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Science to Clinical Practice 1 > Supporting Life > Flashcards

Supporting Life Flashcards

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1
Q

Where in the coronary vessels do plaques usually form?

Which coronary vessel can a plaque form that causes the most damage?

A

Proximal region within 6 cm of aorta

L anterior descending coronary artery

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2
Q

What is the major action of the haemodynamic effects of nitrates?

A

Relaxes veins + venules
↓ CVP, so ↓ cardiac wall tension
↓ cardiac O2 demand

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3
Q

What is the minor action of the haemodynamic effects of nitrates?

A

Dilate larger coronary arteries, ↑ing blood flow thru coronary collaterals
↓ TPR + afterload, so ↓ O2 demand

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4
Q

What are the side effects of nitrates?

Why?

A

Headache, facial flushing
↓ BP, reflex ↑ HR
Due to vasodilatation

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5
Q

What is the most commonly used beta blocker in UK for angina?
Against what receptors?

A

Bisoprolol

Beta 1 selective

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6
Q

How do beta blockers work in angina?

A

Inhibit sympath stimul heart + inhibit renin release
Aim resting HR 55-60 bpm, + ↑ HR of <75% of rate causing ischaemia during exercise
↓ contractility, ↓ O2 demand

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7
Q

How do beta blockers ↑ perfusion of l ventricle?

A

L ventricle gets blood only during diastole - systole squeezes arterioles
Slower HR, more time spent in diastole

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8
Q

Why are beta blockers contraindicated in asthma and vasospastic angina?

A

Asthma - adren bronchodilator via beta receptors

V angina - beta receptors vasodilating effect on coronary arteries

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9
Q

What are the side effects of beta blockers?

A

Fatigue, exercise intolerance, hypoglycaemia, disturbed sleep, cold/tingling extremities

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10
Q

What are the common Ca channel blockers used?

A

Amlodipine (dihydropyridine, DHP)
Verapamil
Diltiazem

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11
Q

What are the effects of the different types of Ca channel blockers in angina?

A

DHPs vasodilate → reducing afterload, so cardiac work
Verapamil acts by direct (–) inotropic effect, some reduction in afterload
Dilate coronary arteries, useful angina associated mit coronary vasoconstriction
e.g. Prinzmetal’s, also oft occurs in mixed angina

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12
Q

What enzyme do statins block?

A

HMG-CoA reductase

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13
Q

What is the coronary flow reserve?

A

Ability of coronary vessels to↑ blood flow during greater O2 demand e.g. exercise

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14
Q

How does nitrous oxide work to prevent vascular smooth muscle cell contraction?

A

Opens K+ channels to prevent depolarisation
Activates Ca2+ pumps - to remove Ca2+ from cells
Ca2+ desensitisation

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15
Q

How is GTN taken so it works immediately?

A

Sublingually

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16
Q

How quickly does tolerance to organic nitrates happen?

How to avoid this?

A

After 12 hours

Daily 8 hour drug free period - usu at night

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17
Q

What is the late Na+ current in cardiac myocytes?

A

Upstroke of AP in cardiac myocytes due rapidly developing Na+ current - inactivates few millisec
Inactivation incomplete - late Na+ current

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18
Q

What can a late Na+ current in cardiac myocytes cause?

A

AP prolongations → arrhythmias
Myocardial stunning - contractile abnormality even after reperfusion
Diastolic stiffness → ↑cardiac work, ↓ coronary blood flow

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19
Q

How does the drug ranolazine help with angina?

A

Inhibits late Na+ current in cardiac myocytes

Reduces cardiac wall tension, ↓ cardiac work

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20
Q

What type of angina is the drug ranolazine used to treat?

A

Microvascular angina
May have anti-oxidant + inflammatory effects
Improve coronary endothelial function

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21
Q

How does the drug nicorandil work to reduce symptoms of angina?

A

Opens ATP-sensitive K+ channels in vascular sm cells
Stimulates guanylate cyclase → ↑ vascular sm cell [cGMP]
Relaxation of sm

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22
Q

How does the drug ivabradine work to reduce symptoms of angina?

A

Blocks If (‘funny’ current), involve SAN pacemaking,
↓ HR, ↑es perfusion
‘Use-dependency’ - ivabradine block more when HR ↑

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23
Q

What are the hemodynamic effects of ivabradine?

A

↓ HR allows more time for blood to perfuse myocardium, reduces ischaemia
↓ HR → ↓ afterload → ↓ O2 demand

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24
Q

What 2 revascularization techniques can be used to treat stenosis in coronary vessels?

A 
Percutaneous intervention (PCI) - stents
Coronary artery bypass grafting (CABBAGE) - pieces of saphenous vein/diverted internal mammary artery
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25
Q

When would a coronary artery bypass be used instead of PCI?

A

Patients with mehr serious/advanced coronary artery disease

Improves survival compared to PCI

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26
Q

What is definition of:

a) Sinus rhythm?
b) Junctional rhythm?

A

a) Heartbeat originate from SAN

b) Heartbeat originate from AVN/Bundle of His

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27
Q

How do tachyarrhythmias arise?

A

Re-entry, impulse delayed/‘trapped’ 1 region of heart
Adjacent tissue finishes depolarising, x refractory
Delayed impulse re-enters adjacent tissue, spreads throughout heart
1nce; premature beat
Indefinitely; sustained tachycardia

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28
Q

What are the classes of antiarrhythmic drugs?

A

Class 1: Na+ channel blockers - suppress conduction
Class 2: beta blockers - reduce excitability, inhibit AVN conduction
Class 3: K+ channel blockers - prolong AP + refractory period
Class 4: Ca 2+ channel blockers - inhibit AVN conduction

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29
Q

What 2 drugs are antiarrhythmic but don’t fit the different classes?

A

Adenosine: slows AV nodal conduction
Digoxin: stimulates vagus, slows AV nodal conduction

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30
Q 
Examples of:
a) Class 1
b) Class 2
c) Class 3
d) Class 4
antiarrhythmic drugs?
A

a) flecainide
b) bisoprolol
c) amiodarone
d) verapamil

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31
Q

What is rate control in treatment of arrhythmias?

A

Reduce proportion of impulses conducted thru AV node

Atrial tachycardia continues, but ventricles slow down, improving cardiac output

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32
Q

What drugs are used in rate control of arrhythmias?

A

Class 2, Class 4, Adenosine, Digoxin

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33
Q

What is rhythm control in treatment of arrhythmias?

A

Target source of arrhythmia/conduct impulse away from source, by blocking re-entrant pathway

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34
Q

What drugs are used in rhythm control of arrhythmias?

