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CSIM > Questions > Flashcards

Questions Flashcards

1
Q

Periductal onionskin fibrosis

A

PSC

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2
Q

Gietlmans

A

Na+Cl- channel leads to hypocalciuria, metabolic alkalosis, hypokalemia and hypomagnesaemia

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3
Q

Subclinical hyperthyroidism

A

Normal T4, low TSH

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4
Q

RET gene

A

Failure activation in utero = Hirschprungs

Failure of inactivation post-natally = MEN2

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5
Q

Tear drop polkilocytes

A

Myelofibrosis

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6
Q

Hereditary spherocytosis

A

Recurrent haemolysis, splenomegaly, raised reticulocytes and spherocytes on blood film.

Osmotic fragility test = diagnostic

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7
Q

Occupational asthma and IgE

A

Low molecule weight antigens often reactive chemical such as isocyanates, acids and paints.

High molecular weight antigens are usually organise products such as proteins or animal fur have specific IgE

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8
Q

Atypical nephrotic syndrome

A 
Age <1 or >11
Elevated creatinine
Macroscopic hematuria
Hypertension
Positive FH of nephrotic syndrome

Requires investigation with renal biopsy before treatment

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9
Q

Di George

A

Presents in many different ways so diagnosis can be difficult

Heart (Outflow tract) defects, hypocalcaemia, immunodeficiency
Velocardiofacial syndrome
Cleft palate/velopharyngeal insufficiency, heart defect, dysmorphic face
Nonspecific learning diffs/short stature
Increased tendency to psychiatric illness

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10
Q

Sarcoidosis and calcium

A

Hypercalcaemia occurs in sarcoidosis commonly due to increased intestinal calcium absorption due to high blood concentrations of 1,25-dihyodroxyvitamin D. This is due to the very large number of macrophages present in a granulomatous disease such as sarcoid which catalyse the production of activated vitamin D independent to PTH. It normally takes place in the kidney.

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11
Q

Brugada ECG and which channel

A

Sodium channel mutation; RBBB + coved ST elevation in leads V1–V3

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12
Q

CPVT

A

Calcium channel mutation; life threatening Ventricular Tachycardia (VT) or Ventricular Fibrillation (VF) during emotional or physical stress, bidirectional and polymorphic tachycardias

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13
Q

ARVT

A

Small positive deflection at end of QRS complex (epsilon waves)

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14
Q

Long QT

A

Potassium channel mutation; polymorphic ventricular tachycardia (torsades de pointes)

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15
Q

Broncholitis obliteratans

A

Bronchiolitis obliterans, also called obliterative bronchiolitis, and constrictive bronchiolitis,] is a rare and life-threatening form of non-reversible obstructive lung disease in which the bronchioles (small airway branches) are compressed and narrowed by fibrosis (scar tissue) and/or inflammation.
Inflammation and scarring occur in the airways of the lung, resulting in severe shortness of breath and dry cough.

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16
Q

Which cytogenetic method is unable to dectect balanced robertsonian translocations

A

Array-CGH. Detects gain or loss

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17
Q

Cirrhosis screening

A

Screen for oesophageal varices at diagnosis and every 2 years
Screen 6 monthly with USS and alpha-FP for HCC

18
Q

Hypo echoic lesion discovery

A

<1cm = 4 monthly USS and aFP

> 1cm = CT or contrast MRI

19
Q

Lung cancer >5cm

A

All tumour >5cm and >3nodes should be staged and should have CXR, US, Bone Scan!

20
Q

Cutaneous paraneoplastic

A

Both conditions starts approximately the same time and follow a parallel course
a specific tumour occurs with a specific skin manifestation
the dermatosis is not common in the general population
a high percentage of association between the two conditions is noted

21
Q

Presence of Cushings

A

24hr urinay free, late night salivary cortisol, low one dexamethasone

22
Q

Finding the cause of Cushings

A

High dose dexamethasone suppression
Plasma ACTH
MRI head
CT chest and abdo

23
Q

Haemolytic anaemia

A

High LDH due to cell destruction, high reticulocyte count as BM tries to replace lost RBC
Low haptoglobin - protein that binds free haemoglobin
Blood film = spherocytes

24
Q

Differentiating between dermatomyositis and polymyositis on biopsy

A

Polymyositis infiltrate contains mainly CD8 + T cells and Dermatomyositis contains CD4 + T cells

