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Year 5 😊✌🏼 > Path 3 > Flashcards

Path 3 Flashcards

1
Q

Risk factors for SSI

A
  • age (>45)
  • ASA 3 or more
  • diabetes
  • malnutrition
  • low serum albumin
  • DMARDs
  • obesity (adipose tissue is poorly vascularised)
  • smoking
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2
Q

Main pathogens causing SSI

A
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3
Q

FC levels of SSI deep superficial etc

A
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4
Q

Measures to decrease number of surgical site infections

A

PRE-OP
- pre-op showering
- nasal décolonisation (for some surgeries, e.g. cardiac)
- antibiotic prophylaxis (at induction of anaesthesia, need to achieve bactericidal levels at the time the incision is made; in prolonged OP or lots of blood loss,
- hair removal not with razor but electrical clippers because prevent micro abrasions

OP
- reduce number of poeple in theatre
- ventilation (+ve pressure, direction of air flow is from theatre to rest of the hospital; 20 air changes/h, all air coming in is filtered, keep theatre doors closed; orthodoxy surgeries in laminar flow theatres)
- sterilised instruments
- skin prep (chlorhexidine in 70% EtOH)
- asepsis and surgical technique
- normothermia
- O2 sats >95%

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5
Q

Incidence of SA

A
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6
Q

Incidence of SA

A
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7
Q

mortality and morbidity in SA

A
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8
Q

RFs for SA

A
  • prosthesis
  • immunosuppression
  • underlying joint disease
  • IVDU
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9
Q

Pathophysiology of SA

A

see screenshot

includes bacterial and host factors

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9
Q

Pathophysiology of SA

A

see screenshot

includes bacterial and host factors

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10
Q

Host factors for SA pathophysiology

A
  • genetic variation in cytokine expression
  • more
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11
Q

bacterial factors in SA pathophysiology

A
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12
Q

Commonest pathogens

A
  • staph aureus
  • streptococci
  • gram -ve organisms
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13
Q

Presentation of SA

A
  • ## 1 red, hot, swollen joint
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14
Q

Ix for SA

A
  • blood cultures
  • synovial aspiration
  • bloods

USS to guide needle aspiration
MRI scan to look at damage and

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15
Q

Abx for SA

A

flucloxacillin
cephalosporin

may need to add vancomycin if MRSA

review after 2 weeks -> switch to oral for 4w if good response, if not good continue for 4 weeks IV

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16
Q

Vertebral osteomyelitis

A
  • acute haematogenous
  • add
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17
Q

Commonest organisms in vertebral osteomyelitis

A
  • staphylococcus
  • streptococci
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18
Q

commonest location of

A

lumbar spin

  1. cervical spine
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19
Q

PC in VOM

A
  • back pain
  • fever
  • may have neurological sx
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20
Q

Ix in VOM

A

MRI?

add mroe

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21
Q

Mx of VOM

A
  • 6w Abx
  • may need longer course if untrained abscess, foreign material
  • may need surgery if there are neurological issues/compression
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22
Q

commonest organisms causing prosthetic joint infection

A
  • coagulase -ve staphylococci
  • staph aureus
  • g-ve less common
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23
Q

what dies the presence of alpha-defensin indicate?

A

infection (in the bone)

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24
Q

what dies the presence of alpha-defensin indicate?

A

infection (in the bone)

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25
Q

What haematological changes are normal in pregnancy?

A
  • mild anaemia (physiological) - plasma volume rises 150%, red cell mass rises 120-130%)
  • macrocytosis (normal - physiological, but does not exclude folate or b12 deficiency)
  • neutrophlia
  • thrombocytopenia (and increased platelet size)
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26
Q

iron deficiency in pregnancy - consequences

A

IUGR
prematurity
PP haemorrhage

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27
Q

Dose of folate pre conception and in first trimester

A

400 ug/day

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28
Q

What happens to platelets in pregnancy?

A

count decreases (15% women will have below 150)

size increases

there may also be some clumping

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29
Q

Causes of thrombocytopenia in pregnancy

A
  • physiological
  • pre-ecclampsia
  • ITP
  • microangiopathic syndromes
  • other (e.g. DIC, leukemia, …)
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30
Q

thrombocytopenia number

A

<140 x 10^8 /L

double check this

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31
Q
A

IgG autoantibodies from ITP can cross the placenta so the baby may be affected

significantly low platelets (<20) in 5% of the babies

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32
Q

How do you manage ITP in pregnancy?

