Day 8 Flashcards

1
Q

Newly diagnosed patient with hypertension (>55 years)-

on atenolol & aspirin. what medication can be added for BP?

A

CCB

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2
Q

What would you expect to find in a water deprivation test of a patient with nephrogenic DI

A

> urine osmolality after fluid deprivation: low

>urine osmolality after desmopressin: low

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3
Q

Normal urine osmolality

A

wide range between 50 and 1200 mOsm/kg

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4
Q

A rise in urine osmolality to >___ mOsm/kg is a normal response to dehydration.

A

700

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5
Q

Side effect of lithium

A

nephrogenic DI

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6
Q

risk factors for cranial DI

A

recent surgery
head injury
signs of pituitary tumour

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7
Q

how is the water deprivation test performed?

A

Method
prevent patient drinking water
ask the patient to empty their bladder
hourly urine and plasma osmolalities

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8
Q

Normal water deprivation test results

A

Starting plasma osm. : normal
Final urine osm: >600
Urine osm. post-DDAVP: >600

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9
Q

Psychogenic polydipsia water deprivation test results

A

Starting plasma osm. : low
Final urine osm: >400
Urine osm. post-DDAVP: >400

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10
Q

Cranial diabetes insipidus water deprivation test results

A

Starting plasma osm: high Final urine osm: <300

Urine osm. post-DDAVP: >600

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11
Q

nephrogenic diabetes insipidus water deprivation test results

A

Starting plasma osm: high Final urine osm: <300

Urine osm. post-DDAVP: <300

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12
Q

What is hodgkins lymphoma

A

malignant proliferation of lymphocytes characterised by presence of reed-stenberg cell

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13
Q

What is the age distribution of hodgkins lymphoma

A

bimodal age

3rd and 7th decades

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14
Q

What are the types of hodgkins?

A

Nodular sclerosing
Mixed cellularity
Lymphocyte predominant
Lymphocyte depleted

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15
Q

What is nodular sclerosing HL associated with

A

good prognosis
common in women
associated with lacunar cells

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16
Q

What is mixed cell HL associated with

A

good prognosis

large number reed-steenberg cells

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17
Q

HL subtypes in order of descending frequency

A

Nodular sclerosing
Mixed Cellularity
Lymphocyte predominant
Lymphocyte depleted

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18
Q

Which HL has the best prognosis

A

lymphocyte predominant

lymphocyte depleted

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19
Q

what are ‘b’ symptoms

A
  • weight loss >10% in last 6 months
  • fever >38
  • night sweats
20
Q

Factors associated with poor prognosis

A
  • age > 45 years
  • stage IV disease
  • haemoglobin < 10.5 g/dl
  • lymphocyte count < 600/µl or < 8%
  • male
  • albumin < 40 g/l
  • white blood count > 15,000/µl
21
Q

Complications of MI

A
> cardiac arrest 
> cardiogenic shock
> chronic HF
> Tachyarrhythmia : VF
> bradyarrhythmias : AV block
> pericarditis 
> left ventricular aneurysms
> left ventricular free wall rupture
> ventricular septal defect
> acute mitral regurgitation
22
Q

when does pericarditis occur post-MI

A

first 48 hours following a transmural MI is common

23
Q

When does dressler syndrome occur

A

2-6 weeks after MI

24
Q

what causes dresslers syndrome?

A

autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

25
Q

when would left ventricular free wall rupture occur after MI

A

1-2 weeks after

26
Q

what would you see in acute mitral regurgitation

A

acute hypotension and pulmonary oedema

early-to-med systolic murmur

27
Q

how is acute mitral regurg treated

A

vasodilator threrapy

surgical repair

28
Q

How is torsades de pointes treated?

A

Treat torsade de pointes VT immediately by stopping all drugs known to prolong the QT interval.

Do not give amiodarone for definite torsade de pointes.

Correct electrolyte abnormalities, especially hypokalaemia.

Give magnesium sulfate 2 g IV over 10 min (= 8 mmol, 4 mL of 50% magnesium sulfate).

29
Q

Treatment for chlamydia

A

doxycycline 7 day course

if pregnant then azithromycin, erythromycin or amoxicillin may be used

30
Q

How common is ALL

A

most common malignancy affecting children and accounts for 80% of childhood leukaemias

31
Q

What are the features of ALL

A

bone marrow failure

> anaemia: lethargy and pallor
neutropaenia: frequent or severe infections
thrombocytopenia: easy bruising, petechiae

And other features
>bone pain (secondary to bone marrow infiltration)
>splenomegaly
>hepatomegaly
>fever is present in up to 50% of new cases (representing infection or constitutional symptom)
testicular swelling

32
Q

Types of ALL

A

common ALL, CD10 present, pre-B phenotype
t-cell ALL
b-cell ALL

33
Q

What are the poor prognostic factors of ALL

A
  • age < 2 years or > 10 years
  • WBC > 20 * 109/l at diagnosis
  • T or B cell surface markers
  • non-Caucasian
  • male sex
34
Q

How are infantile spasms characteristed

A

repeated flexion of head/arms/trunk followed by extension of arms (sallam attacks)
up to 50 times

poor prognosis

35
Q

when does west syndrome present?

A

first 4 to 8 months

36
Q

management of west syndrome

A

poor prognosis
vigabatrin is now considered first-line therapy
ACTH is also used

37
Q

What is IgA nephropathy

A

commonest cause of glomerulonephritis worldwide. It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.

38
Q

What is associated with berger’s disease

A
  • alcoholic cirrhosis
  • coeliac disease/dermatitis herpetiformis
  • Henoch-Schonlein purpura
39
Q

Pathophysiology of IgA nephropathy

A

> mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

40
Q

presentation of IgA

A

> young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients

41
Q

How to differentiate between IgA nephropathy and post-streptococcal glomerulonephritis

A

> post-streptococcal glomerulonephritis is associated with low complement levels
main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis

42
Q

management of berger’s

A

steroids/immunosuppressants not be shown to be useful

43
Q

Prognosis of bergers

A

> 25% of patients develop ESRF
markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

44
Q

what are the features of COA

A
> infancy: heart failure
> adult: hypertension
> radio-femoral delay
> mid systolic murmur, maximal over back
> apical click from the aortic valve
> notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
45
Q

Associations of COA

A

> Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

46
Q

What are contraindications to IUD

A

PID

47
Q

Poorly controlled hypertension, already taking a calcium channel blocker

A

add an ACE inhibitor or an angiotensin receptor blocker or a thiazide-like diuretic