A

Class 1, Class 3

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35
Q

How do the drugs used in rate control of arrhythmias work to treat them?

A

Class 2 drugs suppress norad-mediated stimulation of AVN conduction
Class 4 drugs depress AVN conduction
Digoxin stimulates vagus nerve, suppresses AVN conduction
Adenosine inhibits AVN Ca2+ channels + stimulates K+ channels, ↓ing conduction

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36
Q

How do the drugs used in rhythm control of arrhythmias work to treat them?

A

Both block re-entry
Class 1 - suppress/block conduction (instead of slowed)
Class 3 - prolong refractory period

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37
Q

What class of antiarrhythmic drugs can be used to treat polymorphic VT?

A

Class 2

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38
Q

How do implantable defibrillators work?

A

Connected to electrodes in r ventricle + SVC
Senses + differentiate arrhythmias by rate + location
Delivers an appropriate shock/shock sequence, causing cardioversion i.e. return to sinus rhythm

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39
Q

What is defibrillation?

A

Used to terminate VF/ ‘pulseless’ VT
DC cardioversion: Momentary discharge large current across chest via paddles placed at sternum + RV apex
Applied onset QRS complex (if present)
Stops heart, allows SAN reassert itself
Combined mit cardiopulmonary resuscitation; adrenaline can also be used
Absence any equip, thump to chest can occasionally terminate VF

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40
Q

What is the definition of arteriosclerosis?

What are the 3 distinct morphological variants?

A

Group disorders, thickening + loss elasticity arterial walls

Atherosclerosis, Monckeberg’s medial sclerosis, arteriolosclerosis

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41
Q

What is Monckeberg’s medial sclerosis?

A

Calcification of media of muscular arteries

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42
Q

What is Arteriosclerosis?

A

Proliferative/hyaline thickening of walls of small arteries + arterioles

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43
Q

What are the major risk factors for atherosclerosis?

A

Diet + hyperlipidemias (hypercholesterolaemia, hypertriglyceridemia)
Hypertension – both systolic + diastolic
Cigarette smoking - ↑es heart disease in women
Diabetes mellitus – 2x risk of MI, 8x-150x risk of gangrene of extremities

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44
Q

What are minor risk factors for atherosclerosis?

A 
Obesity
Physical inactivity
Male gender
↑ing age
Family history
Stress (“type A” personality – competitive, stressful lifestyle) - controversial
Oral contraceptives –controversial
High carbohydrate intake - controversial
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45
Q

What are some features of normal aortic intima?

A

Innermost layer of a blood vessel + extends from flattened endothelial cells on luminal surface to internal elastic lamina
Mostly composed of subendothelial collagen

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46
Q

What is the layer deep to the internal elastic lamina in the aorta?

A

Media composed of sm cells + elastin fibres

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47
Q

What features can you see of a Type 1 lesion under a microscope (in atherosclerosis)?

A

Macrophages in aortic intima phagocytose LDLs that progressively accumulate within cytoplasmic vacuoles AKA foamy macrophages from their appearance

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48
Q

What features can you see of a Type 2 lesion under a microscope (in atherosclerosis)?

A

Sm cells migrate from media → intima thru fenestrations in internal elastic lamina
Also phagocytose lipid (seen as cytoplasmic vacuoles in cells with spindle-shaped nuclei).
Modified sm cells (myofibroblasts) also start producing collagen in intima

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49
Q

What is hyperlipoproteinemia?

A

Inability to break down lipids in body, esp cholest/trigly

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50
Q

What is the definition of an infarct?

A

An area of ischaemic necrosis within a tissue/organ, produced by occlusion of either its arterial supply/its venous drainage

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51
Q

What are the usual causes of an infarct?

A

Acute arterial occlusion
1. Thrombosis e.g. coronary arteries → MI
2. Embolism e.g. lung, kidney, spleen
3. Either thrombosis/embolism e.g. brain (but also
hypotension)

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52
Q

Why is venous infarction less common?

A

Most tissues have numerous venous anastomoses

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53
Q

What places can venous infarction take place in?

A

Thrombosis of mesenteric veins → intestinal infarction

Brain following thrombosis in superior sagittal sinus

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54
Q

What is the most common type of myocardial infarct?

A

TRANSMURAL INFARCT
Ischaemic necrosis of full/nearly full thickness of ventricular wall in distribution of single coronary artery
Usu associated mit coronary atherosclerosis, plaque rupture + super-imposed thrombosis

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55
Q

What is another type of myocardial infarct?

A

SUBENDOCARDIAL INFARCT
Ischaemic necrosis, inner 1/3/ 1/2, ventric wall
Diffuse stenosing coronary atherosclerosis + global reduction of coronary flow but x plaque rupture + x thrombosis

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56
Q

What are the 4 morphological complications following MI?

A

Cardiac rupture
Pericarditis
Mural thrombosis
Ventricular aneurysm

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57
Q

Definition of embolism?

A

Transfer of abnormal material by bloodstream + its impaction in a vessel
Impacted material = embolus

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58
Q

What are the types of emboli?

A 
Fragments of thrombus (commonest type)
Material from ulcerating atheromatous plaques (common in distal leg arteries)
Septic emboli
Fragment of tumour growing into a vein
Fat globules
Air emboli
Parenchymal cells
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59
Q

What is the ejection fraction of the heart?

Normal value for healthy individual?

A

Fraction of volume of ventricle pumped out during each beat

- Amount of blood pumped out at each beat >55%

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60
Q

What are the 3 main causes of heart failure?

A

Pressure overload
Volume overload
Contractile dysfunction

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61
Q

What are the 3 phases of heart failure?

A

Short-term acute failure - functional reserves overwhelmed by overload
Compensated hypertrophy - heart enlarges + adapts
Chronic failure - exhaustion, cell death + necrosis

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62
Q

What are the short term mechanisms of the body to cope with acute heart failure?

A

Sympathetic activation
Activation of renin-angiotensin system
↑ secretion of aldosterone
Myocardial hypertrophy

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63
Q

How would you take a sample of fluid in a pleural effusion?

A

Thoracentesis
Patient faces away from practitioner + leans over table
Needle inserted into pleural space to remove excess fluid
Goes above rib

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64
Q

How would you classify pleural fluid based on its protein content?

A

<25g/L - transudate
>35g/L - exudate
If 25-35 use Light’s criteria

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65
Q

What is Light’s criteria when it comes to classifying pleural fluid (based on protein content)?

