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Year 5 😊✌🏼 > Path 3 > Flashcards

Path 3 Flashcards

1
Q

What is the best measure of kidney function?

A

GFR

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2
Q

Functions of the kidney

A
  1. waste excretion
  2. fluid regulation and acid-base balance and
  3. hormone secretion
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3
Q

functional unit of kidney

A

nephron

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4
Q

functional unit of kidney

A

nephron

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5
Q

GFR (normal)

A

120ml/min (7.2L/h)

decreases with age, lower in males

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6
Q

What is serum creatinine influenced by?

A

muscularity
age
sex
ethnicity (higher in afro-caribbean)

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7
Q

ethylene glycol poisoning - sx, ix and mx

A

early sx:
- vomiting
- intoxication
- abdominal pain

late sx
- decreased level of consciousness
- headaches
- seizures

Ix ?

Mx ?

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8
Q

red cell casts

A

cells embedded in ?proteinacious matrix

suggestive of glomerular dysfunction

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9
Q

Renal imaging modalities

A

Plain KUB (x-ray

IVU (intravenous urogram)

CT KUB (e.g. for renal stones)

US KUB

MRI

Functional imaging (status and dynamic renograms)

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10
Q

AKI stage 1-3 definitions

A

AKI Stage 1: Increase in sCr by β‰₯26 Β΅mol/L, or by 1.5 to 1.9x the reference sCr

AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr

AKI Stage 3: Increase in sCr by β‰₯3x the reference sCr, or increase by β‰₯354 Β΅mol/L

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11
Q

Causes of pre-renal AKI

A

True volume depletion
Hypotension
Oedematous states
Selective renal ischaemia (e.g. renal artery stenosis)
Drugs affecting glomerular blood flow

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12
Q

How do different drugs affect pre-renal AKI risk?

A

NSAIDs - decrease afferent arteriolar dilatation

Calcineurin inhibitors - decrease afferent arteriolar dilatation

ACEi or ARBs - decrease efferent arteriolar constriction

Diuretics – affect tubular function, decrease preload

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13
Q

ATN

A
  • intrinsic AKI that follows a condition of severe and persistent hypoperfusion or toxic injury of epithelial cells causing detachment of the basement membrane and tubular dysfunction.
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14
Q

What structures may be involved in intrinsic AKI?

A

Vascular Disease e.g. vasculitis

Glomerular Disease e.g. glomerulonephritis

Tubular Disease e.g. ATN

Interstitial Disease e.g. analgesic nephropathy

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15
Q

Outcomes of AKI

A

40% full recovery
20% death

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15
Q

Outcomes of AKI

A

40% full recovery
20% death

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16
Q

How many stages to define CKD?

A

5

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17
Q

Stages of CKD

A

1.
2. mild
3. moderate
4. severe
5. end stage

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18
Q

Stages of CKD

A

1.
2. mild
3. moderate
4, severe
5. end stage

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19
Q

Causes of CKD

A

Diabetes!!! (mainly T2DM driving CKD here)
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease

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20
Q

Functions of the kidney

A

Excretion of water-soluble waste
Water balance
Electrolyte balance
Acid-base homeostasis
Endocrine functions
EPO, RAS, Vit D

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21
Q

Consequences of CKD

A

1]Progressive failure of homeostatic function
-Acidosis
-Hyperkalaemia
2]Progressive failure of hormonal function
-Anaemia
-Renal Bone Disease
3]Cardiovascular disease
-Vascular calcification
-Uraemic cardiomyopathy
4]Uraemia and Death

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22
Q

Renal acidosis

A

Metabolic acidosis
Failure of renal excretion of protons

Results in:
- Muscle and protein degradation
- Osteopenia due to mobilization of bone calcium
- Cardiac dysfunction

Treated with oral sodium bicarbonate

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23
Q

Hyperkalaemia ECG changes

A
  • tall tented t-waves
  • flattened p-waves
  • wider QRS complex

can lead to VT and VF

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24
Q

NSAIDs and potassium levels

A

NSAIDs increase potassium levels

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25
Q

erythropoietin stimulating agents

A
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25
Q

erythropoietin stimulating agents

A
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26
Q

Renal bone disease

A

Complex entity resulting in reduced bone density, bone pain and fractures:
-Osteitis fibrosa
-Osteomalacia
-Adynamic bone disease
-Mixed osteodystrophy

