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My MRCP > Miscellaneous 2 > Flashcards

Miscellaneous 2 Flashcards

1
Q

Chemotherapy

Give an example of alkylating agent
Give 2 examples of cytotoxic antibiotics
Give 4 examples of antimetabolites
Give 2 examples that act on microtubules
Give 1 example of irinotecan

A
  • Alkylating agent - cyclophosphamide
  • Cytotoxic abs - bleomycin, doxorubicin
  • Antimetabolites - methotrexate, 5FU, 6-mercaptopurine, cytarabine
  • Microtubular action- vincristine, docetaxel
  • Topoisomerase inhibitor - irinotecan
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2
Q

CYCLOPHOSPHAMIDE

MOA
SE [3]

A

Alkylating agent - causes cross-linking in DNA
Haemorrhagic cystitis, myelosuppression, transitional cell carcinoma

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3
Q

Bleomycin
MOA
SE

A

Bleomycin
MOA -degrades preformed DNA
SE- lung fibrosis

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4
Q

Anthracyclines - doxorubicin
MOA
SE

A
  • Stablilise DNA-topoisomerase II complex inhibits DNA & RNA synthesis
  • SE: cardiomyopathy
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5
Q

Antimetabolites

A
  • Methotrexate - inhibits dihydrofolate reductase and thymidylate synthesis
  • 5-FU - pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase
  • 6-mercaptopurine - purine analogue
  • Cytarabine - pyrimidine antagonist, myelosuppression
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6
Q

Acts on microtubules

Vincristine

A
  • Vincristine inhibits formation of microtubule
  • Side effects - peripheral neuropathy reversible, paralytic ileus
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7
Q

Docetaxel

A
  • Prevents microtubule depolymerisation and disassebly, decreasing free tubulin
  • Neutropaenia
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8
Q

Topoisomerase inhibitors

A
  • Irinotecan - inhibits topoisomerase I which prevents relaxation of supercoiled DNA - myelosuppression
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9
Q

Cisplatin
MOA
SE

A

MOA - causes cross linking in DNA
SE - peripheral neuropathy, hypoMg

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10
Q

What is the action of IL-1, and what are its main sources?

A

IL-1 is produced by macrophages. Its main functions include inducing acute inflammation and fever.

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11
Q

What is the action of IL-2, and what are its main sources?

A

IL-2 is produced by Th1 cells. It stimulates the growth and differentiation of T cell responses.

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12
Q

What is the action of IL-3, and what are its main sources?

A

IL-3 is produced by activated T helper cells. It stimulates the differentiation and proliferation of myeloid progenitor cells.

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13
Q

What is the action of IL-4, and what are its main sources?

A

IL-4 is produced by Th2 cells. It stimulates the proliferation and differentiation of B cells.

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14
Q

What is the action of IL-5, and what are its main sources?

A

IL-5 is produced by Th2 cells. Its main function is to stimulate the production of eosinophils.

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15
Q

What is the action of IL-6, and what are its main sources?

A

IL-6 is produced by macrophages and Th2 cells. It stimulates the differentiation of B cells and induces fever.

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16
Q

What is the action of IL-8, and what are its main sources?

A

IL-8 is produced by macrophages. It is involved in neutrophil chemotaxis.

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17
Q

What is the action of IL-10, and what are its main sources?

A

IL-10 is produced by Th2 cells. It inhibits Th1 cytokine production and is known as an ‘anti-inflammatory’ cytokine.

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18
Q

What is the action of IL-12, and what are its main sources?

A

IL-12 is produced by dendritic cells, macrophages, and B cells. It activates NK cells and stimulates the differentiation of naive T cells into Th1 cells.

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19
Q

What is the action of TNF-α, and what are its main sources?

A

TNF-α is produced by macrophages. It induces fever and neutrophil chemotaxis.

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20
Q

What is the action of IFN-γ, and what are its main sources?

A

IFN-γ is produced by Th1 cells. It activates macrophages.

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21
Q

Monitoring of hereditary angioedema

associated with low plasma levels of the C1 inhibitor

A
  • MOA - the probable mechanism behind attacks is uncontrolled release of bradykinin resulting in oedema of tissues.
  • C1-INH level is low during an attack
  • Low C2 and C4 levels are seen, even between attacks.
    Serum C4 is the most reliable and widely used screening tool
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22
Q

Hereditary angioedema
Presenation
Management acute

A

Symptoms
attacks may be proceeded by painful macular rash
painless, non-pruritic swelling of subcutaneous/submucosal tissues
may affect upper airways, skin or abdominal organs (can occasionally present as abdominal pain due to visceral oedema)
urticaria is not usually a feature

Management
acute
HAE does not respond to adrenaline, antihistamines, or glucocorticoids
IV C1-inhibitor concentrate, fresh frozen plasma (FFP) if this is not available

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23
Q

HOCM management

A

Management
* Amiodarone
* Beta-blockers or verapamil for symptoms
* Cardioverter defibrillator
* Dual chamber pacemaker
* Endocarditis prophylaxis

Drugs to avoid
* nitrates
* ACE-inhibitors
* inotropes

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24
Q

Complement deficiencies

C1 inhibitor protein deficiency

A

causes hereditary angioedema
C1-INH is a multifunctional serine protease inhibitor
probable mechanism is uncontrolled release of bradykinin resulting in oedema of tissues

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25
Q

What is c1q, c1rs, c2, c4 deficiency

A

predisposes to immune complex disease
e.g. SLE, Henoch-Schonlein Purpura

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26
Q

What does C3 complement deficiency cause?