A

Classed as exudate if 1/more is true
Pleural protein > half of serum protein
Pleural LDH > 0.6 of serum LDH
Pleural LDH > 2/3 upper limit of lab normal LDH

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66
Q

What are the common causes of transudates (pleural fluid)?

A

L ventricular failure
Liver cirrhosis
Renal failure

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67
Q

What are the common cause of exudates (pleural fluid)?

A

Lung cancers
Parapneumonic effusions
TB

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68
Q

What are the general causes of transudates and exudates (pleural fluid)?

A

Transudates - systemic problemos

Exudates - local problemos

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69
Q

What measurement can mirror pleural fluid glc?

A

Pleural pH - if it’s low, glc is low
If <7.20 - complicated parapneumonic effusion
Indication for tube drainage

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70
Q

What is empyema? (in context of lungs)

A

Pus in the pleural space
Have to drain pus
Very smelly

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71
Q

What is cachexia?

A

Extreme weight loss and muscle wasting

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72
Q

What are some causes of a malignant pleural effusion?

A

Lung/breast/ovarian cancer

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73
Q

What can you use to stick together 2 layers on pleural membrane?
Why?

A

Medical grade talc
Causes inflammation so 2 layers stick together
Can survive with it, helps reduce efflusion

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74
Q

What is orthopnea?

A

Breathlessness when lying down

Relieved by sitting/standing

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75
Q

What would a chest X-ray show in heart failure?

A

Bilateral pleural effusions

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76
Q

What is a PEA arrest?

A

Pulseless Electrical Activity

ECG shows heart rhythm but no pulse produced

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77
Q

What are viridans streptococci?

What do they cause?

A

Gram +ve bact, green colouration on blood agar plates

Pneumonia. emphysema, sepsis, meningitis

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78
Q

What are the 4 types of hypersensitivity?

A

Type I: Immediate Hypersensitivity (Allergy Anaphylaxis + Atopy)
Type II: AntiBody Mediated
Type III: Immune Complex Mediated
Type IV: Cell Mediated (Delayed)

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79
Q

What is kyphoscoliosis?

A

Abnormal curvature of spine in coronal (side-side) and sagittal plane (back-front)

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80
Q

What are some environmental causes of ILD?

A

Pneumoconiosis - occupational lung disease related to inhalation exposures to inorganic dusts e.g. silicon, asbestos
Henoch-Schonlein Purpura (HSP) - exposure to protein antigens e.g. farmer’s lung, pigeon breeder’s lung
Radiation e.g. radiotherapy

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81
Q

What are some drugs that can cause ILD?

A

Cytotoxic drugs e.g Amiodarone, Nitrofurantoin, Bleomycin, Chemotherapy, Methotrexate

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82
Q

What does IIP mean in causes of ILD?

What are the IIP classifications?

A 
Idiopathic Interstitial Pneumonia
UIP - Usual IP (aka IPF, Idiopathic Pulmonary fibrosis)
NSIP - Non Specific IP
AIP - Acute IP
COP - Cryptogenic Organising Pneumonia
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83
Q

What are the risk factors of IPF/UIP?

A

Smoking (2-3x day)
Metal/wood dust
Genetic (familial)

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84
Q

What is the aim of treatment in IPF/UIP?

What are the treatment options?

A

Reduce disease progression
Oxygen
Pulmonary Rehabilitation
Palliative Care
Lung transplant
Pirfenidone- antifibrotic, oral, slows disease progression (FVC) + reduces mortality
Nintedanib- Triple tyrosine kinase inhibitor (similar effect)

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85
Q

What are the main causes of death in IPF/UIP?

A 
Resp failure
Heart failure
PE
Pneumonia
Lung cancer
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86
Q

What are some CT findings in non-specific interstitial pneumonia?

A

Ground glass opacities + fibrosis

Treatment response + prognosis better that UIP/IPF

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87
Q

What are the drug therapies in the different ILDs?

A

IPF/UIP - pirfenidone, nintedanib
NSIP/AIP/COP - steroids (cortico)
HP (hypersensitivity) - steroids
CTD (connective tissue disease) - immunosuppressants

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88
Q

What are the hallmarks of type I hypersensitivity?

A

IgE production, activation of Th2 cells

Mediated IgE-mast cells

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89
Q

What is contained in the storage granules of mast cells?

What do they do?

A

Histamine → ↑ed vascular permeability, sm contraction

Tryptase → tissue remodelling, ↑ed mucus secretion

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90
Q

What are the characteristics of the main allergens in type I hypersensitivity?

A

Individuals repeatedly exposed to them

X induce macrophage/dendritic cell typical responses

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91
Q

What are some examples of the main allergens in type I hypersensitivity?

A

Inhaled: pollens, spores, dander, dust mite
Ingested: peanut, egg, fruits, sesame
Venoms: bee, wasp stings and bites (Hymenoptera)
Drugs: antibiotics, chemotherapeutics

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92
Q

What are some symptoms of type I hypersensitivity?

A 
Lung – asthma, wheezing
Nose – rhinitis, sneezing, runny nose
Eye – conjunctivitis
Skin – atopic dermatitis
Gut – food allergy
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93
Q

What are some diagnostic tests of type I hypersensitivity?

A 
Skin prick test > 3 mm wheal (swelling)
Laboratory tests:
- Total IgE (>100 IU/mL)
- Specific IgE raised (e.g. RAST)
- Tryptase levels – transient (24-48h)
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94
Q

What happens in type II sensitivity?

A

Antigens bound on cell membranes

Activate complement cascade + recruit immune cells

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95
Q

What is the most severe form of type I hypersensitivity?

A

Anaphylaxis

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96
Q

What are some examples of antigens in type II hypersensitivity?

A

Drugs e.g. penicillin, quinine
Bacteria
Rhesus antigen

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97
Q

What are the main types of antibodies in type II and III hypersensitivity?

A

IgM, IgG

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98
Q

What does the complement cascade lead to in type II hypersensitivity?

A

↑ed inflammatory mediators
Opsonization - phagocytosis
MAC (membrane attack complex) formation, cell lysis
NK cell activation

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99
Q

What are some examples of antigens in type III hypersensitivity?

A

Foreign serum - antivenom, monoclonal antibody

Group A streptococcus

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100
Q

What is an arthus reaction in type III hypersensitivity?

A

Inflammation caused by deposition of immune complexes at localised sites

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101
Q

What is serum sickness in type III hypersensitivity?

A

Foreign serum from animal/monoclonal antibodies cause systemic adaptive immune response
Antibody production against foreign serum/MA

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102
Q

What is type IV hypersensitivity?