A
  • steroids
    ?check IViG?
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33
Q

HUS and I think there is a lot more to say here and I think there is so much more to say here

A
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34
Q

What medication can be given to women to increase uterine contraction?

A

syntosin

(synthetic oxytocin)

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34
Q

What medication can be given to women to increase uterine contraction?

A

syntosin

(synthetic oxytocin)

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35
Q

When around pregnancy is the risk of VTE highest?

A

6 weeks following delivery

VTE risk assessment done before, throughout and after pregnancy

good hydration is important during pregnancy

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36
Q

Causes of DIC

A
  • infections
  • obstetric causes

fill out this list

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37
Q

Scan to check for metabolically active metastases?

A

FDG-PET

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38
Q

Scan to check for bone metastases?

A

Tc bisphosphoante scan

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39
Q

What happens to the apex beat in LV hypertrophy?

A

the apex beat is normal

LV hypertrophy does not cause apex displacement.

tall R waves and deep s-waves because the muscle is huge.

you only see displacement if there is also heart failure

do not confuse a dilated heart with a hypertrophic heart

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40
Q

commonest cause of LV hypertrophy

A

untreated HTN

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41
Q

What type of bacteria are neisseria gonorrhoeae?

A

gram -ve diplococci

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41
Q

What type of bacteria are neisseria gonorrhoeae?

A

gram -ve diplococci

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42
Q

What can cause gram -ve meningitis in children? (rods)

A
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43
Q

g-ve diplococci on LP in meningitis Sx

A

Neisseria meningitidis

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44
Q

g-ve rods causing meningitis Sx in a 6yo child - organism?

A

Haemophilus influenzae

less common in vaccinated kids but in the unvaxxed

E coli is also a gram -ve rod and causes meningitis in neonates and premies

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45
Q

gram +ve diplococci causing sepsis that we are worries about

A

strep pneumoniae

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46
Q

19 yo with PUO cultures -ve for 2 months but cold agglutinins are positive - organism?

A

mycoplasma

  • gives you cold agglutinins
    ?also takes long to culture?
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47
Q

gram+ve cocci in clusters from pus of a boil

A

staph aureus

the clusters make it likely to be staph aureus

it is the aggressive organism that attacks joints, foreign material etc.

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48
Q

staph epidermidis

A

found on skin

can also cross the skin and cause sx
much less aggressive than staph aureus

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49
Q

Strep viridans

A

gram +ve cocci

can cause strep viridans endocarditis
PUO
slowly can damage the endocardium

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50
Q

Which organism are you more likely to get endocarditis/sepsis from?

strep pyogenes and strep viridans

A

strep pyogenes kills you by sepsis before it can settle on valves

strep viridans can cause PUO and endocarditis because it is less virulent and can settle on the valve

more virulent bugs may be less likely to cause endocarditis thereby

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51
Q

Signs of subacute endocarditis

A
  • splenomegaly
  • haematuria
  • splinter haemorrhages
  • heart murmurs
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52
Q

Where does strep viridans come from

A

teeth

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53
Q

What is the commonest cause of meningitis

A

viral

e.g. coxsackie B virus

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54
Q

what is aseptic meningitis?

A

viral meningitis

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55
Q

how do you manage viral meningitis?

A

?supportive management

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56
Q

LP result in SAH

A
  • red cells
  • yellow colour
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57
Q

Stain in TB

A

Ziehl nielsen

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58
Q

LP result in TB meningitis

A

normal LP but culturign shows TB

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59
Q

Commonest cause of secondary immunodeficiency worldwide

A

malnutrition

especially protein loss malnutrition

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60
Q

measles induced immunodeficiency

A
  • lasts months to years
  • implicated in increased morbidity and mortality
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61
Q

How does TB lead to immunodeficiency?

A

???

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62
Q

TB IRIS

A

TB immune reconstitution syndrome

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63
Q

Drugs as a cause of immunodefiocicnet

A
  1. small molecules (steroids, cytotoxic agents, calcineurin inhibitors, anti epileptic drugs, DMARDs)
  2. Jak inhibitors
  3. biologics and cellular therapies
  4. haematological cancers (B-cell and plasma cell cancers; chemotherapy; Goods’ syndrome)
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64
Q

Goods’ syndrome

A
  • thymoma associated with Ab deficiency
  • combined T- and B-cell problem
  • absent B cells, no antibodies
  • increased risk of PJP, CMV, fungal and AI disease
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65
Q

Ix for ?secondary ID

A

FISH

FBC
Immunglobulins
S??
HIV test

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65
Q

Ix for ?secondary ID

A

FISH

FBC
Immunglobulins
S??
HIV test

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66
Q

How many people are living with HIV?