A

Recurrent bacterial infections

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27
Q

What does C5 deficiency cause?

A

predisposes to Leiner disease
recurrent diarrhoea, wasting and seborrhoeic dermatitis

28
Q

What does C5-9 deficiency cause?

A

encodes the membrane attack complex (MAC)
particularly prone to Neisseria meningitidis infection

29
Q

Primary immunodeficiency

Neutrophil disorders (name 3)
B-cell disorders (name 3)
Name 1 T-cell genetic disorder
Name some 4 combined B- and T- cell disorders

A

Neutrophil disorders
* Chronic granulomatous disease
* Chediak-Higashi syndrome
* Leukocyte adhesion deficiency
B- cell disorders
* CVID
* Brutons congenital agammaglobulinaemia
T-cell genetic disorder
* Digeorge syndrome
Combined B-cell and T-cell disorder
* Severe combined immunodeficiency
* Ataxic telangiectasia
* Wiskott-Aldrich syndrome
* Hyper IgM syndromes

30
Q

Chronic granulomatous disease

Underlying defect
Clinical manifestation

A

Underlying defect
* Lack of NADPH oxidase reduces ability of phagocytes to produce ROS

Clinical manifestation
* Recurrent pneumonias and abscesses
* Catalase-positive staph aureus and fungi

31
Q

Chediak Higashi syndrome

Underlying defect
Clinical manifestation

A

Underlying defect
* Microtubule polymerization defect leading to decrease in phagocytosis

Clinical manifestation
* Affected children have ‘partial albinism’ and peripheral neuropathy.
* Recurrent bacterial infections are seen
Giant granules in neutrophils and platelets

32
Q

Leukocyte adhesion deficiency

Underlying defect
Clinical manifestation

A

Underlying defect
* Defect of LFA-1 integrin (CD18) protein on neutrophils

Clinical manifestation
Recurrent bacterial infections.
Delay in umbilical cord sloughing may be seen
* Absence of neutrophils/pus at sites of infection

33
Q

B-cell disorders

CVID
Underlying defect
Clinical manifestation
Increases risk of…

A

CVID
* No specific underlying genetic defect
* Low antibody levels specifically Ig types IgG, IgM, IgA
* Recurrent chest infections
* Predispose to autoimmune disorders & lymphoma

34
Q

Brutons congenital agammaglobulinemia

Underlying defect
Clinical manifestations

A

Underlying defect
* Defect in Bruton’s tyrosine kinase (BTK) gene that leads to a severe block in B cell development
Clinical manifestations
* X-linked recessive.
* Recurrent bacterial infections are seen
* Absence of B-cells with reduced immunoglogulins of all classes

35
Q

Selective IgA deficiency

Underlying defect
Clinical manifestations

A

Underlying defect
* Maturation defect in B cells

Clinical manifestations
* Most common primary antibody deficiency.
* Recurrent sinus and respiratory infections
* Associated with coeliac disease and may cause false negative coeliac antibody screen
* Severe reactions to blood transfusions may occur (anti-IgA antibodies → analphylaxis)

36
Q

How does DiGeorge immunodeficiency manifest?

A

Recurrent viral or fungal diseases

37
Q

Severe combined immunodeficiency
What is the most common genetic defect?
How is it inherited?
Clinical manifestation

A

Most common due to defect in the common gamma chain, a protein used in the receptors for IL-2 and other interleukins.
X-linked disease.
Clinical manifestation
* Recurrent infections due to virus, bacteria, fungi.

38
Q

Ataxic telangiectasia

Defect
Clinical manifestation
Inheritance pattern
Features

A

Defect
* Defect in DNA repair enzymes

Inherited pattern - AR
Features
* cerebellar ataxia, telangiectasia (spider angiomas)
* recurrent chest infections
* 10% risk of developing malignancy, lymphoma or leukaemia

39
Q

Hyper IgM syndromes
Mutation
Features

A

Mutation
* CD40 gene
Features
* Infection/ pneumocystis pneumonia
* Hepatitis
* Diarrhoea

40
Q

Water deprivation test & post- DDAVP test

What is the diagnosis if
Urine osmolality after water deprivation remains <300
Post desmopressin test, the urine osmolality is >600

A

Cranial DI

41
Q

Water deprivation test & post- DDAVP test

What is the diagnosis if urine osmolality after water deprivation is <300
Post desmopressin is <300

A

Nephrogenic DI

42
Q

Water deprivation test & post- DDAVP test

What is the urine osmolality result for psychogenic polydipsia for post-water deprivation and post-desmopressin