A

Antibody independent, 24-48 hr after antigen exposure

Cytokine mediated inflamm, T cell mediated cytotoxicity

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103
Q

What are the 5 types of asthma?

ICS - inhaled corticosteroids

A

Allergic asthma: childhood, past/FHx allergic disease, eosinophilic airway inflamm, good response to ICS
Non-allergic asthma: sputum neutrophilic/eosinophilic / mit few inflammatory cells, less response to ICS
Late-onset asthma: more common women, tendency non-allergic, ↑er doses ICS required
Asthma mit fixed airflow limitation: long-standing asthma, airflow limitation due airway wall remodelling
Asthma with obesity: prominent respiratory symptoms, little eosinophilia

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104
Q

What types of cells are responsible for producing large amounts of IL-5 and IL-3 in asthma?

A

Type 2 Innate Lymphoid Cells (ILC2)

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105
Q

What is the dominant cause for asthma exacerbation?

A

Viruses

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106
Q

What are the bronchodilators used in the treatment of asthma?

A

Selective β-2 adrenoceptor agonists: Inhaled/IV in intensive care
Short-acting: Salbumatol
Long-acting: e.g. Formoterol (12h), Vilanterol (24h)
Anticholinergic / muscarinic receptor antagonists: Inhaled
Short-acting: Ipratropium
Long-acting: Tiotropium, Umeclidinium

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107
Q

What is the action of salbutamol in the treatment of asthma?

A

Stimulates β2adrenergic receptors – predom receptors in bronchial sm
↑ levels cAMP relaxes bronchial sm + inhibits release bronchoconstrictor mediators e.g His + leukotrienes from mast cells in airway

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108
Q

What is the mechanism of anticholinergic / muscarinic receptor antagonists in treating asthma?

A

Block AcH effects released from cholinergic parasympathetic nerve fibres to sm + mucus glands
Prevents airway sm contract + mucus hypersecretion
Less effective than β-2 adrenoceptor agonists
Side effects unusual: dry mouth, palpitations, headache, dizziness, blurred vision

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109
Q

How do leukotriene receptor agonists help treat symptoms of asthma?
What types of patients benefit from this?

A

CysLT1 receptor mediates bronchoconstrictive + proinflammatory effects of cysteinyl-leukotrienes (LTC4, LTD4, + LTE4)
Montelukast comp antagonist of CysLT1 receptor
1nce daily oral administration
Work best subgroup asthma patients mit ‘aspirin exacerbated respiratory disease’ (AERD)
- ↑ed production of cysteinyl-leukotrienes
Side effects rare: headache + GI disturbances

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110
Q

How do inhaled corticosteroids (ICS) reduce asthma symptoms?

A

Suppress Th2 / ‘Type 2’ airways inflammation

Reduce infiltration + activation of eosinophils, Th2 cells, + other inflammatory cells

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111
Q

Example of long lasting ICS for asthma?

How does it work?

A 
Fluticasone furoate (FF) enhanced affinity glucocorticoid receptor (fast association + slow dissociation)
Longer duration action + prolonged retention in lung; enables use as once-daily ICS
Improve patient convenience + enhance compliance
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112
Q

When are steroids more effective in asthma?

A

If asthmatic has eosinophil inflammation

113
Q

What is the aim of drug treatment in angina?

A

↓ing myocardial O2 demand

↑ing O2 supply

114
Q

Why is it good to have a drug free period at night with nitrates in the treatment of angina?

A

Nitrates build up to form superoxides

Cause vasoconstriction, opposite action of nitrates

115
Q

What happens to the alveoli in pneumonia?

A

Fill with pus
Congestion - vascular engorgement, intra-alveolar fluid
Red hepatisation - exudation of red cells, neutrophils, fibrin
Grey hepatisation - disintegration RBC, persisting inflammatory cells

116
Q

What is the common pathogen that causes pneumonia?

A

S. pneumoniae, esp post influenza

117
Q

What are some complications of pneumonia?

A 
Septic shock
Adult Respiratory Distress Syndrome
Parapneumonic effusion & empyema
Cavitation & abscess
MI
118
Q

What are the signs of acute exacerbation in COPD?

A

Any 2: ↑ed dyspnoea/sputum volume/ purulence

Any 1 above + any 1: ↑ed cough, wheeze, sore throat, cold

119
Q

What are the signs of severe exacerbation in COPD? (Non-invasive ventilation)

A

Respiratory acidosis (PaCO2 >6 kPa, pH <7.35)
Fatigue + ↑ed work of breathing
Persistent hypoxaemia

120
Q

What are the signs of severe exacerbation in COPD? (Invasive ventilation)

A 
Unable tolerate NIV/NIV failure
Post cardiorespiratory arrest
Reduced consciousness
Haemodynamic instability/arrhythmia
Life threatening hypoxaemia
Aspiration/vomiting
pH <7.25
121
Q

What are the emergency treatments of acute exacerbation of COPD?

A 
Bronchodilators e.g salbutamol 
Corticosteroids e.g. prednisolone
Antibiotics e.g doxycycline
Controlled oxygen - consider target levels
Consideration of NIV/intubation
122
Q

What symptoms would help with a diagnosis of COPD in a patient over 35?

A

Progressive persistent SOB, usu worse exercise
Chronic cough (maybe intermittent + unproductive)
Chronic sputum
Frequent ‘winter bronchitis’

123
Q

What are the 3 high value interventions for COPD?

A

Treating tobacco dependance
Providing vaccination
Support patient to complete pulmonary rehab
SUPPORTING BEHAVIOUR CHANGE

124
Q

What type of patients would you treat with inhaled corticosteroids in COPD?

A

History of hospitalization for exacerbations of COPD
2/more moderate exacerbations per yr
Blood eosinophils > 300 cells/microlitre
History/Concomitant asthma

125
Q

What type of patients would you NOT treat with inhaled corticosteroids in COPD?

A

Repeated pneumonia events
Blood eosinophils < 100 cells/microlitre
History of mycobacterial infection

126
Q

What is pulsus paradoxus AKA paradoxical pulse?

A

Abnormally large ↓ in stroke volume, systolic BP + pulse wave amplitude during inspiration

127
Q

What is the difference between hypoxia and hypoxaemia?

A

Hypoxia - insufficient O2 at cellular level

Hypoxaemia - reduced O2 tension in blood (arterial hypoxaemia – low PaO2)

128
Q

What are the 4 types of hypoxia?