A

37 million

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67
Q

How many of the people living with HIV are taking ART

A

21 million of 47 million

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68
Q

How many poeple in the UK are living with HIV?

A

101 200

approx 100 000

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69
Q

virus family of HIV

A

lentivirus family

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70
Q

what kind of virus is HIV?

A

double stranded RNA virus

structural, replicative and accessory proteins

retrovirus

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71
Q

What does HIV bind to?

A

CD4

CCR5

CXCR4

72
Q

How does HIV replicate?

A

via DNA intermediate

integrates into host genome

HIV DNA transcribed to viral mRNA

viral RNA translated to viral proteins

packaging and release of mature virus

73
Q

Origin of HIV

A

4 distinct linneages

MNOP

74
Q

commonest variant of HIV worldwide

A

Group M

75
Q

natural history of HIV infection

A
  1. acute (flu-like illness in 70% people)
  2. asymptomatic but progressive for 8-10 years
  3. AIDS
76
Q

what is the risk of HIV transmission related to?

A

viral load

therefore risk of transmission is highest in the acute phase

77
Q

driving force for viral diversity in HIV

A

error prone nature of HIV RT

short generation time of viral cycle and length of infection

78
Q

Characteristic features of untreated HIV imunlogy

A

insert

79
Q

loss of tetanus vaccine responses in HIV

A
80
Q

ART in UK

A

-reverse transcriptase inhibitor (NRTI, NNRTI)
- boosted protease inhibitors (ritonavir + PI)
- integrates inhibitor (

……..

81
Q

who is typically affected by MDS?

A

elderly

82
Q

signs and sx of myelodysplasia

A

of general BM failure

83
Q

Issues in MDS

A
  1. cytopenias
  2. quality decline of the cells
  3. increased risk of AML
84
Q

Pelger Heut abnormallity

A

bi-lobed neutrophils

seen in MDS

85
Q

Blood and BM morphological features of MDS

A
  • Pelger Huet abnomrality
  • dysgrabnulopoiesis of neutrophils
  • dyseryhtropoiesis of erythrocytes
  • myelokathexis
  • ringed sideroblasts
  • myeloblasts with Auer rods (seen in AML)

….. more

86
Q

what do Auer rods indicate?

A

AML

87
Q

Scoring system for MDS

A

IPSS-R

revised international prognostic scoring system

the higher the score the higher the lower the survival and time to progress to AML

87
Q

Scoring system for MDS

A

IPSS-R

revised international prognostic scoring system

the higher the score the higher the lower the survival and time to progress to AML

88
Q

MDS genetic abnormalities

A
  • driver mutations in MDS (carry prognostic significance)

add more info

89
Q

Myelodysplasia - Evolution

A
  1. deterioration of blood counts (worsening consequences of marrow failure)
  2. development of AML (in 5-50% <1 year, some cases of MDS are much slower to evolve, AML from MDS has an extremely poor prognosis and is usually not curable
  3. 1/3 will die of infection
    1/3 will die of bleeding
    1/3 will die of acute leukaemia
90
Q

Treatment of MDs

A
  1. allogenic SCT
  2. intensive chemotherapy

only a minority of MDS patents can really benefit from this

91
Q

Supportive care in MDS

A
  1. Supportive care
    - blood transfusion
    - antimicrobial therapy
    growth factors (Epo, G-CSF, TPO-receptor agonist)
  2. Biological modifiers
    - immunosuppressive therapy
    - azacytidine
    - decitabine
    - lenalidomide
  3. oral chemotherapy
    hydroxyurea/ hydroxycarbamide
  4. low dose chemotherapy )s.c. low dose cytarabine)
  5. intensive chemo/sct
    in a minority of patients
92
Q

when do you use lenalidomide

A

MM

5qdel variant of MDS

93
Q

Primary causes of BM failure

A
94
Q

Secondary causes of BM failure

A
95
Q

What is more common - primary or secondary BM failure?

A

secondary is much more common

96
Q

Drugs and BM failure

A
  1. predictable (dose dependat, common) - cytotoxic drugs
  2. idiosyncratic (NOT dose dependant, rare
  3. Antibiotics

etc/

97
Q

What is chloramphenicol used for?

A

it is used as an antibiotic in eye drops

used to be a systemic medication; can cause BM failure

98
Q

incidence of aplastic anaemia?

