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22 Cards in this Set
- Front
- Back
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What are 3 bacteria to look for in CSF?
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Neisseria menigitidis, strep pneumoniae, Hib
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What is the formula to calculate plasma osmolality?
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Osmolarity = 2 Na + glucose + urea
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Formula to calculate plasma ormolarity corrected to body weight?
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Osmolarity = 0.55 (assumption of body fluid ratio, 55% or 60%) x weight (kg) x normal body osmolarity (285 mOsm)
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What are the differences of clinical presentation between UMN lesion with LMN lesion?
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UMN:
- No muscle wasting - Hypertonicity - Hyperreflexia - spasticity - Clasp -knife response LMN lesion - Muscle wasting - Hypotonicity - Hyporeflexia - Paralysis |
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Describe the attachment and mechanism of injury of the ACL and MCL
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ACL
o ATTACHMENTS– From the intercondylar area of the upper surface of the tibia (in between the anterior ends of the menisci) and pass posteriorly, laterally and upwards to the posteromedial surface of the lateral femoral condyle o FUNCTION = Prevents anterior translation of the tibia on a fixed femur and helps control medial rotation MCL o ATTACHMENTS – From the medial tibia just below the level of the articular cartilage to the medial femoral condyle. There is a deep component which has fibres that attach to the medial meniscus and blend into the posterior capsule. o FUNCTION = Helps prevent excessive valgus force of the knee. |
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What would you look for in examination for ACL and MCL tears?
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Look - gait
Feel - swelling (effusion), medial joint line for medial meniscus tear (MCL) Move - restriction in both flexion and extension and also catching or locking. Restricted strength due to pain Special tests: ACL tear - Lachmans test and anterior drawer test Valgus stress test - MCL McMurrays - medial meniscus, associated with MCL tear |
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How do you reverse bleeding due to heparin overdose?
Why not plasma? |
Protamine, +ve ly charged protein which binds to -vely charged heparin.
Heparin works by binding to AT III, plasma has AT III so it will lead to potentiation rather than reversal. |
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What are required in medicalisation?
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ADAPT
A current preoccupation Diagnosis,a method Authority voice Plausability, biological Treatment |
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Graph of hearing loss – Similar in R and L ears particularly low at high frequency sounds. Which patient is it most likely from?
a) Man who suffered hearing loss after gun going off near right ear b) Elderly lady who can no longer hear her husband speaking c) Older man who has suffered hearing loss due to occupational exposure and says that he cant hear the bats at night anymore |
C.
mainly because bilateral hearing loss tends to be due to exposure i.e work or constant earphone use (??didn't Stricker said that high frequency is normally due to gun shot? but in this case it s bilateral,so work is likely) |
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What are the acute complications of blood transfusions?
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IMMUNOLOGICAL
o Acute haemolytic transfusion reaction o Febrile non haemolytic reaction - mild temp o Allergic reaction o Anaphylaxis o Transfusion related Acute Lung Injury (TRALI) NON IMMUNOLOGICAL o Bacterial contamination o Circulatory overload o Non immune hemolysis |
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How do you manage acute transfusion reaction?
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o Stop the transfusion
o Maintain the IV access o Maintain BP (if required) IV crystalloid Adrenaline for anaphylaxis if required o Monitor and maintain O2 and urine output Diuretic Supplementary O2 o Order appropriate lab tests o Initiate the appropriate clerical work/blood bank process o Antibiotics if infection is suscpected o Corticosteroid is suspect TRALI |
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What are the pathological markers of Alzheimers disease in the brain?
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Neurofibrillary tangles and senile plaques.
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In which part of the brain do neurofibrillar tangles accumulate in Alzheimer's?
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In all parts but particularly the hippocampus
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What are neurofibrillary tangles?
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Tangles aggregate inside neurons & are formed from hyperphosphorylated proteins associated with microtubules (called tau).
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What are the principal interneurons of the neocortex?
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Stellate cells
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What is the supporting cells (non neuronal cells) of the CNS called? What are they and what are their functions?
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Neuroglia, include:
- Astrocytes: control contraction of BV (control BBB), clear excess NT, supporting cells - Microglia: macrophages of the CNS - Ependymal cells: lining the cerebral aqueduct, specialised to secrete CSF. - Oligodendrocytes: wrap around neuron to produce myelin sheath. |
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What are the 3 types of prevention?
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Primary prevention: prevention before it happens by controlling risk factors.
Secondary prevention: preventing progression, further episodes by early diagnosis, diagnosing non symptomatic people, and prompt treatment Tertiary prevention: preventing complications/disability by treatment. |
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Describe the principles of radiotherapy.
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4Rs.
Repair - In the cells that don’t die, the repair process is impaired in cancerous cells compared with normal cells. Repopulation – in breaks between treatments, the population doubling time halves (as more cells move into mitosis) Redistribution - non replicating cells in the population of cancerous cells are redistributed to the mitotic stage of cell cycle, where they are more radiosensitive. Re-oxygenation – oxygen binds to damaged DNA and ‘fixes it’ – note: fix is not repair, but rather makes the damage permanent ->more vascularised cancer cells are more affected. |
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Briefly describe the different seizure types. What are the clinical features?
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1. Partial - focal/regional cortical abnormality causing a local imbalance between excitation and inhibition.
Clinical features: preserved consciousness, 2. Generalised -seizure that involves entire cortex right from the onset. Clinical features: loss of consciousness at the time of onset. Special generalised: absence seizures, primary general tonic-clonic, myoclonic seizures. 3.Mix |
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What viruses are linked to cancer? Name the virus and cancer type.
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HIV - Kaposi's sarcoma
HPV - cervical cancer Epstein-Barr Virus - Burkitt's lymphoma Hepdnavirus (HepB) & Flavivirus (Hep C) - hepatic carcinoma |
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Describe the pathway of the auditory nerve.
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Auditroy nerve -> ipsilateral cochlear nucleus -> contralateral olivary nucleus -> lateral lemniscus -> inferior colliculus -> medial geniculate nucleus -> internal capsule -> primary audition area (contralateral) - Brodman's 41 & 42
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Describe the process of primary haemostatic plug formation.
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1. Adhesion - endothelial injury exposes the underlying subendothelial matrix. Platelet GP Ib/IX/V adherence to matrix vWF.
2. Activation - Adhesion triggers GP IIb/IIIa exposure/activation. GP IIb/IIIa is irreversibly bind to subendothelial matrix. This leads to shape change (spherical), spreading and granule secretion (Ca2+, ADP, TX A2-> vasoconstrictor and platelet activator). 3. AggregationActivated GPIIb-IIIa mediates aggregation via fibrinogen and vWF. Release of granules recruits more platelets (ADP, TXA2) and coagulation cascade activation (Ca2+) Local activation of the coagulation cascade results in fibrin polymerisation, which "cements" the platelets into a definitive hemostatic plug. |