A

Hypoxic hypoxia - low arterial blood PO2, inadequate Hb saturation
Anaemic hypoxia - reduced O2-carrying capacity of blood.
Circulatory hypoxia - too little oxygenated blood delivered to tissues
Histotoxic hypoxia - normal O2 delivery to tissue, cells unable use O2 available to them (cyanide poisoning).

129
Q

What are routine lung function tests?

A

Spirometry - (inspired/expired volume/flow)
Lung volume (+/- airway resistance)
Gas transfer
Resp muscle strength (volitional tests)

130
Q

What 2 types of drugs can reduce oxidative stress caused by smoking?

A

Antioxidants

Antiproteases

131
Q

What molecules are involved in inflammation in COPD?

A

↑ed neutrophils, macrophages + T cells
(CD8 > CD4) in lungs
Eosinophilic inflammation

132
Q

What are sources of oxidants? (COPD)

A

Cigarette smoke

Reactive O2 + N2 species from inflamm cells

133
Q

What happens during oxidative stress?

A

Inactivates antiproteases
Stimulates mucus production
Amplifies inflamm by enhancing transcrip factor activation + gene expression of pro- inflamma mediators

134
Q

What happens to the lung parenchyma in COPD?

A

Proteolytic enzymes destroy alveolar tissue

Elastin + collagen, loss of elastic recoil

135
Q

What happens to the airways in COPD? (Mucus)

A

Hypertrophy + hyperplasia of bronchial submucosal
glands + ↑ no goblet cells
LEADS TO MUCUS HYPERSECRETION
Destruction of cilia – Difficulty expelling mucus

136
Q

What happens to the airways in COPD?

A

Narrowing of airways due remodelling
- starts mit smaller airways <2mm
↑ed airways resistance

137
Q

What does compliance mean in relation to lungs?

A

Extend to which lungs can expand

138
Q

What is FRC?
How is it affected in:
a) Lung fibrosis?
b) Emphysema?

A

Inward recoil of lung exactly balances outward recoil

a) ↑ed lung recoil → reduced FRC
b) Reduced lung recoil → ↑ed FRC (barrel chest)

139
Q

What is the state of the lungs at rest during COPD?

A

Hyperinflated, FRC + RV ↑ed

140
Q

What is expiratory flow limitation?

A

Flow ceases ↑ mit ↑ing expiratory effort
Can occur tidal breathing (in COPD)
Max expiratory flow reached during Vt, min time lung emptying fixed
X empty lungs faster by pushing harder in expiration

141
Q

What is the hoover sign in COPD?

A

Inward movement of lower rib cage during inspiration instead outward - flat but functioning diaphragm

142
Q

What are the common causes of COPD exacerbation?

A

Bacterial infections e.g influenza, catarrhalis, pneumonia

Viral infections less common cause

143
Q

How is the severity of COPD exacerbations classified?

A

Mild (treat mit shrt acting bronchodilators only, SABDs)
Moderate (treat mit SABDs + antibiotics +/ oral corticosteroids)
Severe (patient requires hospitalization/visit ER)

144
Q

What are the 5 common causes of hypoxaemia?

A 
Ventilation-Perfusion mismatch
Impaired diffusion
Alveolar hypoventilation
Low pp of inspired O2
Anatomical R-L shunt e.g. PAVM, lobar pneumonia
145
Q

What happens during impaired ventilation?

A

O2 x move from alveoli → blood

Causes: ILD, thickened alveoli so x diffuse

146
Q

What can be the causes of low pp inspired O2?

A

High altitude non commercial flights

High altitude mountaineering

147
Q

What happens during a shunt in V-P mismatch?

A

Perfusing under ventilated lung
Gases alveoli equate venous blood - low O2, high CO2
Re-enters systemic circulation, blood with alveoli gas

148
Q

What happens in dead space in a V-P mismatch?

A

Ventilating under-perfused lung
X blood flow, x GE
Wasted ventilation + energy

149
Q

What are the main causes of hypercapnia?

A

↑ed resp load
Reduced internal resp drive
Reduced muscle capacity

150
Q

Is oxygen useful in cases of MI or stroke?

Why?

A

No as it can worsen area ischaemia,
High level of O2 causes vasoconstriction, affects delivery of O2 - worsens hypoxia
Only use O2 in cases of hypoxia

151
Q

What are some reasons a patient would need acute non-invasive ventilation?

A

Hypercapnic resp failure, is decompensated (acidosis)

Failed standard therapy

152
Q

What are the common conditions for acute non-invasive ventilation?

A

COPD

Obesity related resp failure

153
Q

What is ECMO in ventilation?

A 
Extra Corporeal Membrane Oxygenation
Removes blood from circulation
Replaces O2, removes CO2
Returns to Venous circulation
Requires anticoagulation
154
Q

When does COPD cause resp failure?

What lung function measurements can reassure you COPD x cause resp failure?

A

Other pathologies e.g. obesity, obstructive sleep apnoea

FEV1> 1L

155
Q

How would you detect:
a) Type 1 resp failure
b) Type 2 resp failure
in COPD patients?

A

a) Pulse oximetry

b) ABG for diagnosis, unlikely in COPD without hypoxia

156
Q

What is Obesity hypoventilation syndrome?

A

Obesity - BMI >30kg/m^2
Sleep disordered breathing
Daytime hypercapnia
Absence of another pathology explaining hypoventilation

157
Q

What is:

a) Pharmacodynamics?
b) Pharmacokinetics?

A

a) what effects drugs have on body

b) how body processes drug

158
Q

What are the common induction agents (anaesthetics) used?

A 
Propofol
Barbiturates
Etomidate
Benzodiazepines
Ketamine
159
Q

What are the common opioids used?

A 
Morphine
Fentanyl
Codeine
Tramadol
Remifentanil
160
Q

What are the uses of propofol?

A

Anaesthetic induction
Maintenance of anaesthesia
Sedation
Anti-emesis - effective against nausea + vomiting

161
Q

What are the pros of using propofol as an anaesthetic?

A

X Malignant Hyperpyrexia trigger
Pleasant dreams
Relieves pruritus from opiates
Anti-emetic

162
Q

What is malignant hyperpyrexia?

A

Cause: Underlying disease of muscle
Trigger: Volatile anesthetic gas
Drastic, sustained rise body temp, metabolic acidosis, widespread muscular rigidity

163
Q

What are the con of using propofol as an anaesthetic?

A

Anaphylaxis (v rare)
Pancreatitis (Hypertriglyceridemia)
Pain on injection (rare); thrombophlebitis

164
Q

What is thrombophlebitis?

