Third Flashcards
Entamoeba histolytica liver image findings suggestive of an amoebic liver abscess may demonstrate?
‘double-target’ sign, where there is central low attenuation fluid surrounded by an outer ring with high attenuation on the inside of the ring and lower attenuation on the outside
Necrotising fasciitis bacteria
Type 1, or polymicrobial
Streptococcus pyogenes , Escherichia coli and Clostridium perfringens
Familial Mediterranean Fever features and Mx
presents by the second decade.
common in Turkish, Armenian and Arabic descent.
Features - attacks typically last 1-3 days
pyrexia
abdominal pain (due to peritonitis)
pleurisy
pericarditis
arthritis
erysipeloid rash on lower limbs
Management
colchicine may help
Creutzfeldt-Jakob disease
EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
MRI: hyperintense signals in the basal ganglia and thalamus
CSF Findings in CJD is 14-3-3 protein which has a sensitivity of 95% , PPV of around 92% and NPV of around 94%.
bulging fissure sign is classical
Klebsiella pneumonia
high risk for refeeding syndrome
BMI of <16 kg/m2 and no nutritional intake for >10 days
Unintentional weight loss of more than 15% over 3-6 months
hypophosphataemia and hypokalemia
drugs causing pulmonary eosinophilia
drugs: nitrofurantoin, sulphonamides
abnormal coag for hemophilia
DIC
HUS / HIT / TTP /ITP
Von willebrand
Both normal in hemophilia
haemophilia ( same as Von willebrand) - prolonged aPTT or normal
haemophilia A (same as Von willebrand) - severely reduced factor VIII levels
Haemophilia occur due to extreme lyonization, homozygosity, mosaicism, or Turner syndrome.
X linked recessive disease as males
haemophilia B - reduced factor 9
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To distinguish between vin willebrand and Hemophilia A -
Von willebrand has prolonged bleeding time and secondly, the platelet aggregation is impaired in response to ristocetin
DIC
DIC
fibrinogen can be normal or elevated in over 50% of cases especially early on (as fibrinogen is an acute phase marker)
PROLONGED PT and APTT
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PT/APTT are usually normal in ITP, TTP, HUS and HIT
risk of developing breast and ovarian cancer by age 70 for BRCA1 and BRCA2
breast
55-65% = BRCA1
45% for BRCA2
ovarian
40% for BRCA1 a
15% for BRCA2 mutations.
cholestasis (+/- hepatitis) causing drug?
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
Cardiac failure of QRS is between 120 and 149ms without evidence of left bundle branch block
cardiac resynchronisation therapy - without defibrillator!!!
hyperventilation syndrome (HVS) needs what score in Nijmegen questionnaire
More than 23
HVS - SOB with repeated admission
Rapidly improve in hospital with nebs
And Spirometry is normal
Langerhans cell histiocytosis presentation
affects smokers 20-40 years due to proliferation of Langerhans cells (antigen presenting cells containing Birkbeck bodies on electron microscopy).
Presentation of LCH is with exertional dyspnoea and cough, spontaneous pneumothorax, clubbing and manifestation of granuloma infiltration in bones and the hypothalamus
Lymphangioleiomyomatosis (LAM) presentation
interstitial lung disease, pneumothorax or chylous pleural effusion. Lung damage is similar to emphysema with pulmonary function tests showing reduced FVC, TLCO
reticulonodular changes in the bases bilaterally
cystic changes in the lung bases with a minimal left sided pleural effusion.
immunosuppressant therapy currently being researched for use in non-small cell lung cancer?
Pembrolizumab
small cell cancer staging and tx
Early stage (T1-2a,N0,M0) - surgery
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(T1-4,N0-3,M0)
4-6 cycles cisplatin based chemotherapy carboplatin
if poor renal function/poor performance status +/- radiotherapy
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Extensive disease
6 cycles platinum based combination chemotherapy + thoracic radiotherapy if good response
how to treat hypertriglyeridemia?
fenofibrate and nicotinic acid
how to treate high ldl levels ?
statin and Evolocumab, a PCSK9 inhibitor
hiccup mx ?
Hiccup due to gastric distension may be helped by a preparation incorporating an antacid with an antiflatulent.