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27
Q

Renal bone disease

A

Complex entity resulting in reduced bone density, bone pain and fractures:
-Osteitis fibrosa
-Osteomalacia
-Adynamic bone disease
-Mixed osteodystrophy

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28
Q

Mx of renal bone disease

A

Phosphate control
- Dietary
- Phosphate binders

Vit D receptor activators
- 1-alpha calcidol
- Paricalcitol

Direct PTH suppression
Cinacalcet

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28
Q

Mx of renal bone disease

A

Phosphate control
- Dietary
- Phosphate binders

Vit D receptor activators
- 1-alpha calcidol
- Paricalcitol

Direct PTH suppression
Cinacalcet

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29
Q

What is cinacalcet

A
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29
Q

Is HIV a CI for renal transplant?

A

no, not anymore

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30
Q

BMI >30 is a CI to renal transplant, T or F?

A

F

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31
Q

Active sepsis - CI for renal transplant?

A

YES

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32
Q

Types of diaysis

A

haemodialysis (more common, can be done at home)
peritoneal (10%)

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32
Q

Types of diaysis

A

haemodialysis (more common, can be done at home)
peritoneal (10%)

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33
Q

PUO definition

A

prescriptive set of mandatory investigations

3 days of hospital investigations

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34
Q

Durack and Street criteria for PUO - categories

A

classic

nosocomial

immune deficient (neutropenic)

HIV-associated

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35
Q

DUKE criteria

A

can come up in exams

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36
Q

RIPL

A

rare and imported pathogens laboratory

you send a sample with the story and then they do the appropriate tests.

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37
Q

Campylobacter vs Salmonella

A

Campylobacter
- diarrhoea
- cramps
- bloating
- no fever
- no manegemtn

Salmonella
- diarrhoea
- vomiting
- may have fever
- usually supportive management, in typhi and paratyphi might give AABx

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38
Q

Abx for salmonella

A
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39
Q

Causes of polycythaemia in foetuses

A

 Twin-to-twin transfusion
 Intrauterine hypoxia
 Placental insufficiency

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40
Q

Causes of anaemia in foetuses

A

 Twin-to-twin or Foetal-to-maternal (rare) transfusion
 Parvovirus infection (virus not cleared by immature immune system)
 Haemorrhage from cord or placenta

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41
Q

haem -> causes of damage to the foetus

A

 Irradiation
 Damage by something crossing the placenta (e.g. drugs, chemicals, antibodies)
 Anticoagulants (οƒ  haemorrhage or foetal deformity (e.g. vitamin K if given in the first trimester))
 Antibodies can destroy red cells, white cells or platelets
 Substances in breast milk (e.g. G6PDD-baby may suffer from haemolysis if mother eats fava beans)

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42
Q

transient abnormal myelopoiesis / TAM

A
  • remits spontaneously
  • often transforms into a leukemia that does not remit
  • occurs in trisomy 21
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43
Q

Splenic sequestration

A

in children

sickled cels move into spleen -> infarcts -> spleen enlarges -> can be very dangerous and cause

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43
Q

Splenic sequestration

A

in children

sickled cels move into spleen -> infarcts -> spleen enlarges -> can be very dangerous and cause

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43
Q

Splenic sequestration

A

in children

sickled cels move into spleen -> infarcts -> spleen enlarges -> can be very dangerous and cause

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44
Q
A

Stroke risk is higher in infants with SCD than in adults

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45
Q

Inherited haemolytic anaemias n children - where can the defects be?

A

Red cell membrane
Haemoglobin molecule
Red cell enzymesβ€”glycolytic pathway
Red cell enzymesβ€”pentose shunt
Not to mention other rare conditions that you really don’t want to hear about

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45
Q

Inherited haemolytic anaemias n children - where can the defects be?

A

Red cell membrane
Haemoglobin molecule
Red cell enzymesβ€”glycolytic pathway
Red cell enzymesβ€”pentose shunt
Not to mention other rare conditions that you really don’t want to hear about

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46
Q

Haemolytic anaemias in chldern

A

Red cell membrane defects
Hereditary spherocytosis
Hereditary elliptocytosis
Haemoglobin defects
Sickle cell anaemia
Glycolytic pathway defects
Pyruvate kinase deficiency
Pentose shunt defects
G6PD deficiency

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47
Q

spherocytes on film

A

reduced central pallor

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48
Q

Heinz body

A
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48
Q

Heinz body

A
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49
Q

What can precipitate haemolytic in G6PD deficency?