A

2-5 cases/million/year

slightly more common in Asian pop

99
Q

Which age groups are affected by aplastic anaemia

A

all age groups can be affceted

bimodal incidence in 20s and 60s

100
Q

Causes of aplastic anaemia

A

70-80% are idiopathic

inherited: dyskeratosis congenita, Fanconi anaemia, Schwachmann-diamond syndrome

secondary anaemia: radiation, drugs, viruses, immune e.g. SLE

miscellaneous: PNH (paroxysmal nocturnal haemoglobinuria), thymoma

101
Q

idiopathic aplastic anaemia

A

failure of BM to produce blood cells

stem cell problem (CD34, LTC-IC

immune attack

102
Q

triad of BM failure

A
  1. anaemia (fatigue, breathlessness)
  2. leucopenia (infections)
  3. thrombocytopenia (bruising)
103
Q

diagnosis of MDS

A
  1. blood (cytopenia)
  2. marrow (hyopcellular)
104
Q

Ddx of pancytopenia and hypo cellular marrow

A
  • hypoplastic MDS / AML
  • hypocellular ALL
  • hairy cell leukemia
  • mycobacterial (usually atypical infection)
  • anorexia nervosa
  • idiopathic thrombocytopenic purpura (BM tap will be normal)
105
Q

Camitta criteria

A

low reticulocyte count
low neutrophils
low platelets

BM <25% cellularity`

106
Q

Mx of BM failure

A
  1. seek and remove cause (detailed drug and occupational hx)
  2. supportive (blood transfusion, abx, iron chelation therapy)
  3. Immunosuppressive therapy (anti-thymocyte globulin, steroids, CyA)
  4. drugs to promote marrow recovery (G-CSF, TPO R agonists, oxymethome)
  5. SCT
  6. other treatments in refractory cases e.g. aletuzumab (anti-CD52, high dose cyclophosphamide)
107
Q

Specific treatment of idiopathic aplastic anaemia is based on…

A
  • illness severity
  • age of patient
  • potential stem cell donor
108
Q

Specific treatment of idiopathic aplastic anaemia

A

insert

109
Q

late complications following immunosuppressive therapy for AA

A
  1. relapse of AA (35% over 3 years)

etc

small risk fo solid tumours

110
Q

cure rate of young patients with AA treated with SCT

A

80%

110
Q

cure rate of young patients with AA treated with SCT

A

80%

111
Q

Fanconi anaemia

A

most common form of inherited AA
AR x-linked inheritace

etc

112
Q

Fanconi anaemia

A

most common form of inherited AA
AR x-linked inheritace

etc

113
Q

What is the most common cause of inheritedAA?

A

Fanconi anaemia

114
Q

somatic/congential abnormalities in Fanconi anaemia

A

short stature
cafe au lait spots
abnormality of thumbs
developmental delay
hypo pigmented patches
skeletal abnormality

check and add details

115
Q

complications of fanconis anaemia

A

AA (90%) median age 9
leukemia 10% - 14
liver disease
cancer\

????

116
Q

dyskeratosis congenita

A

inherited d/o characterised by

  • BM failure
  • cancer predisposition
  • somatic abnormalities

nail dystrophies
leukoplakia
white patches n skin

rare!!

add more details

117
Q

dyskeratosis congenita

A

inherited d/o characterised by

  • BM failure
  • cancer predisposition
  • somatic abnormalities

nail dystrophies
leukoplakia
white patches n skin

rare!!

add more details

118
Q

DC genetic basis

A

telomere shortening

X-linked, AD or AR possible

DKC1 gene and TERC gene

119
Q

which genes are implicated in DC (dyskeratosis congenita)?

A
120
Q
A

telomere shortening is a feature of idiopathic aplastic anaemia and also of dyskeratosis congenital

121
Q

mx options for hypoglycaemia

A

Alert and orientated
- juice/sweets
- sandwish

drowsy/confused but swallow intact
- buccal glucose
- hypostop/glucofgel
- start thinking about IV access

unconscious or concerned about swallow

-IV access
- 20% glucose

…

im iv etc

122
Q

Sx of hypoglycaemia

A
  1. adrenergic
    - tremor
    - palpitations
    - sweating
    - hunger
  2. neuroglycopaenic
    - somnolescnece
    - confusion
    - incoordination
    - seizures, coma
  3. None = impaired awareness of hypoglycaemia (could be people that take insulin)