25
Q

Lysosomal storage disorders enzyme deficiency

A

Gaucher’s disease- Deficiency in beta-glucosidase/glucererosidase leads to accumulation of glucocerebroside in cells as unable to breakdown ganglioside/globoside

Niemann-Pick disease- Deficiency in sphyingomyelinase leads to inability to break down sphyingomyelin. Type A- neurological disorders, Type B-Organomegaly

Tay-Sachs disease- Deficiency in hexosaminisidase A leads to G2-ganglioside accumulation

26
Q

Iron absorption

A

HCP1 is the receptor in which haem is absorbed into the enterocytes
DMT1 is the receptor for Fe2+
ferroportin is to export Fe2+ from cells to the circulation
FLVCR1 is to export haem from the cells to the circulation

27
Q

Immunoassay microarray

A

HLA

28
Q

Malignant vs non malignant ascites

A

In malignant ascites the treatment is usually paracentesis as sodium (and fluid) retention is not the cause. Therefore the diuretics would not be helpful.

In non-malignant ascites the first line treatment is salt and fluid restriction followed by a combination therapy of furosemide and spironolactone.

29
Q

Hypomagnesemia and hypocalcemia

A

Very low magnesium blocks the PTH receptor preventing the ability of PTH to raise Ca2+ levels

Low magnesium stimulates the PTH receptor

30
Q

Recombinant human growth hormone treatment is recommended for the treatment of adults only if:

A

They have severe GH deficiency, defined during an insulin tolerance test or a cross-validated GH threshold in an equivalent test.

They have a perceived impairment of quality of life (Sx include depression, reduced strength, reduced energy and abdominal fat)
They are already receiving treatment for any other pituitary hormone deficiencies

Short stature would not be modifiable in adults with recombinant GH due to growth plate fusion, it is a big indication in childhood GH deficiency.

31
Q

T cell tolerance vs B cell tolerance

A

T-cell
central tolerance - @thymus - positive and negative selection
peripheral tolerance - @secondary lymphoid tissue - 4 mechanisms (suppression by Treg, deletion by Fas, anergy by absence of costimulatory signal, and immune privilege site for example eye.

B-cell
central tolerance - @bone marrow - 1. deletion (of high affinity or strong binding) antigen recognition - which also called negative selection but this happens in BM and not in thymus. 2. Receptor editing (to make it no longer self reactive)
peripheral tolerance - 1. with the help of helper T cells (as T cells underwent tolerance process earlier, so most of the cells now are ‘acceptable’ to the whole system. And as helper T cells help in the tolerance of B cells, the normal helper T cells will help development of normal B cells too. The two cells are interrelated!). 2. Anergy - downregulation of IgM

32
Q

Pagets disease

A

Bone pain, deformity at extremities, seen in old age. Can = enlarged skull and deafness if compression of CNVIII

Can have cardiovascular, neurological and kidney stones

Progressive disease of excessive turnover. Excessive osteoclast activity with low osteoblast activity leads to deformed bones

High ALP, normal levels of PTH, Ca2+

33
Q

Drug induced Pulmonary fibrosis

A

Amiodarone, bleomycin, methotrexate, amiodarone, nitrofurantoin, sulfazalazine

34
Q

Indications for LTOT

A

Polycythemia, PaO2 <7.3, signs of RHF

35
Q

Mx COPD

A

FEV1 >50% = LABA/LAMA

FEV1 <50% = LAMA / LABA + ICS

36
Q

PC HUS

A

Renal failure, thrombocytopenia and micorangipoathic haemolytic anaemia

37
Q

Medications that cause gum hypertrophy

A

Nifedipine, phenytoin, ciclosporin

38
Q

Hyperprolactinemia

A 
Prolactinoma, High TSH - hypothyroidism 
dopamine antagonist (dopamine inhibits prolactin)
39
Q

Nelsons syndrome

A

Bilateral adrenalectomy leads to huge enlargement of pituitary (macro adenoma) due to increased ACTH.

PC headaches, tunnel vision

40
Q

Response to desmopressin

A

Confirmed cranio DI

41
Q

Synacthen test

A

Short = no increase in cortisol destruction of adrenal i.e. Addison Primary adrenal failure

Small or large increase in secondary. May need a long to confirm

42
Q

Budd Chiari

A

Thrombosis in the hepatic vein. Triad of abdo pain, ascites and liver enlargement

1 - Polycythemia, COCP, pregnancy, coagulation disorders, SLE

2 - Extrinsic compression of hepatic vein - HCC

CSIM (12 decks)

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