A
  • Infections
  • Drugs
  • Naphthalene
  • Fava beans

falafel now sometimes made with a mixture of chickpeas and broad beans

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50
Q

Defects of coagulation in children

A

Haemophilia
vWD
?

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51
Q

When do you see Auer rods?

A
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52
Q

mutation in polycythaemia vera

A

JAK2 V617F

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53
Q

What does roleaux on blood film indicate?

A
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53
Q

What does roleaux on blood film indicate?

A
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54
Q

thrombotic thrombocytopaenic purpura

A

The underlying defect in thrombotic thrombocytopenic purpura is a deficiency of a plasma protein called von Willebrand factor cleaving protease (or ADAMTS13)

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55
Q

Presentation of FMF

A
  • episodic fevers for 48-96 hours

associated with:
- Abdominal pain due to peritonitis
- Chest pain due to pleurisy and pericarditis
- Arthritis
- Rash

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56
Q

Complication of FMF

A

Complication - AA amyloidosis
Liver produces serum amyloid A as acute phase protein
Serum amyloid A deposits in kidneys, liver, spleen

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57
Q

Dx of FMF

A

High CRP, high SAA
Blood sample to specialist genetics laboratory to identify MEFV mutation

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58
Q

Management of FMF

A

Colchicine 500mcg bd - binds to tubulin in neutrophils and disrupts neutrophil functions including migration and chemokine secretion

IL-1 blocker (anakinra, canukinumab)

TNF alpha blocker

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59
Q

What is IPEX?

A

Immune dysregulation, polyendocrinopathy, enteropathy, X- linked syndromeIPEX

mutations in FoxP3 cause it -> failure to negatively regulate Tregs

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60
Q

What is ALPS?

A

Auto-immune lymphoproliferative syndrome

Mutations within FAS pathway

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61
Q

ALPS symptoms

A

High lymphocyte numbers with large spleen and lymph nodes

Auto-immune disease
commonly auto-immune cytopenias

Lymphoma

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62
Q

Why do we worry about infections in pregnancy?

A

Maternal complications (Influenza, VZV, Hep E)
Miscarriage / stillbirth (rubella, measles, Hep E)
Teratogenicity (VZV, Zika)
IUGR / prematurity (rubella / CMV)
Congenital disease (CMV, HSV)
Persistent infection (HIV, Hep B/C)

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63
Q

pregnant woman with rash - which viruses?

A

Varicella Zoster virus (chickenpox/ shingles)
Epstein barr virus
Herpes simplex virus
Cytomegalovirus
Parvovirus B19
Enterovirus
Measles
Rubella

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64
Q

HSV details

A
  • transmission vii close contact
  • incubation: oropharyngeal/oro-facial 2-12 days; genetical infection 4-7 days
  • Sx: Asymptomatic
    Painful vesicular rash
    Lymphadenopathy
    Fever
  • latency: established in nerve cells
  • lesion swab for viral PCR
65
Q

Foetal HSV infection

A
  • very uncommon
  • foetal infection ascending in PROM
66
Q

Neonatal HSV infection

A
  • can be very dangerous

Routes of infection:
- Direct contact with infected maternal secretions during delivery
- Oral herpes : kissing baby
- Non familial transmission: other relatives, hospital staff etc

67
Q

HSV vertical transmission in pregnancy

A

VERTICAL TRANSMISSION
Greatest risk of transmission is primary genital infection in the 3rd trimester
- If active HSV in final 6 weeks before delivery then C-section is recommended

68
Q

What do you do with a woman that has active HSV in pregnancy>

A
  • GUM clinic referral
  • aciclovir in primary infection
  • HSV Ab testing
  • consider planned C-section
69
Q

mortality in neonatal HSV f untreated

70
Q

Why is HSV under diagnosed in babies?