A

Both remain >400

43
Q

Describe mitochondrial inheritance

A

Mitochondrial inheritance has the following characteristics:
* inheritance is only via the maternal line as the sperm contributes no cytoplasm to the zygote
* none of the children of an affected male will inherit the disease
* all of the children of an affected female will inherit the disease
* generally, encode rare neurological diseases
* poor genotype:phenotype correlation - within a tissue or cell there can be different mitochondrial populations - this is known as heteroplasmy

44
Q

Give 4 examples of mitochondrial inherited diseases

A
  • Lebers optic atrophy
  • MELAS -mitochondrial encephalomyopathy lactic acidosis
  • MERRF- myoclonus epilepsy with ragged-red fibres
  • Kearns- Sayre syndrome
45
Q

Psoriasis exacerbating factors

A

The following factors may exacerbate psoriasis:
* trauma
* alcohol
* drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab
* withdrawal of systemic steroids
Streptococcal infection may trigger guttate psoriasis.

46
Q

Sideroblastic anaemia

A

Sideroblastic anaemia is a condition where red cells fail to completely form haem, whose biosynthesis takes place partly in the mitochondrion. This leads to deposits of iron in the mitochondria that form a ring around the nucleus called a ring sideroblast. It may be congenital or acquired.

47
Q

Causes of sideroblastic anaemia

Congenital vs acquired

A

Congenital cause: delta-aminolevulinate synthase-2 deficiency

Acquired causes
myelodysplasia
alcohol
lead
anti-TB medications

48
Q

Sideroblastic anaemia

Investigations
FBC
Iron studies
Blood film
Blood marrow

A

full blood count
* hypochromic microcytic anaemia (more so in congenital)
* iron studies
* high ferritin
* high iron
* high transferrin saturation
blood film
* basophilic stippling of red blood cells
bone marrow
* Prussian blue staining will show ringed sideroblasts

49
Q

Haematological malignancies- genetics

t(9;22) - Philadelphia chromosome

A

CML

50
Q

Haematological malignancies- genetics

t(15;17)

A

seen in acute promyelocytic leukaemia (M3)
fusion of PML and RAR-alpha genes

51
Q

t(8;14)

A

seen in Burkitt’s lymphoma

52
Q

t(11;14)

A

Mantle cell lymphoma

53
Q

t(14;18)

A

follicular lymphoma

54
Q

Renal transplant infections

Over 50% of renal transplant patients have a significant infection within the first 12 months of having a renal transplant. Why do we test CMV serology?

A

At the time of transplant the CMV-serological status of the donor and recipient are noted. The highest risk is seen in CMV-seronegative recipients who receive a kidney from a CMV-seropositive donor. These patients are usually given antiviral prophylaxis.

55
Q

Renal transplant infections

What is the usual time frame you would expect cytomegalovirus infection in renal transplant patients and why?

A

Cytomegalovirus tend to be seen after four weeks as before this time the immune system has not been fully affected by the immunosuppressants.

56
Q

Upper zone vs Lower zone fibrosis

CHARTS

A

Acronym for causes of upper zone fibrosis:

CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

57
Q

Causes of lower zone lung fibrosis

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

58
Q

What is the purpose of measuring ABPI and the normal value

A

a ‘normal’ ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease.

59
Q

ABPI

What indicates arterial calcification?

A

Interestingly, values above 1.3 may also indicate arterial disease, in the form of **false-negative **results secondary to arterial calcification (e.g. In diabetics)

60
Q

Drug induced lupus

A

Features
* arthralgia
* myalgia
* skin (e.g. malar rash) and pulmonary involvement (e.g. pleurisy) are common

61
Q

Drug induced lupus - immunology

A
  • ANA positive in 100%, dsDNA negative
  • anti-histone antibodies are found in 80-90%
  • anti-Ro, anti-Smith positive in around 5%
62
Q

Drug induced lupus

Causes - and indicate the top two

A

Most common causes
* procainamide
* hydralazine

Less common causes
* isoniazid
* minocycline
* phenytoi

63
Q

Lateral medullary syndrome

A

PICA
Presentation
* Ipsilateral CN palsy eg facial numbness
* Contralateral body loss of pain sensation
* Nystagmus, ataxia

64
Q

Describe AICA and difference in presentation with PICA or lateral medullay syndrome

A

An anterior inferior cerebellar artery infarct would present in the same way but with the additional symptoms of a same-sided facial weakness and loss of hearing.

65
Q

Subacute combined degeneration of the spinal cord

A

dorsal column involvement
* distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
* impaired proprioception and vibration sense
lateral corticospinal tract involvement
* muscle weakness, hyperreflexia, and spasticity
* upper motor neuron signs typically develop in the legs first
* brisk knee reflexes
* absent ankle jerks
* extensor plantars
spinocerebellar tract involvement
* sensory ataxia → gait abnormalities
* positive Romberg’s sign

My MRCP (43 decks)

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