Neurology and microbiology and haematology Flashcards

1
Q

Label the constituent portions of the cerebral cortex

A

Frontal - Contains motor cortex (anterior to central sulcus). Also has large influence on all executive control. Contains Brocas area for speech.

Parietal - Contains main somatosensory area. Also involved in calculation and the non-dominant lobe is responsible for spatial awareness and positioning.

Occipital - Mainly involved in vision

Temporal - Contains Werneckes area superiorly. Involved in emotion, memory, olfaction and auditory capabilities.

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2
Q

Describe the syndromes that would arise from a lesion in cerebral hemispheres

A

Focal neurological deficits:
Damage to the Premotor cortex would result in apraxia (inability to execute movements)
Damage to Temporal lobe could result in amnesia.
Damage to the language area may give aphasia or dysphasia.
Damage to parietotemporal cortex will give agnosia (inability to recognise).

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3
Q

Describe the syndromes that would arise from a lesion in brainstem

A

Depends on where the lesion is:
May result in Problems with sleep/wake cycle, balance, cardioresp control os reticular formation affected.
If cerebellar communicants affected then cerebellar symptoms will persist.
Cranial nerves may also be affected

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4
Q

Describe the syndromes that would arise from a lesion in the cerebellum

A
Dysdiadochokineses
Ataxia
Nystagmus
Intention tremor
Slurred speech (dysarthria)
Hypotonia

IPSILATERAL

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5
Q

Describe the syndromes that would arise from a lesion in the basal ganglia

A
Parkinsons - 
Tremor
Rigidity
Akinesia
Postural instability

Huntingtons:
Dyskinesia
Chorea
Athetosis (serpentine twisting)

Tourette’s:
Tics

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6
Q

Name the location of the causative lesion in homonymous hemianopia

A

Lesion from optic radiation to the visual cortex

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7
Q

Name the location of the causative lesion in bitemporal hemianopia

A

Optic chiasm

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8
Q

Describe the clinical difference between upper and lower motor neuron facial weakness

A

The forehead is spared in an unilateral UMN lesion to CNVII.

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9
Q

Describe the clinical difference between upper and lower motor neuron limb weakness, with specific reference to findings on inspection, tone, deep tendon reflexes and pattern of weakness.

A
UMN: 
Decreased power, (weakness in extensors - upper limbs and flexors - lower limbs = pyramidal weakness. strength in antigravity muscles)
increased tone, 
increased reflexes
No wasting
Spaticity (clasp knife)
Extensor plantar response
Loss of abdominal reflexes
LMN
Decreased power
Decreased tone
Decreased reflexes
Wasting
plegia and paresis of specific muscles.
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10
Q

Describe the clinical syndrome that would arise from C5 lesion

A

Sensory loss to lateral part of arm
Loss of biceps reflex
Motor loss: Shoulder abduction and elbow flexion

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11
Q

Describe the clinical syndrome that would arise from median nerve lesion

A

Sensory loss to palmar side of first 3.5 digits - paraesthesia
Motor loss: Wasting of pollicis brevis.
Patient wakes up at night with pain/paraesthesia radiating down forearm into hand. Relieved by hanging arm down.
RFs: RA, pregnancy, hypo T4, obesity, acro, dialysis

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12
Q

Describe the clinical syndrome that would arise from an ulnar nerve lesion

A

Sensory loss to median 1.5 digits

Wasting of hypothenar muscles, interossei, medial 2 lumbricals.

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13
Q

Describe the clinical syndrome that would arise from a radial nerve lesion

A

Sensory loss to the dorsum of the hand
Motor loss to brachoradialis and finger extensors
Compression of nerve against humerus leads to wrist drop.

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14
Q

Describe the clinical syndrome that would arise from a S1 nerve root lesion.

A

Sensory loss to posterior of calf and lateral border of foot.
Loss of ankle reflex.
Loss of plantar flexion.
Sudden onset during lifting/bending/twisting.