A

Inflammatory process

Blood clot forms + blocks 1/more veins, usu in legs

165
Q

What are the uses of barbiturates?

A

Thiopental: Induction, cerebral protection (e.g. status epilepticus)
Methohexital: Induction (for ECT)
Phenobarbital: Seizure suppression
Anxiolysis

166
Q

What are the endocrine effects of etomidate?

A

Dose dependent inhibition of 11B-hydroxylase - formation of cortisol + aldosterone
Potential acute adrenal insufficiency
Impaired stress response may be harmful

167
Q

What are common benzodiazepines?

A

Midazolam (short acting)
Lorazepam (intermediate)
Diazepam (long acting)

168
Q

What are the adverse effects of benzodiazepines?

A

All have extended effects
Post-op amnesia, drowsiness, cognitive dysfunction
Paradoxical reactions, irritability, aggressiveness (oft elderly patients)

169
Q

What is flumazenil?

A

Reverse sedating effect of benzodiazepines
Comp antagonist
Short 1/2-life, may get rebound agonist effect
Infusion may be necessary
Can cause seizures in:
Patients on chronic benzodiazepines
Mixed overdoses (tricyclic antidepressants)

170
Q

What are the uses of ketamine?

A

Dissociative anaesthesia
Sedation
Analgesia
Bronchodilatation

171
Q

What are the 2 pain pathways?

A

Ascending - transmitting stimulus

Descending - inhibiting transmission

172
Q

What area of the spinal cord do pain fibres travel?

A

Dorsal horn

Substantia Gelatinosa

173
Q

What are the 4 opioid receptors?

A

MOP (mu)
KOP (kappa)
DOP (delta)
NOP (nociceptin)

174
Q

What receptor do opioid analgesics mostly bind to?

A

MOP

175
Q

What opioid receptor does morphine act on?

A

MOP

176
Q

What are the uses of morphine?

A

Analgesia
Palliation
Peri-operative

177
Q

How can morphine be administered?

A

Oral (poor bioavailability; 40-60%) - metabolised liver b4 reaches brain
Subcutaneous/IV/intrathecal/transdermal

178
Q

What other effects can morphine have on the body?

A

Constipation (GI receptors)

Pruritus

179
Q

How does fentanyl work?

A

Synthetic analogue of morphine - 80-100x more potent
Targets DOP + MOP, rapid onset
Few cardiovascular effects, less His release

180
Q

What type of fentanyl is available for use in cancer?

A

Transdermal fentanyl - patch on skin

Replace patch every 72 hrs

181
Q

How does codeine work?

A

50% analgesic potency compared to morphine
Weakly targets MOP + KOP
Given orally

182
Q

What is a pro drug?

A

Metabolized into pharmacologically active drug by body

183
Q

When is codeine banned?

A

Neonate

Risk breastfeeding mother are rapid metabolizers, infant can overdose via breast milk

184
Q

How does tramadol work?

A 
Atypical opioid
Dual action i) mu agonist (weak)
ii) serotinergic / noradrenergic reuptake inhibition
Safer cardio - respiratory profile
Risk of serotonin syndrome
185
Q

How is tramadol administered?

A

Oral/IV

186
Q

What is naloxone?

A

Reduce side effects of opioids
Pure opioid antagonist
Short acting
Rebound agonist effect possible - may need infusion

187
Q

What are the adverse effects of naloxone?

A

Hypertension
Pulmonary oedema
Cardiac arrhythmias

188
Q

How does remifentanil work?

A

Synthetic derivative of fentanyl
Potent MOP agonist
Ultra-short acting drug

189
Q

What are the pharmacokinetics of remifentanil?

A

Metabolized by non specific blood/tissue esterases

Rapid onset + offset

190
Q

What are the uses of remifentanil?

A

Pain relief during surgery
Sedation in ICU
PCA in obstetrics - patient controlled analgesia
Total IntraVenous Anaesthesia ( TIVA)

191
Q

What are the pros of TIVA?

A 
Propofol + Remifentanil infusions
Avoids conventional anaesthetic gases
Improved cardiovascular profile
Less nausea + vomiting
Improved tube tolerance
192
Q

What are the cons of TIVA?

A

Need dedicated IV line
Based on algorithms (Compartment model assumptions)
Risk of awareness

193
Q

What are the common outcomes of delirium?

A

↑ed rates of:
cognitive impairment + functional disability
length of hospital stay/institutionalisation
death
falls

194
Q

What acronym can help remember causes of delirium?

A 
Drugs (withdrawal/toxicity, anticholinergics)/Dehydration
Electrolyte imbalance
Level of pain
Infection/Inflamm (post surgery)
Resp failure (hypoxia, hypercapnia)
Impaction of faeces
Urinary retention
Metabolic disorder (liver/renal failure, hypoglycaemia)/MI
195
Q

What NT are implicated in delirium?

A

Cholinergic deficiency

Dopaminergic excess

196
Q

How does having dementia affect risk of delirium?

A

↑ risk 5x

197
Q

What would you look out for in a full examination of a patient to look out for frailty?

A

Causes of delirium/presence of delirium
Look for infection, dehydration, sensory impairment
Baseline cognitive assessment (e.g. AMT, MMSE)
Assess for pain

198
Q

What medications are high risk for delirium?

A 
Analgesics - opioids
Anticholinergics
Antidepressants
Sedative-hypnotics
Corticosteroids
Dopamine agonists
199
Q

When should pharmacological management of delirium be used?

A

If non-pharmacological methods have failed
If patients: severely distressed by delirium symptoms
At risk to self/others
Requires urgent medical interventions

200
Q

What is the strongest RF for persistent delirium?

A

Pre-existing dementia

201
Q

What is persistent delirium?

A

Cognitive disorder, meets criteria for delirium on/after admission to hospital + continues meet criteria at discharge + beyond

202
Q

How is sleep entered?

A

Via nonREM (NREM)

203
Q

What stages of sleep dominate the:

a) 1st third of the night?
b) last third of the night?

A

a) SWS - slow-wave sleep, phase 3 sleep

b) REM

204
Q

What stage of sleep is the majority of sleep?

A

Stage 2

205
Q

How does SWS change as we get older?

A

↓s by 2% per decade until 60

206
Q

What are the 2 types of circadian rhythm sleep disorders?

A

Intrinsic (primary) - alterations circadian timekeeping system e.g DSPD (delayed sleep phase), ASPD (advanced sleep phase)
Extrinsic (2ndary) - misalignment between intrinsic + extrinsic signals e.g shift work disorder, jet lag disorder

207
Q

What is delayed sleep phase disorder (DSPD)?