A
  • can be small lesions
  • can be mistaken for other things
71
Q

types of neonatal HSV

A
  • SEM (skin, eye, mouth)
  • CNS involvement (+/- SEM)
  • disseminated

-> prevent HSV! Swab them, if concerned, treat with acyclovir)

72
Q

Why are we worried about VZV in pregnancy>

A

MATERNAL VARICELLA
- 10-20% of women in childbearing age susceptible
- 10-20%
- of pregnant women with varicella will have varicella pneumonia.
Encephalitis is rare but mortality is 5-10%

CONGENITAL VARICELLA SYNDROME
- 0.4% if maternal infection weeks 0-12
- 2% if weeks12-20
- skin scarring and limb abnormalities

Find out if this woman has had a varicella infection/vaccination or not? or check IgG

73
Q

PEP for maternal VZV

A
  • consult guidance
  • within 7d of exposure (Oral aciclovir 800mg
    OR
    Oral Valaciclovir 1000mg TDS
    from day 7-14 after exposure)
  • present after 7d of exposure (Oral aciclovir 800mg QDS
    OR
    Oral Valaciclovir 1000mg TDS
    up until day 14 post exposure)
74
Q

How do you treat maternal VZV?

75
Q

How common is CMV in pregnancy>

76
Q

How does foetal CMV infection present?

77
Q

How do we manage CMV infection in pregnancy?

A
  • check serology and compare to booking serology
  • refer to foetal medicine team, regaular USS perhaps amniocentesis
  • no treatment
78
Q

Rubella presentation

A
  • Starts on face and spreads to trunk/limbs within hours
  • lymphadenopathy
  • most people in the UK are vaccinated so not that big of an issue at the moment
79
Q

When in pregnancy is Rubella a problem?

A

Greatest risk is in the 1st trimester
- If infection before 8 weeks -> 20% spont abortion
- If infection before 10 weeks 90% incidence of fetal defects
- If infection after 18-18 weeks -> hearing defects and retinopathy
- If infection after 20 weeks risk is much lower

80
Q

CRS

A

congenital rubella syndrome

Sx:

  • bone lesions
  • microcephalau
81
Q

What may you be able to see in the mouth in rubella infection?

A

Froschheimer spots

82
Q

How does measles spread?

A

Measles starts behind the hairline, around the ears, spreads cephaocaudally over a few days (~3d)

83
Q

Measles - complications for mother

A
  • secondary bacterial infection
  • otitis media
  • pneumonia (10% mortality)
  • gastointestinal
  • encephalitis
84
Q

Risk of measles infection in pregnancy

A
  • foetal loss
  • preterm delivery
  • SSPE
  • no congenital abnormalities
85
Q

Risks of parvovirus B19 in pregnancy

A
  • before 20w transmission 33%
  • 9% risk of infection in trransmission
  • 3% hydros foetalis f infection
  • 1% foetal anomalies
  • 7% foetal loss
  • no risk documented after 20w
86
Q

What is hydros foetal is aand what can cause it?

A
  • cytotoxic to foetal red bood precurrsos cels -> anemie aanaard accumulaton of fluid in soft tissues and serous cavities, and can
86
Q
A

Refer to fetal medicine for monitoring
May require intrauterine transfusion

87
Q

Questions to ask a pregnant woman presenting with rash?

A
  • Gestation of pregnancy (date of last menstrual period/Due date by scan)
  • Date of onset, clinical features, type and distribution of rash, associated features
  • Past relevant history of infection
  • Past relevant history of antibody testing
  • Past immunisation history (and dates/places)
  • Any known contacts with rash illness (dates)
  • Travel history
88
Q

Investigations for pregnant woman with rash

A

Antenatal booking bloods
Antibody test to determine immunity/susceptibility
Swab/scrape from rash (if vesicular)
Blood sample
Antibody
+/- PCR
Postpartum vaccination if not had

89
Q

Complications of PID

A

peritonitis
bacteraemia
infertility
intestinaal….?

90
Q

Meaan age for cervical cancer

A

45-50 years

91
Q

High risk HPVs for cancer

92
Q

When does dysplasia/carcinoma in situ change to invasive cervical cancer?

A

When the basement membrane is crossed?

92
Q

When does dysplasia/carcinoma in situ change to invasive cervical cancer?

A

When the basement membrane is crossed?

93
Q
A

CIN -> squamous carcinoma
CGIN -> cervical adenocarcinoma

94
Q

Adenomyosis

A

endometrium is present in areas within the muscle wall

95
Q

Staging for endometrial Ca

A

FIGO

includes
- depth of invasion
- local and/or regional spreads the tumour
- metastases
- lymph nodes

96
Q
A

Serous carcinoma of ovary - origin is often the Fallopian tube

97
Q

Which cancer is associated with endometriosis?

