Day 8 Flashcards
Newly diagnosed patient with hypertension (>55 years)-
on atenolol & aspirin. what medication can be added for BP?
CCB
What would you expect to find in a water deprivation test of a patient with nephrogenic DI
> urine osmolality after fluid deprivation: low
>urine osmolality after desmopressin: low
Normal urine osmolality
wide range between 50 and 1200 mOsm/kg
A rise in urine osmolality to >___ mOsm/kg is a normal response to dehydration.
700
Side effect of lithium
nephrogenic DI
risk factors for cranial DI
recent surgery
head injury
signs of pituitary tumour
how is the water deprivation test performed?
Method
prevent patient drinking water
ask the patient to empty their bladder
hourly urine and plasma osmolalities
Normal water deprivation test results
Starting plasma osm. : normal
Final urine osm: >600
Urine osm. post-DDAVP: >600
Psychogenic polydipsia water deprivation test results
Starting plasma osm. : low
Final urine osm: >400
Urine osm. post-DDAVP: >400
Cranial diabetes insipidus water deprivation test results
Starting plasma osm: high Final urine osm: <300
Urine osm. post-DDAVP: >600
nephrogenic diabetes insipidus water deprivation test results
Starting plasma osm: high Final urine osm: <300
Urine osm. post-DDAVP: <300
What is hodgkins lymphoma
malignant proliferation of lymphocytes characterised by presence of reed-stenberg cell
What is the age distribution of hodgkins lymphoma
bimodal age
3rd and 7th decades
What are the types of hodgkins?
Nodular sclerosing
Mixed cellularity
Lymphocyte predominant
Lymphocyte depleted
What is nodular sclerosing HL associated with
good prognosis
common in women
associated with lacunar cells
What is mixed cell HL associated with
good prognosis
large number reed-steenberg cells
HL subtypes in order of descending frequency
Nodular sclerosing
Mixed Cellularity
Lymphocyte predominant
Lymphocyte depleted
Which HL has the best prognosis
lymphocyte predominant
lymphocyte depleted
what are ‘b’ symptoms
- weight loss >10% in last 6 months
- fever >38
- night sweats
Factors associated with poor prognosis
- 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
Complications of MI
> 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
when does pericarditis occur post-MI
first 48 hours following a transmural MI is common
When does dressler syndrome occur
2-6 weeks after MI
what causes dresslers syndrome?
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.
when would left ventricular free wall rupture occur after MI
1-2 weeks after
what would you see in acute mitral regurgitation
acute hypotension and pulmonary oedema
early-to-med systolic murmur
how is acute mitral regurg treated
vasodilator threrapy
surgical repair
How is torsades de pointes treated?
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).
Treatment for chlamydia
doxycycline 7 day course
if pregnant then azithromycin, erythromycin or amoxicillin may be used
How common is ALL
most common malignancy affecting children and accounts for 80% of childhood leukaemias
What are the features of ALL
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
Types of ALL
common ALL, CD10 present, pre-B phenotype
t-cell ALL
b-cell ALL
What are the poor prognostic factors of ALL
- age < 2 years or > 10 years
- WBC > 20 * 109/l at diagnosis
- T or B cell surface markers
- non-Caucasian
- male sex
How are infantile spasms characteristed
repeated flexion of head/arms/trunk followed by extension of arms (sallam attacks)
up to 50 times
poor prognosis
when does west syndrome present?
first 4 to 8 months
management of west syndrome
poor prognosis
vigabatrin is now considered first-line therapy
ACTH is also used
What is IgA nephropathy
commonest cause of glomerulonephritis worldwide. It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.
What is associated with berger’s disease
- alcoholic cirrhosis
- coeliac disease/dermatitis herpetiformis
- Henoch-Schonlein purpura
Pathophysiology of IgA nephropathy
> mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3
presentation of IgA
> 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
How to differentiate between IgA nephropathy and post-streptococcal glomerulonephritis
> 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
management of berger’s
steroids/immunosuppressants not be shown to be useful
Prognosis of bergers
> 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
what are the features of COA
> 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
Associations of COA
> Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
What are contraindications to IUD
PID
Poorly controlled hypertension, already taking a calcium channel blocker
add an ACE inhibitor or an angiotensin receptor blocker or a thiazide-like diuretic