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15
Q

Define cerebrovascular disease with specific reference to time course

A

Stroke - Loss of cerebral function lasting >24 hours or leading to death, with no other cause than a vascular one.
TIA - A focal neurological deficit lasting seconds to 24hrs, with complete recovery.
Amaurosis fugax - Temporal loss of vision in one eye prior to a carotid system TIA.

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16
Q

List the irreversible 8 and reversible 10 risk factors leading toward the development of stroke

A

Reversible: Cholesterol, obesity, T2DM, hypertension, smoking, carotid stenosis, sleep apnoea, endocarditis, neurosyphilis, COX-2 inhibitors.

Irreversible: Age, gender, SLE, AF, thrombohilia/hyperviscosity, amyloidosis, hyperhomocysteinaemia, migraine

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17
Q

Describe the pathological causes and consequences of ischaemic stroke

A

Caused by local arterial disease. Rupture of atheromatous plaque, eventually causing ischaemia of the effected area. Emboli from the heart common -
AF. Unlikely to be cause by stenosis - Although a slight drop in BP can result in watershed effect.

Initially little evidence of infarction. 24 hrs after onset, boundary between white and grey matter become blurred. Eventually necrotic material begins to organise and macrophages infiltrate and oedema lessens. Eventually ischaemic area shrinks and ventricle enlarges to fill area.

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18
Q

Describe the pathological causes and consequences of haemorrhagic stroke.

A

Most commonly occurs in hypertensive patients.
Microaneursyms develop and when they rupture blood is released which eventually may form a haemotoma (often in MCA branches to BG, pons and cerebellum) if death does not ensue.

Headach - increased ICP - death. Result is a cyst, containing yellow-brown fluid, walled by glia.

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19
Q

Describe how atrial fibrillation gives rise to stroke

A

Blood is turbulent and relatively static in the atria giving rise to thrombus formation. 80% of strokes are due to thromboemboli and 70% of TIAs.

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20
Q

Describe the clinical presentation of a subarachnoid haemorrhage, with specific reference to features in the history and examination including the rate of onset of symptoms, and signs arising from the event.

A
Sudden onset of a thunderclap headache, followed by nausea and vomiting. 
Coma and death may then follow.
Other signs and symptoms:
Neck stiffness
Positive Kernigs sign
Pappiloedema
Photosensitivity
Brudzinskis signs: flexion of the elbow in response to pressure to the cheek; flexion of the hip in response to flexion of the neck, and abduction and flexion of the hip in response to pubic symphysis pressure.
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21
Q

Describe the clinical features of meningism

A

Neck stiffness
Headache
Photophobia

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22
Q

Describe the vascular abnormalities which may predispose a patient to developing a subarachnoid haemorrhage.

A

Berry aneurysm - Congenital weakness in the elastic tissue surrounding arteries
Most common at branch points
May be multiple in number
Arteriovenous malformations - Abnormality in the arterio-venous connections causing rupture due to the abnormal pressure distribution.

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23
Q

List the potential complication of a subarachnoid haemorrhage.

A
Increased ICP
Arterial spasm
Subdural haemorrhage
Coma
Death
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24
Q

List the predisposing factors which make a patient vulnerable to developing subdural haemorrhage