relief of sx with glucose administration

122
Q

Sx of hypoglycaemia

A
  1. adrenergic
    - tremor
    - palpitations
    - sweating
    - hunger
  2. neuroglycopaenic
    - somnolescnece
    - confusion
    - incoordination
    - seizures, coma
  3. None = impaired awareness of hypoglycaemia (could be people that take insulin)

relief of sx with glucose administration

123
Q

Counter-regulation in hypoglycaemia

A

low glucose -> decrease in insulin, increase in glucagon

  1. reduces peripheral uptake of glucose
  2. increases glycogenolysis
  3. increases gluconeogenesis
  4. increases lipolysis

increased lipolysis increases FFAs -> become ATP via beta oxidation; a by-product of this is ketone body production

the minute you have insulin you will have no lipolysis

Low neuronal glucose is sensed in the hypothalamus and leads to
1. sympathetic activation - catecholamines
2. ACTH, cortisol, GH

124
Q

Ix in hypoglycaemia

A
  • confirm that there is hypoglycaemia with glucometer
  • may be more difficult in person that is otherwise healthy because it might be difficult to get a sample at the time they are hypo whereas people with diabetes monitor their blood glucose regularly
125
Q

venous vs capillary BG measurement

A

capillary - poor precision and low levels of glucose

if you think there is hypoglycaemia the gold standard is lab measured venous glucose

126
Q

Reasons why people without diabetes develop hypoglycaemia

A
  • post gastric bypass
  • organs failure
  • extreme weight loss
  • factitious
  • hyperinsulinism
  • critically unwell

fasting or active
paediatric vs adult

127
Q

What to consider in hypoglycaemia in people with diabetes?

A

medications
inadequate CHO intake / missed meals
impaired awareness
excessive alcohol
strenuous exercise
co-existing AI conditions (e.g. exclude Addisons)

128
Q

Which meds can cause hypglyxameia

A

glucose lowering drugs (sulphonylureas, meglitinides, GLP-1 agents)

Insulin (rapid acting with meals, inadequate meal. long acting at nighty or in between meals)

Other drugs (b-blockers, salicylates…) add

129
Q

Impaired awareness of hypoglycaemia

A

insert

130
Q

Ix for hypoglycaemia in someone w/o diabetes?

A
  • thorough hx and examination

biochemical tests (do them at the right time)
- insulin levels *
- c-peptide*
- drug screen* (e.g. sulfonylurea)
- auto-antibodies
- cortisol/GH
- FFA/blood ketones*
- lactate

  • indicates the most basic tests. you would not do an autoantibody screen on everyone
131
Q

Why do we measure both insulin and c-peptide in hypoglycaemia

A

because c-peptide is a marker for endogenous insulin.

endogenous and exogenous insulin contribute to the insulin level but only endogenous contributes to c-peptide level

132
Q

hypoglycaemia with high insulin, low c-peptide - what could this be?

A

hypoglycaemia in a diabetic

factitious disaese

someone has injected the insulin.

133
Q

Hypoinsulinaemic hypoglycaemia

A
  • fasting/starvation
  • exercuse

etc

134
Q

neonatal hypoglycaemia

A

hypoinsulinaemic hypoglycaemia

go over slide

could also be due to inborn error of metabolism e.g. in FA oxidation pathway, would not have ketones

134
Q

neonatal hypoglycaemia

A

hypoinsulinaemic hypoglycaemia

go over slide

could also be due to inborn error of metabolism e.g. in FA oxidation pathway, would not have ketones

135
Q

What is the appropriate / inappropriate response in hypoglycaemia?

A
135
Q

What is the appropriate / inappropriate response in hypoglycaemia?

A
136
Q

reactive/postprandial hypoglycaemia

A
137
Q

main reason for hypoglycaemia in anorexia

A

not enough glycogen stored in liver

138
Q

What is Km? (Michaelis menten constant)

A

subtrate concentration at which the reaction velocity is 50% of maximum

139
Q

what do elevate serum enzymes point to?

A

disasesd organ

140
Q

ALP

A

alkaline phosphatase

intra/extrahepatic bile ducts
bone
placenta (physiological increase in pregnancy)
intestine

there is also a physiological increase in childhood

141
Q

what happens in ALP deficiency

A

osteomalacia

indicates that it is important for bones

142
Q

What should you also check if there is a raised ALP?

A

hx

check LFTs (GGT and ALT) -> liver
check vitamin D -> bone

143
Q

which organs do AST and ALT come from which one is more specific for the liver?

A

ALT is more specific for liver

both found in heart, liver muscle, kidney

144
Q

Raised ALT - what could it be?