A

Clear cell carcinoma

98
Q

Normal K+ levels

A

3.5-5.0 mol/L

99
Q

What is the main Xcellular ion?

100
Q

Hormones in the regulation of potassium?

A

angiotensin II
aldosterone

101
Q

stimuli for aldosterone release

A

Angiotensin 2
potassium

102
Q

Main causes of hyperkalaemiaa

A
  1. decreased GFR (renal failure,
  2. decreased renin (type 4 renal tubular acidosis - rare (diabetic nephropathy), NSAIDs)
  3. ACE1
  4. ARBs (e.g. losartan)
  5. Addison’s disease
  6. Aldosterone antagonists (e.g. spironolactone)
  7. rhabdomyolysis (K+ leaks from cells)
  8. acidosis (K+ is lost to maintain electroneutrality)
103
Q

where is renin produced/relased?

A

juxtaglomerular apparatus

104
Q

Which drugs reduce renin?

105
Q

Mian ca

A

renal impairment
drugs (ACEi, ARBs,spironolactone, NSAIDs)
low aldosterone
release from cels

106
Q

ECG finding with hyperkalaemia

A
  • peaked T-waves
107
Q

Management of patients with hyperrkalaemia

A
  • 10ml 10% calcium gluconate
  • 100ml of 20% dextrose + 10 units of insulin
  • nebulised salbutamol
  • treat the underlying cause
108
Q
A
  • loop diuretics
  • batter syndrome
  • thiazide diuretics
  • gitelman syndrome

more sodium to distal tubules or excess aldosterone

109
Q

Causes of hypokalaemiia

A
  • GI loss (vomiting)
  • Renal loss (hyperaldosteronism, excess cortisol); increased sodium delivery to distil nephron; osmotic dieresis)
  • redistribution into cells (insulin, beta-agonists, alkalosis)
  • rare causes: renal ……
110
Q

Clinical features of hypokalaemia

A
  • muscle weakness
  • cardiac arrythmia
  • polyuria and polydipsia (nephrogenic DI)
111
Q
A

aldosterone renin ratio

112
Q

What diuretic causes hypokalaemia?

A

Furosemide

113
Q

Why does cutanoues exposure to allergens promote allergy and oral exposure promote tolerance?

A

oral -> IgG responses and promotion of tolerance via Treg cells

cutaneous and resp -> IgE response, promotion of Th2 responses

114
Q
A

Results of skin prick test do not correlate to severity of reaction

115
Q

Advantages and disadvantages of skin prick tests

116
Q

skin prick vs intradermal test for allergy

117
Q

What tests can you do for allergy>

A
  • Skin prick
  • intradermal tests
  • sensitisation (IgE antibody) blood tests
  • component resolved diagnostics
117
Q

What tests can you do for allergy>

A
  • Skin prick
  • intradermal tests
  • sensitisation (IgE antibody) blood tests
  • component resolved diagnostics
118
Q
A

Detection of IgE is necessary but not sufficient to make a diagnosis of allergic disease

allergy is a clinical diagnosis

119
Q

Biomarkers for anaphylaxis

A

mast cell tryptase (pre-formed protein in mast cell granules; systemic degranulation of mast cells during anaphylaxis results in increase in serum tryptase)

120
Q

Biomarkers for anaphylaxis

A

mast cell tryptase (pre-formed protein in mast cell granules; systemic degranulation of mast cells during anaphylaxis results in increase in serum tryptase)

anaphylaxis not allergy

serial measurements at 30 minutes and 2h and then at least 24h

121
Q

Management of anaphylaxis

A
  • correct positioning (supine, legs up)
  • IM adrenaline
  • ABCDE
  • antihistamines only one ABC have been corrected
  • if no response to IM adrenaline, repeat and give IV crystalloid fluids

-> refer to allergy/immunology clinic and give IM epipen; liaise with school/nursery in children.

121
Q

Management of anaphylaxis

A
  • correct positioning (supine, legs up)
  • IM adrenaline
  • ABCDE
  • antihistamines only one ABC have been corrected
  • if no response to IM adrenaline, repeat and give IV crystalloid fluids

-> refer to allergy/immunology clinic and give IM epipen; liaise with school/nursery in children.