A

Sleep out of phase mit socially acceptable sleep-wake times
Prevalence 0.2 to 16%, depending on age
Evening chronotype preference
About 9.25h of sleep required
Sleep deprivation may → worse academic performance, health + wellbeing

208
Q

What are clinical features of DSPD?

A

Unable to advance sleep onset
Restriction to conventional bedtimes results in sleep deprivation
Insomnia +/ excessive sleepiness
Sleep normal when can sleep at desired times

209
Q

How would you treat DSPD?

A 
Does person want treatment?
Combo of:
1. Phototherapy
2. Melatonin
3. CBT-I
4. Examine for psychiatric co-morbidity
210
Q

What is a chronotype?

A

Behavioral manifestation of underlying circadian rhythms of myriad physical processes
i.e circadian typology

211
Q

What is the shift work disorder?

A

Insomnia/excessive sleepiness mit recurring work schedule, overlaps usual time for sleep
Symptoms associated mit work schedule for 1 month
Sleep disturbance X explained by another sleep disorder, medication/substance misuse
Supported by sleep log/actigraphy

212
Q

How is sleep deprivation defined?

A

Sufficient lack of restorative sleep over cumulative period so it causes physical/psychiatric symptoms
+ affects daily performance

213
Q

What are the parasomnias?

A 
Abnormal behaviours occur in association mit sleep
Occur during NREM + REM sleep
Diagnostically challenging
Poor patient recall
Limited history if x witness account
Routine investigations oft normal
214
Q

When do SWS/NREM parasomnias occur?

A

1st third of the night
1-3 episodes p/night
Frequency varies
Onset in childhood

215
Q

What are some examples of SWS/NREM parasomnias?

A 
Confusional arousal
Sleep Walking (somnambulism)
Night terrors (pavor nocturnus)
Sleep-related Eating Disorder
Sexsomnia - engaging in sexual acts while in NREM
216
Q

What are treatments for night terrors?

A

Education. CBT-I to stabilise sleep-wake patterns
Scheduled awakening: 30min alarm method for children
Keep room safe; be aware of new environs
Only wake fully if episode lasts >45 mins
Pregablin, Clonazepam

217
Q

What are some RF of SWS/NREM parasomnias?

How do patients describe selves after night terrors?

A

Family History
Exacerbated: sleep depriv, stress, alcohol, OSA, fever
Patient oft amnesic for event, partial recollection
Partner may describe tearfulness/confusion

218
Q

What is the treatment for SWS/NREM parasomnias?

A

Reassurance (benign)
Education – CBT-I to improve sleep pattern
Avoid triggers
Safety
Antidepressants (e.g. Fluoxetine, Trazadone)
Clonazepam
Melatonin

219
Q

When do REM parasomnias occur?

A

2nd half of night
1-2 episodes p/night
Frequency varies

220
Q

What are some examples of REM parasomnias?

A

REM sleep Behaviour Disorder
Nightmares – Rx: Stop causative meds (e.g. β-blockers, L-Dopa), CBT, Prazosin
Recurrent sleep paralysis

221
Q

What is REM sleep Behaviour Disorder? (RBD)

A

Loss of muscle atonia during REM sleep + history of abnormal behaviours in sleep
Oft correlate mit recalled vivid dreams – usu aggressive
May injure patient / bed partner

222
Q

What is the relationship between RBD and Parkinson’s disease?

A

Non-motor predictor of developing Parkinson’s
Disease, predictor of early cognitive impairment
Present other neurodegenerative conditions (mainly
synucleinopathies) such as MSA/DLB

223
Q

How would you diagnose RBD?

A

Clinical history highly suggestive but a v-PSG would confirm diagnosis (catching episode/REM without atonia)

224
Q

What are some differential diagnoses of RBD?

A

Severe OSA
Severe PLMS, RMD (sleep related rhythmic movement)
Sleep talking, confusional arousals, night terrors (possible overlap disorders)
Nocturnal seizures
Nocturnal dissociative episodes

225
Q

How would you treat RBD?

A

Patient education
If possible, discontinue meds, may be contributing
Safety - separate beds from partner
Consider simple home oximetry (rule out OSA)

226
Q

How can pneumonia be classified based on area of infection?

A 
Lobar - lobe of 1 lung
Bronchopneumonia - parts of both lungs
Interstitial - fibrosis of interstitium
Cryptogenic organising pneumonia - autoimmune?
inflamm of alveoli + bronchioles
227
Q

What pathogen is the common cause of pneumonia in IVDU?

A

Staphylococcus aureus

S, aureus already present on skin

228
Q

What are some rheumatological/CT (connective tissue) causes of ILD?

A

Scleroderma
Rheumatoid arthritis
Mixed CT disease
SLE

229
Q

What are some idiopathic causes of ILD?

A

Chronic fibrosing from -
Idiopathic pulmonary fibrosis
Non-specific IP
Acute/subacute IP

230
Q

What acronym help remember what affects upper lobe CT?

A 
C - Coal Worker's Pneumoconiosis
H - Histiocytosis
A - Ankylosing spondylitis
R - Radiation
T - TB
S - Sarcoidosis + Silicosis
231
Q

What acronym help remember what affects lower lobe CT?

A 
R - RA
A - Asbestosis
S - SLE, Slerdoma, Sjogren's syndrome
I - Idiopathic
O - Other e.g. drugs
232
Q

How would you approach a patient to try and tackle harmful drug use/dependance?

A

F - Feedback, discuss risks associated mit that
person’s drug use + listen to responses
R - Responsibility, up to them to change
A - Advice, harm minimisation advice + how to change
M - Menu, give people options
E - Empathy, non-judgemental, warm clinical approach
S - Self-efficacy, project optimism, ability make +ve change

233
Q

What are some common symptoms of alcohol withdrawal symptoms?

A 
↑ed pulse, BP, temp
Sweating, Shaking, Agitation
Sensitivity light + sound
May be confused, hallucinating: tactile, auditory, visual
May develop seizures
X have to be BAC 0.00mg/l
234
Q

What receptor does alcohol affect?

A

GABA-A receptor, brain’s major inhib system
↑ activity of system, lead to:
Reduced anxiety, ataxia, slurred speech, disinhibition, sedation, reduced levels of consciousness

235
Q

What happens to the sensitivity of GABA-A receptor with chronic alcohol?

A

Receptor sensitivity is reduced

236
Q

How does GHB affect the body? (What receptors act on?)