If this fails, metoclopramide hydrochloride by mouth or by subcutaneous or intramuscular injection can be added;
if this also fails, baclofen, or nifedipine, or chlorpromazine
haloperidol, gabapentin are also used
dexamethasone is also used, particularly if there are hepatic / cerebral lesions
type 1 diabetes BM aim
5-7 waking
4-7- before meals
5-8-after meal
Difference between duchenne and Becker
Duchenne - progressive proximal muscle weakness from 5 years
Becker muscular dystrophy- at 10 years
High cholesterol MX
Statin
Evolocumab - for high LDL
ezetimibe in cases of primary hypercholesterolaemia
What gives eruptive xanthoma?
Familial hypertriglycerdemia
Familial hypercholestrolemia - xanthoma and tendon xanthoma
intermittent claudication
sodium / urine osmolality snd plasma osmolality
Plasma osmlarity
Low < 282- true hypotonic hyponatraemia. - check volume status
Normal 282-295 - pseudohyponatraemia and should prompt you to measure proteins and lipids\
High >295- hypertonic hyponatraemia and should prompt you to check for high levels of solutes in the plasma, hyperglycaemia being the most common.
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Low- sodium (<20) in the presence of hyponatraemia suggest that the kidneys are conserving sodium. This should prompt you to consider extra-renal sodium losses (e.g. via GI tract or skin).
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Beer potomania - urine osmolarity to be <100 also serum osmolarity
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· High->20 in the presence of hyponatraemia suggests renal sodium loss
Addison’s,
primary polydipsia (urine osmolarity to be <100)
SIADH
diuretics: thiazides, loop diuretics
diuretic stage of renal failure
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
euvolaemic hyponatraemia : SIADH , HYPOTHYROIDISM AND Addison
drugs known to cause pleural effusion
nitrofurantoin, methotrexate, and amiodarone
measure the anticoagulant effect (doac)
aPTT and, if available, the thrombin time (TT)
apt will be prolonged
plasma renin for renal artery stenosis ?
high plasma renin - response to the low pressure sensed by the constricted renal artery
pathognomonic hallmark of chronic lead poisoning is
radial nerve palsy, or wrist drop, although many peripheral nerve palsies may be seen.
proximal renal tubular failure, particularly with increased excretion of phosphate and glucose and acidification of the urine
lead poisoning with a pronounced anaemia, often with dimorphic picture and reticulocytosis
Basophilia with stippling is seen and bone marrow trephine may show ring sideroblasts.
Abdominal pain, constipation, neuropsychiatric features
occupational lead poisoning testing
erythrocyte zinc protoporphyrin (ZPP) levels and delta aminolevulinic acid dehydratase (ALAD)
coupled with skeletal analysis and blood lead levels are used to test for occupational lead poisoning
ational choice for chemotherapy or post-operative related nausea
Ondansetron
suitable choice where the cause of nausea is unknown and in the last days of life
Levomepromazine is correct. This is a broad-spectrum anti-emetic - a ‘dirty drug’ targeting many receptors
what would make you not give doc to an AF patient ?
If this patient had mitral stenosis, weighed over 120kg
Angina tx
1st line: PRN GTN
2nd line: BB or CCB
3rd line (if no hypotension after 2nd line) ISMN/nicorandil
3rd line (if hypotension after 2nd line) RANOLAZINE in HR<70, IVABRADINE in HR >70
recommend the use of no more than 2 antianginals prior to consideration of reperfusion therapies
patients with complex anatomy, triple vessel disease or proximal left mainstem disease report better long-term survival and freedom from MI is greater with CABG
Nicorandil is only contraindicated in LV failure and cardiogenic shock
Ranolazine - contra in severe kidney disease liver dysfunction, an absolute contraindication
riteria for a treatment break for bone protection ?
her age (< 75 years),
femoral neck/ hip bone mineral density > -2.5
lack of history of fragility fracture
no Previous history of hip or vertebral fracture
not Taking oral glucocorticoids ≥7.5mg prednisolone/day or equivalent
Allpatients on bisphosphonate treatment for ≥10 years should be reviewed
repeat DEXA scan is recommended after two years or in the event of fragility fracture
Tx break after 3-5 years on bisphosoabte of low risk t score more than 2.5
MPO and pr3 association antibodies
MPO antibodies - churg
pr3 positive Wegener’s granulomatosis
Microscopic polyangiitis is a small-vessel ANCA vasculitis.
pANCA (against MPO) - positive in 50-75%
cANCA (against PR3) - positive in 40%
RAAS system for different disease
High Renin+ Aldosterone= RAS
Low Renin+ HIGH Aldosterone= conn syndrome
Low Renin + low Aldosterone= Liddile syndrome
high aldosterone, high renin, normotension, low K = bartter syndrome
High renin and low aldosterone - gitleman syndrome
what can trigger bullous pemphigoid ?
