/waist circumference, lipodystrophy, oral candidiasis, CVS

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18
Q

When to start HIV therapy in setting of an opportunistic infection

A

When the patient is stable on OI treatment

Delayed further if cryptococcal or TB meningitis

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19
Q

nucleoside reverse transcriptase inhibitors

A

tenofovir
emtricitabine
abacavir
lamivudine

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20
Q

non-nucleoside reverse transcriptase inhibitors

A

rilpivirine
efavirenza
nevirapine
etravirine

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21
Q

when are protease inhibitors used

A

to boost levels of ritonavir or cobicistat

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22
Q

What are examples of protease inhibitors

A

atazanavir

darunavir

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23
Q

integrase inhibitors

A

dolutegravir
elvitegravir + cobicistat
raltegravir

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24
Q

types of HIV treatment failures

A

virologic
immunological
clinical progression

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25
Q

reasons for treatment failure (virologic or immunologic)

A 
adherence - psychosocial, toxicity
drug resistance
suboptimal potency of regimen
suboptimal pharmacokinetics (drug interactions)
more advanced immunodeficiency
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26
Q

HIV drugs that increase risk of cardiovascular diseases

A 
Abacavir
Protease inhibitors (darunavir)
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27
Q

What HIV drugs have CNS toxicities

A 
Efavirenza
Integrase inhibitors (gravirs)
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28
Q

What endocrine AE do all ARTs have

A

osteoporosis/osteopenis

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29
Q

Common reasons for switching ART

A

Simplification of regimen
Enhance tolerability
Mitigate drug-drug interactions
Eliminate food requirements

30
Q

How long after therapy would you expect the viral load to fall below 50 copies/mL

A

3 months

31
Q

Interactions between CVS risk and HIV

A

General RFs of CVS
Abacavir increases risk of AMI
Immuno dysregulation causing atherosclerosis in untreated individuals

32
Q

Biggest issue between HIV and transplant

A

drug-drug interaction (esp CNI)

33
Q

Cyclosplorin AE

A 
nephrotoxicity
neurotoxicity
gum hyperplasia
hirsutism
DM
Hypophospho/hypomag
34
Q

What SE does tacrolimus have more than cyclosplorin

A

Post transplant diabetes mellitus and neurotoxicity

35
Q

MOA of mycophenolate

A

blocks purine synthesis and stops proliferation of T and B cells

36
Q

splenectomy vaccines

A

pneumococcal
meningococcal
HIb
flu vaccine

37
Q

Definition for metabolic syndrome

A

Central obesity (WC men >94cm >80 women)/BMI >30

PLUS

any 2 of:
raised triglycerides
low HDL
hypertension
elevated fasting glucose
38
Q

autoantibody in mixed connective tissue disease

A

U1RNP positive

39
Q

treatment of mixed connective tissues disease

A

as per predominant disease

40
Q

definition of osteoporosis

A

minimal trauma fracture
T score < -2.5 on DEXA
T score < -1.5 taking corticosteroids

41
Q

Lifestyle treatment of patients with osteoporosis

A 
optimise dietary calcium
vit D replacement
weight bearing exercise
smoking cessation
falls prevention
42
Q

Secondary causes of osteoporosis

A 
malnutrition
hyperthyroidism
coeliacs disease
testosterone deficiency
estrogen deficiency
diabetes
myeloma
43
Q

Pharmacological therapy for osteoporosis

A

Antiresorptive

  • bisphosphonates
  • denosumab

Anabolic agents
- teriparatide

44
Q

what is teriparatide

A

parathyroid hormone analog

45
Q

how to monitor therapy in osteoporosis treatment

A

DEXA 1-2 years
Bone turnover markers (C-telopeptide, P1NP) - expect lower range of normal
Drug holiday after 3-5 years of bisphosphonate if fracture risk is low

46
Q

what kind of vasculitis is polyarteritis nodosa

A

medium muscular arteries

47
Q

what organs does polyarteritis nodosa affect

A

most organs can be affected except for lungs

48
Q

treatment of polyarteritis nodosa

A

steroids, cyclophosphamide
?PLEX

tx hypertension

49
Q

What is vasculitis in rheumatoid arthritis associated with

A

positive rheumatoid factor

50
Q

How does vasculitis in rheumatoid arthritis manifest

A

Polyneuropathy, mononeuritis multiplex
Skin ulcers, gangrene
Affected organ infarction

51
Q

Link between osteoporosis and rheumatoid arthritis

A

steroid use and inflammatory disease

52
Q

sarcoidosis staging on CXR

A 
Stage 0 ->  4
0 - nothing
1 - hilar
2 - hilar + infiltrates
3 - infiltrates alone
4 - fibrosis
53
Q

Investigations for sarcoidosis

A 
CXR
ACE levels
HRCT
Biopsy of affected tissues
Resp func tests
DLCO
ECG/holer
54
Q

What does CREST syndrome stand for

A 
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerdactyl
Telangiectasia
55
Q

Organ involvement of scleroderma

A 
Skin
Vascular
Renal
Lung
GI
Cardiac
MSK
Neurological
56
Q

Scleroderma GI manifestations

A

Oesophageal problems - dysmotility, stricture, dysphagia
Bowel dysmotility - alternating diarrhoea and constipation, pseudoobstruction, bacterial small bowel overgrowth
Biliary cirrhosis

57
Q

Cardiac manifestations of scleroderma

A

pericardial disease
myocarditis
myocardial fibrosis
conduction abnormalities

58
Q

Scleroderma MSK manifestations

A 
oedema
swelling
loss of function
contractures
myositis (overlap syndrome)
arthralgias
59
Q

risk factors for systemic sclerosis skin hypertensive renal crisis

A

steroid use

diffuse skin disease

60
Q

What is the criteria for systemic lupus erythematosus

A

4 of 11:

  • malar rash
  • discoid rash
  • photosensitivity rash
  • oral ulcers
  • pleuritis/pericarditis
  • haematological (cytopenia)
  • renal lupus
  • non erosive arthritis
  • neurological disorder (seizure, psychosis)
  • immunological disorder (andit ds DNA, anti Sn, antiphospholipid antibody)
  • positive ana
61
Q

Clinical markers of SLE severity

A 
fatigue/malaise
hair loss
arthralgias
pleuritic chest pain
sx suggesting new organ involvement
62
Q

Laboratory markers of SLE severity

A

ds DNA
decreased complement
cytopenias
evidence of organ dysfunction

63
Q

Wilson’s disease inheritance

A

autosomal recessive

64
Q

Laboratory diagnosis of wilsons

A 
ceruloplasmin screening test
urine copper (high)
serum copper (low)

LIVER BIOPSY

65
Q

Patterns of liver disease in Wilson’s

A

Chronic liver hepatitis
Cirrhosis
Fulminant liver failure

66
Q

Neuropsychiatric features of Wilson’s disease

A 
asymmetric tremor
excessive salivation
ataxia
masklike facies
personality changes
psychiatric abnormalities - behavioural, affective, schizophrenic, cognitive
67
Q

MSK manifestations of wilson’s disease

A

OA like arthropathy

spine and large joints

68
Q

What does Kayser-Fleischer rings look like

A

greenish gold brown

69
Q

Familial screening of Wilson’s disease

A

ceruloplasmin, urine copper, LFTs

70
Q

Treatment for Wilson’s disease

A

chelating agents:
- penacillamine, trientine
Copper absorption blocking agents
- zinc

treatment of complications

FRACP clinicals (24 decks)

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