122
Q

What are the types of adverse reactions to food

A

1) Food intolerance Food poisoning (bacterial, scromboid toxin)

				Enzyme deficiencies (lactase)

				Pharmacological (caffeine, tyramine )

2) Food aversion Fads, eating disorders

3) Food allergy
- IgE mediated reactions (anaphylaxis, OAS)
- Mixed IgE and cell mediated (atopic dermatitis)
- Non IgE mediated (coeliac disease)

				Cell mediated (contact dermatitis)
123
Q
A

90% of food allergies are caused by 8 foods (peanuts, milk, egg, shellfish, tree nut, fish)

124
Q

Important risk factors for food allergy

A

Moderate/severe atopic dermatitis is an important risk factor for food allergy (indication for allergy testing even in absence of clinical history)

125
Q

skin prick in food allergies

A

positive skin prick is good at a confirming the diagnosis

negative is good at excluding disease

126
Q

Food associated exercise induced anaphylaxis

A
  • ask in history if they exercised within 4-6 h of ingestion
  • Food induces anaphylaxis if individual exercises within 4-6 hours of ingestion
  • Common food triggers are wheat, shellfish, celery
127
Q

Delayed food-induced anaphylaxis to beef, pork, lamb

A
  • Symptoms occur 3-6 hours after eating red meat and gelatin
  • IgE antibody to oligosaccharide alpha-gal (Ξ±1, 3-galactose) found in gut bacteria (lipid from meat is released, you are exposed to alpha-gal)

0 Induced by tick bites

128
Q

Coroner’s toxicology reasons (deaths reported to coroner)

A

o Violent
o Unnatural or sudden
o Cause of death is unknown

129
Q

What is the only specimen that can give a chronic drug history

130
Q

Timeframe of drug use based on PM samples

A
  • In Blood/serum, drugs typically can be detected for <12 hours
  • In Urine, drugs typically can be detected for 2-3 days
  • Hair: detects long term drug use (months/years e.g. 6months ago -> 6th centimetre)
131
Q

How do you calculate osmolality

A

2(Na+K)+urea+gulcose

132
Q

anion gap forula

A

Na+K-Cl-bicarb

133
Q

nomal anion gap

134
Q

High anion gap causes

A
  • ketones
  • methanol
  • ethanol
  • lactate (rare)
135
Q

Mx of HHC

A

gradual IV saline on ICU

136
Q

How can metformin cause acidosis?

A

if you OD it increases lactate -> lactic acidosis

137
Q

Definition of type 2 diabetes

A

FG >7.0 mM

GTT >11.1 mM at 2h

138
Q

What is smouldering myeloma? (general)

A
  • a stage between MGUS and MM
  • premalignant condition
  • there are no CRABs Sx but some of the lab values are β€˜worse’ than with MGUS classification
139
Q

What condition precedes MM?

A

MGUS (monoclonal gammopathy of unknown significance)

140
Q

Incidence of MGUS in the elderly?

141
Q

What is the risk of progression with MGUS?

A

1% annual risk

(IgA and IgG progress to MM; IgM progress to lymphoma)

142
Q

What are some primary and secondary events that lead to MM?

A

PRIMARY

a. Hyperdiploidy (odd number of chromosomes) - occurs in 60%

b. IGH rearrangements (Chr 14q32)
- t(11;14) IGH/CCND1
- t(4;14) IGH/GFR3
- t(14;16) IGH/MAF

SECONDARY

  • KRAS, NRAS
  • t(8;14) IGH/MYC
  • 1q gain / 1p del
  • del 17p (TP53)
  • 13-/ del 13q
143
Q

What are some primary events that lead to MM?

A

a. Hyperdiploidy (odd number of chromosomes) - occurs in 60%

b. IGH rearrangements (Chr 14q32)
- t(11;14) IGH/CCND1
- t(4;14) IGH/GFR3
- t(14;16) IGH/MAF

144
Q

What are some secondary events that lead to MM?

A
  • KRAS, NRAS
  • t(8;14) IGH/MYC
  • 1q gain / 1p del
  • del 17p (TP53)
  • 13-/ del 13q
145
Q

In what ways do MM cells interact with the bone marrow microenvironment? What effects to they have?

A
  • Bone destruction
  • anaemia
  • angiogenesis
  • immunosuppression and inflammation
146
Q

What is cast nephropathy in the context of MM?

A

formation of plugs (=urinary casts) in renal tubules from the free Ig light chains leading to renal failure

146
Q

What is cast nephropathy in the context of MM?