A

hepatocyte damage

(toxins, hepatitis, NAFLD, cancer, ischaemia e.g. post cardiac arrest)

not really used as a biomarker of kidney, heart or pancreas damage because we have better biomarkers

145
Q

How can you detect intestinal ALP?

A

usually ALP should not be secreted when you are fasting

so get the person to fast and then measure ALP, it should be back to mnromal

146
Q

is raised ALP in a pregnant person worrying

A

it is normal to have elevated ALP in pregnancy as it is secreted from the placenta

147
Q

gamma-GT

A

released from liver and biliary system

if it is high the problem is in the RUQ

can also be increased in response to alcohol or certain drugs

148
Q

LDH

A

lactate dehydrogenase

important for anaerobic metabolism

149
Q

where is LDH found?

A

WBC
RBC
Placenta (germ-cell testicular cancer (seminoma))
skeletal muscle (myositis)
liver injury
cardiac (better biomarkers available)

149
Q

where is LDH found?

A

WBC
RBC
Placenta (germ-cell testicular cancer (seminoma))
skeletal muscle (myositis)
liver injury
cardiac (better biomarkers available)

150
Q

in what cancer is the LDH level proportional to tumour size

A
151
Q

causes of increased amylase

A

acute pancreatitis
perf duodenal ulcer
bowel obstruction *and secondary disease to pancreas
salivary gland stones or infection (e.g. mumps)
macro-amylase (benign)

152
Q

CK - where is it found?

A

skeletal muscle
cardiac muscle

153
Q

Where is CK used as a biomarker?

A

rhabdomyolysis
myositis
polymyositis
dermatomyositis
severe exercise
……..
MI

add more

not used as a cardiac biomarker anymore because there are better markers (troponin)

154
Q

Troponin I

A

we measure cardiac troponin
elevation indicates damage to cardiac myocytes

155
Q

Reference range of troponin in men and women - same?

A

no, higher in men because they have bigger hearts

156
Q

What regulates release of BNP?

A

stretch
hypoxia
cytokines
hormones

157
Q

BNP

A

b-na… peptide

t1/2 18 minutes

difficult to measure in blood due to short half life

that is why we measure NT-proBNP because it is secreted in equimolar amounts to BNP

NT pro BNP is also a lot more stable

158
Q

artiest - drug, what is it and what is it used for?

A

can cause false low levels of BNP so measure NT-pro-BNP

159
Q

epitope for CAR T cells

A

CD19

159
Q

epitope for CAR T cells

A

CD19

160
Q

T-cell markers

A

CD3+ (all t-cells)
CD4
CD8
CD5

immature T cells can be 4+8+ but mature ones are wither 4+ or 8+

161
Q

descrbe spherocytes

A

smaller than normal RBCs
loss of cerntal pallor

162
Q

causes of spherovytosis

A
  • AIHA
  • hereditary spehrocytosis
163
Q

causes of acquired non-immune haemolytic anaemia

A

malaria
HUS
drugs
MAHA
snake venom
drinking anti-freeze

164
Q

Medication for CML

A

imatinib (Gleevec)

it is a tyrosine kinase inhibitor
(ABL kinase inhibitor)

165
Q

Blast crisis

A

chronic leukemia progressing to an acute leukemia

transformed as it acquired new mutations

166
Q

Test for polycythaemia vera

A

Jak2…17 mutation
check this!!!

167
Q

which drug to treat CLL?

A

Ibrutinib

168
Q

what is imatinib?

A

ABL kinase inhibitor

169
Q

Ibrutinib

A

brutin tyrosine kinase inhibitor

170
Q

Venetoclax - what is it?

A

BCL2 inhibito

171
Q

Cause of renal failure in melanoma

A

cast nephropathy is most likely

AL amyloid, hypercalcaemia and ATN are also possible.

If there is a very high serum free light chain it is likely to be cast neohropathy, because they can pass through eh basement membrane and precipitate in the tubules

171
Q

Cause of renal failure in melanoma

A

cast nephropathy is most likely

AL amyloid, hypercalcaemia and ATN are also possible.

If there is a very high serum free light chain it is likely to be cast neohropathy, because they can pass through eh basement membrane and precipitate in the tubules

172
Q

what FFP do you give in an emergency

A

AB +/-

173
Q

Who can you give 0+ blood too in emergencies

A

men and postmenopausal women

174
Q

what would you give in bleeding with low fibrinogen and normal PT/APTT

A

cryoprecipitate

Year 5 😊✌🏼 (53 decks)

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