A

Elderly
Alcoholic
Anticoagulant therapy

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25
Describe the clinical presentation of a chronic subdural haemorrhage
``` May present with a long prodome Time between initial trivial trauma and SBH may be weeks. Headache, drowsiness, confusion, coma stupor Focal deficits ```
26
Describe the clinical presentation of meningo-encephalitis
``` Malaise Drowsiness Meningism Photophobia Fever Rigors Nausea and vomiting Focal neurological deficits Papilloedema ``` ``` Pointers to causative organism: Recent travel Petechial rash Skull fracture/ear infection immunocompromise ```
27
Describe the typical rash found in meningococcal septicaemia
Blotchy | Non-blanching
28
List the complications that may arise from meningitis 11
``` Chronic headache Venous sinus thrombosis Cerebral oedema Hydrocephalus Seizures Death Hearing loss Septic shock Cortical blindness Peripheral infection/gangrene Papilloedema ```
29
List the typical symptoms 6 of a patient with anaemia.
``` Fatigue SOB Angina Intermittent claudication Faintness Headaches ``` Signs: Pallor Tachycardia Flow systolic murmur, cardiac failure. ``` Specific anaemias may cause: Angular stomitis Koilonychia Jaundice, Bone abnormalites Brittle hair and nails Plummer Vinson syndrome Leg ulcers ```
30
What is microcytic anaemia and what are the causes? 6
``` Low Hb with a low MCV due to small cells. Causes include Iron deficiency anaemia (main cause) sideroblastic anaemia Thalessaemia Anaemia of chronic disease ```
31
What is normocytic anaemia and what are the causes? 7
``` Acute blood loss Inflammation Malignancy CKD Endocrine disorders Haemolytic and aplastic anaemias Malnutrition ```
32
What is macrocytic anaemia and what are the causes? 7
``` Megaloblastic and non-megaloblastic Megaloblastic more common. Lack of B12 - vegetarians Lack of intrinsic factor - Pernicious anaemia, gastrectomy Lack of absorption of B12 -Ilial disease ``` Lack of folate intake: alcoholics elderly Lack of absorption: coeliac Failure to meet demands: Pregnancy, haemolytic anaemias
33
Discuss the common causes of iron deficiency anaemia
``` Blood loss (blled, pregnancy, hookworm) Supply not meeting demand = Pregnancy, growth Decreased absorption (postgastrectomy) Poor intake ```
34
Discuss appropriate investigations to confirm that a patient has iron deficiency
FBC with serum ferritin -indication of iron stores Serum iron and transferrin receptors are other tests that can be used to confirm diagnosis Bone marrow sampling can be done in extreme cases
35
Outline appropriate investigations for a patient with confirmed iron deficiency anaemia
``` Find underlying cause: Endoscopy if bleed suspected Check menstrual cycle Diet should also be checked May be given iron supplements to see if this corrects problem. ```
36
Outline the physiological absorption of vitamin B12 and folate
B12 present in eggs, meat, fish and milk. Bound to intrinsic factor secreted by parietal cells of the stomach. Absorbed in the terminal ileum Stored in the liver, takes a while for stores to deplete. Folate is present in vegetables and offal. Broken down in the upper GI. Stores take longer to wear down.
37
List the common causes of neutrophilia 5
``` Tissue damage Infection corticosteroids Physiological Malignancy ```
38
List the common causes of neutropenia 6
``` Autoimmunity Severe viral or bacterial infection (typhoid) Feltys syndrome Ethnicity ELA2 gene mutation Alcohol and other drugs ```
39
List the common causes of lymphocytosis 5
Chronic infection Viral infection CLL and some lymphomas Post-splenectomy
40
List the common causes of lymphopenia 5
``` Renal failure Lymphoma HIV Transient following infection Inflammation/corticosteroids ```
41
Describe the mechanism of action of aspirin
A COX enzyme inhibitor. | Prevents the production of thromboxane, prostaglandins and prostacyclins.
42
Outline the clinical features of thrombocytopenia 2 and major causes 4
CFs - Bleeding from mucus membranes, purpura Causes: Decreased production in BM - bone marrow failure, HIV infection Excess destruction peripherally - SLE, DIC May be idiopathic Hypersplenism will increase sequestration Massive blood transfusion, dilution
43
Describe the laboratory tests that are used to assess the clotting system and recognise patterns of abnormality.
FBC - May pick up thrombocytopenia PT - Measures extrinsic pathway (and common pathway). Standardised using INR, raised by Warfarin APTT - Measures intrinsic pathway (and common pathway). Raised by heparin (unfractionated has to be monitored more than LMWH) TT - Measures common pathway.