A

formation of plugs (=urinary casts) in renal tubules from the free Ig light chains leading to renal failure

147
Q

What is the 2nd commonest blood cancer?

A

multiple myeloma

(prevalence is increasing)

147
Q

What is the 2nd commonest blood cancer?

A

multiple myeloma

(prevalence is increasing)

148
Q

Bence Jones protein

A

urine monoclonal free light chains

indicates MM

149
Q

What does β€˜M-spike’ refer to?

A

it is a pattern on electrophoresis indicative of MM

150
Q

RFs for MM

A
  • m>f
  • obesity/overweight
  • genetics (sometimes there is familial MM)
  • older age
  • black > caucasian/asian
151
Q

What is Waldenstrom’s lymphoplasmacytic lymphoma

A
  • low grade lymphoma
  • B-cells (have features of lymphocytes and of plasma cells hence the name)
  • IgM monoclonal gammopathy seen
152
Q

CRAB features

A

-> mm

C - calcium > 2.75 mmol/L
R - renal disease (Creatinine >177umol/ or eGFR <40ml/L
A - anaemia (Hb <100g/L or drop of 20g/L)
B - bone disease (one or more bone lytic lesions on imaging)

152
Q

CRAB features

A

-> mm

C - calcium > 2.75 mmol/L
R - renal disease (Creatinine >177umol/ or eGFR <40ml/L
A - anaemia (Hb <100g/L or drop of 20g/L)
B - bone disease (one or more bone lytic lesions on imaging)

153
Q

What % pts with MM present with bone disease?

154
Q

What type of bone lesions do people with MM get?

A
  • osteolytic, never osteoblastic
  • Proximal skeleton
  • Back (spine), chest wall and pelvic pain
  • Osteolytic lesions, never osteoblastic
  • Osteopenia
  • Pathological fractures
  • Hypercalcaemia
155
Q

On which chromosome are HLA genes encoded?

A

Chromosome 6

155
Q

On which chromosome are HLA genes encoded?

A

Chromosome 6

156
Q

Which HLA are for MHC I and II?

A

MHC I: show antigen to CD8+ T-cells
HLA-A
HLA-B
HLA-C

MHC II: show antigen to CD4+ T-cells
HLA-DP
HLA-DQ
HLA-DR

157
Q

Which HLAs are usually typed for compatibility purposes in SCT?

A

HLA-A
HLA-B
HLA-DR

158
Q

What is GvHD?

What is affected in acute/chronic GvHD?

A

An immune response when donor cells recognise the patient as β€˜foreign’

Acute GvHD affects skin, gastrointestinal tract and liver

Chronic GvHD affects skin, mucosal membranes, lungs, liver, eyes, joints

158
Q

What is GvHD?

What is affected in acute/chronic GvHD?

A

An immune response when donor cells recognise the patient as β€˜foreign’

Acute GvHD affects skin, gastrointestinal tract and liver

Chronic GvHD affects skin, mucosal membranes, lungs, liver, eyes, joints

159
Q

RFs for GvHD

A

Degree of HLA disparity
Recipient age
Conditioning regimen
R/D gender combination
Stem cell source
Disease phase
Viral infections

160
Q

Treatment of acute GvHD

A

Corticosteroids
Calcineurin inhibitors: cyclosporin A, tacrolimus, sirolimus
Mycophenylate mofetil
Monoclonal antibodies
Photopheresis
Total lymphoid irradiation
Mesenchymal stromal cells

161
Q

Prevention of acute GvHD

A

Methotrexate
Corticosteroids
Calcineurin inhibitors: cyclosporin A, tacrolimus, sirolimus
CsA plus MTX

T-cell depletion
Post-transplant cyclophosphamide

162
Q

How is neutropenic sepsis defined?

A
  • temperature >38 sustained for one hour or single fever >39
  • in a patient with neutrophils <1.0 x 10^9/L
163
Q

How do you manage neutropenic sepsis?

A

Defined as temperature >38 sustained for one hour, or single fever >39, in a patient with neutrophils <1.0 x 10^9/L

164
Q

Manifestations of CMV disease

A
  • Pneumonitis
  • Retinitis
  • Gastritis – colitis
  • Encephalitis
165
Q

What is PTLD?

A
  • post transplant lymphoproliferative disease
  • life threatening
  • associated with EBV

Year 5 😊✌🏼 (53 decks)

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