Furosemide
C captopril derivative
P penicillin & penicillamine derivatives
S sulfasalazine
primary pulmonary hypertension causes
primary
hiv
apetite suppressant - fenfluramine
connective tissue disease
vasculitis
secondary
thromboembolic
Surgery for aortic regurgitation is indicated if
significant enlargement of the ascending aorta
severe regurgitation with symptoms
asymptomatic patients with severe AR who have LV systolic dysfunction ejection fraction of less than 50%
surgery in MR indication
EF < 60%
2. Left ventricular end systolic diameter > 40mm
3. New onset of AF or pulmonary hypertension
4. High likelihood of durable repair with low surgical risk and absence of risk factors
indication for surgery in parathyridectomy ?
Symptoms of hypercalcaemia
b. Osteoporosis and/or fragility fractures
c. Renal stones or nephrocalcinosis
2. Age <50 years
3. Serum adjusted calcium of 2.85 mmol/L or above
4. Estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m²
patients admitted within three days of an acute stroke should have
intermittent pneumatic compression
LMWH - has a high chance of covering to hemorrhagic stroke
Evan’s syndrome is
immune thrombocytopenic purpura (ITP) and autoimmune haemolytic anaemia (AIHA).
The body’s immune system mistakenly targets and destroys platelets and red blood cells leading to symptoms of both thrombocytopenia such as easy bruising, petechiae, and bleeding, as well as symptoms of haemolytic anaemia like fatigue, pallor and jaundice.
Diagnosis is typically based on the presence of these two conditions with a positive Direct Coombs Test (DCT) confirming AIHA
Glanzmann Thrombasthenia
defective platelet aggregation due to a deficiency or dysfunction of the glycoprotein IIb/IIIa
causing mucocutaneous bleeding such as epistaxis, menorrhagia or gum bleeding.
confirmed by flow cytometry showing GPIIb/IIIa negativity
or Platelet Aggregation Tests using ADP, collagen or adrenaline which show abnormal results
while ristocetin-induced agglutination remains normal.
Bernard-Soulier Disease
deficiency or dysfunction in the glycoprotein Ib-IX-V complex
prolonged bleeding time despite having normal platelet count but larger than average size (macrothrombocytes).
Diagnosis can be confirmed by flow cytometry showing GPIb/IX negativity
Platelet Aggregation Test showing decreased agglutination with ristocetin.
Paroxysmal nocturnal haemoglobinuria
haemolytic anaemia
pancytopaenia may be present
haemoglobinuria: classically dark-coloured urine in the morning (although has been shown to occur throughout the day)
thrombosis e.g. Budd-Chiari syndrome
aplastic anaemia may develop in some patients
Diagnosis
flow cytometry of blood to detect low levels of CD59 and CD55
tx
blood product replacement
anticoagulation
eculizumab
stem cell transplantation
AIP
Acute intermittent porphyria
Acute intermittent porphyria (AIP) defect in porphobilinogen deaminase,
abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common
classically urine turns deep red on standing
Diagnosis
raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
assay of red cells for porphobilinogen deaminase
raised serum levels of delta aminolaevulinic acid and porphobilinogen
Management
avoiding triggers
acute attacks
IV haematin/haem arginate
IV glucose should be used if haematin/haem arginate is not immediately available
chronic demyelinating polyneuropathy
motor and sensory involvement
multifocal motor neuropathy with conduction block
immune-mediated disorder, commonly associated with anti-GM1 antibodies
multifocal areas of demyelination and motor block, with f waves and H-reflexes
Anti-GM1b are antibodies typically present
without sensory or bulbar involvement
pure motor peripheral neuropathy
respond well to intravenous immunoglobulin.
differentiate MND from multifocal motor neuropathy with conduction block
does not have nerve block ,
typically nerve conduction normal
how to differentiate haemophilia A from von willebrand
von willebrand - prolonged bleeding time
platelet aggregation is impaired in response to ristocetin