44
Describe the role of the liver in normal clotting
The liver produces clotting factors: I (fibrinogen), II (prothrombin), IV, V, VI, VII. It also produces bile which enables the absorption of vitamin K, a fat soluble vitamin. Portal hypertension causes splenomegaly and increased sequestration of platelets there. Vitamin K is absorbed in the upper ileum and stored in the liver. Vitamin K dependent clotting factors: II, VII, IX, X
45
Describe the ABO blood group and outline their significance in blood transfusion.
A - 42% A antigens on surface and anti-B antibodies in serum B - 8% B antigens on surface and anti-A antibodies in serum AB - 3% A, B antigens on surface and no antibodies in serum O - 47% No antigens on surface and A, B antibodies in serum
46
Describe the principles of cross matching blood.
Group and save takes around 40 minutes and involves typing a sample of a patients blood and testing it for different antibodies which have the potential to cause haemolysis. Cross matching takes a further 40 minutes and involves mixing patients blood with donor blood to observe any reactions which may take place.
47
List common causative organisms of infectious disease
Bacteria, viruses, helminths, fungi, protozoa
48
Define infection
Infection is the presence of micro organisms in an area which is usually sterile. Infectious disease is accompanied by tissue damage.
49
List the complications of bacterial infection 9
``` Septic shock Endotoxic shock Hypersensitivity Septicaemia Bacteraemia Pyaemia Abscess Gangrene Granulomas ```
50
What are the general consequences of infection?
Weight loss Dehydration Pyrexia Raised CRP and ESR and WBC
51
Outline the microbiological investigation of a patient presenting with infective endocarditis
Take blood cultures from 3 different sites prior to starting antibiotics
52
Outline the microbiological investigation of a patient presenting with CAP
Blood cultures Sputum cultures - ZN stain for TB? Serology Urinary serology - TB, legionella
53
Outline the microbiological investigation of a patient presenting with EBV (infectious mononucleosis)
20% of peripheral lymphocytes must have atypical morphology | Heterophile antibody must be present
54
Outline the microbiological investigation of a patient presenting with gastroenteritis and food poisoning.
Stool sample and culture
55
Outline the microbiological investigation of a patient presenting with travellers diarrhoea
Stool sample
56
Outline the microbiological investigation of a patient presenting with acute hepatitis
A, B, C, D, E can all cause acute hepatitis, whereas, B and C can cause chronic hepatitis.
57
Outline the microbiological investigation of a patient presenting with an UTI
MSU sample for urine dip
58
Outline the microbiological investigation of a patient presenting with meningitis
Lumbar puncture unless contraindicated by signs of raised ICP, hedrocephalus.
59
Outline the microbiological investigation of a patient presenting with surgical infection
Gram stain, cultures and sensitivities should be done.
60
Describe the basic principles of prevention of infection in hospitals
Hand hygiene at 5 appropriate points. Use sterile equipment as much as possible Sterilise patient before any procedures Isolation to rooms with self containing sink and toilet can be used to isolate infectious disease. Cohort nursing is also acceptable where patients who have the same disease are placed together and told to move around as little as possible.
61
Describe the basic principles of prevention of infection in the community.
Many infectious diseases are notifiable and require reporting to public health. In addition to this, everyone over the age of 65 and with a chronic disease will be offered pneumococcal vaccination via the flu jab. Healthcare professionals are also vaccinated against Hep B, TB and chickenpox. Travellers also receive vaccinations for the area they are visiting.
62
What are endotoxins? Describe their features
They are part of bacterial cell walls Released when gram negative bacteria die They are complex polysaccharides which are heat stable They do not stimulate antibody production. In low does, stimulate protective immunity, but in high doses stimulate endotoxic shock.
63
What are exotoxins? Describe their features
Secreted by living gram negative and positive bacteria. They are simple proteins which are not heat stable They are neutralised by specific antibodies and the fatal dose is low.