A

Presynaptic GABA-B + GHB receptors, ↓ GABA release
High concs binds postsynaptic GABA-B receptors – inhibit postsynaptic neuron
GHB metabolised to GABA

237
Q

How do opioids suppress respiration?

A

Central control of resp occurs in brainstem + medulla
Chemoreceptors detect pO2 + pCO2, usu stimulate resp drive
MOP in brainstem, medulla, chemoreceptors
Stimulation receptors slows resp

238
Q

What is the half life of naloxone?

A

60-90 min

239
Q

What is delirium tremens?

A

Delirium occurring cos of alcohol withdrawal

240
Q

What is Wernicke-Korsakoff’s syndrome?

Common symptoms?

A 
Secondary to thiamine deficiency
Triad ophthalmoplegia (weakening of eye muscles), ataxia, confusion
241
Q

What is ataxia?

A

Degenerative disease of nervous system, damage to cerebellum

Symptoms mimic being drunk: slurred speech, stumbling, falling

242
Q

What are 2 ways to care for patients in uncomplicated alcohol withdrawal?

A

Symptom triggered - measure withdrawal every 2-4 hrs for 24 hrs and dose accordingly
Fixed dose - prescribe fixed dose, estimate what you think patient needs

243
Q

What are the cons of the 2 ways to care for patients in uncomplicated alcohol withdrawal?

A

Symptom triggered - needs adequate nursing staff trained in assessment of alcohol withdrawal
Fixed dose - risks excess sedation, longer stay than needed

244
Q

What drugs are used for patients in uncomplicated alcohol withdrawal?

A

Benzodiazepines, reduces dose over 5 days
Diazepam/Chlordiazepoxide
Lorazepam/oxazepam (cirrhosis)

245
Q

How would you treat patients with delirium tremens?

A

Universal intervention to peeps mit delirium - 1:1 nurse, side room, family present
Manage delirium - hrly ↑ dose lorazepam/diazepam until symptoms controlled
Monitor resp depression and have flumazenil prn

246
Q

What drugs would you use to treat Wernicke’s Encephalopathy?

A

Parenteral thiamine - window for effect is short
Pabrinex - cocktail thiamine + other B vitamins
Preventative: 1 pair of ampoules x 3 IM or IV
Treatment: 2 pairs ampoules 3x day for 5 days

247
Q

How would you care for a patient that’s G intoxicated?

A

Supportive - keep airways clear, O2
Aware of mixed intoxication e.g. X hypotension + bradycardia if also taken cocaine
X intubate unless vomiting, seizing/other indication
X naloxone unless picture ambiguous

248
Q

How would you classify G dependance?

A 
Using every couple of hours every day
Using alcohol/benzos manage withdrawal symptoms
Waking at night to use
Preoccupation
Prioritising G over other things
249
Q

How would you carry out a GBL detox if it’s planned?

A

CIWA evaluate withdrawal severity
Give baclofen 10mg tds week before, increase to 20mg tds
In withdrawal, add benzodiazepines (diazepam/librium) May need large doses, 10-14 days treatment

250
Q

What receptor does naloxone have the highest affinity for?

A

Mu opioid receptor

251
Q

What are medically unexplained symptoms?

A

Physical symptoms x explained by underlying pathology
Cause signif functional disability/distress
X soley attribute anxiety, depression, health anxiety, psychosis

252
Q

What are common medically unexplained symptoms?

A

Pain, fatigue, dizziness, headaches, changes gut motility. visual + auditory disturbances
Singly/symptom clusters

253
Q

What is chronic fatigue syndrome?

A

Persistent/relapsing, debilitating fatigue

At least 6 months

254
Q

What is fibromyalgia?

A

Widespread pain index + symptom severity scores
Symptoms present at similar level for at least 3 months
Patient X have disorder otherwise explain pain

255
Q

What are insensible losses of water from the body?

A

Skin + Lungs

X measure water loss

256
Q

What percentage of total body sodium is non-exchangeable?

A

25% e.g in bones

257
Q

What 3 mechanisms regulate sodium excretion?

A

Kidneys: Renin-Angiotensin-Aldosterone
Natriuretic Peptides
Intrinsic Renal mechanisms

258
Q

Where is potassium mainly stored?

A

In cells

259
Q

What mnemonic can help remember causes of increased AG acidosis?

A 
G - Glycols (ethylene, propylene)
O-  Oxyproline
L - L-lactate
D - D-lactate
M - Methanol
A - Aspirin
R - Renal failure
K - Ketoacidosis
260
Q

What are some causes of normal anion gap (AG) acidosis?

A

GI losses bicarb: diarrhoea, surgical drains/fistulae

Renal losses bicarb: renal tubular acidosis

261
Q

What can cause lactic acidosis?

A

Lactate production from anaerobic resp

Shock e.g hypovolaemic, Cardiogenic, Septic, Anaphylactic

262
Q

What is:

a) Anuria?
b) Oliguria?

A

a) failure kidneys produce urine, patient x produce urine

b) Reduced urine output

263
Q

What hormones do the kidneys produce?

A

Renin, Vit D, Erythropoietin, Prostaglandins

264
Q

What is uremia?

What can it cause?

A

Retention metabolic waste products (sulphate, urea, ammonia, creatinine, phosphate etc)
Pericarditis, Pleurisy, Encephalopathy

265
Q

Why would you consider renal replacement therapy/dialysis in a patient with AKI?

A

Life threatening complication of AKI e.g.
Life threatening pulmonary oedema
Severe metabolic acidosis
Severe hyperkalaemia, esp if ECG changes present
Uraemia: uraemic pericarditis/encephalopathy

266
Q

What is an AVM in the brain?

A

Arteriovenous malformation, tangle of abnormal blood vessels connecting arteries + veins in brain

267
Q

Who is more at risk to blood in subdural space? Why?

A

Elderly, wider subdural spaces

268
Q

What is diffuse spectrum imaging (DSI)?

A

Tracks how water molecules through nerve fibres of brain to expose large-scale pics of axons

269
Q

How can you modulate spinal reflexes?

A

↑ sensitivity flexor network - anticipate heat

Inhibit flexor response - still touch heat but x withdraw

270
Q

What are the motor areas of the cortex and what do they do?

A

Premotor cortex: conceptualization of movement goal
PLAN
Supplementary cortex: strategy → achieve goal PROGRAMME
Primary motor cortex: activate spinal motor neurones
INITIATE MOVEMENT

271
Q

What is the blood supply of the motor cortex?

A

Middle cerebral artery (MCA)

Anterior cerebral artery (ACA)

272
Q

Where do the pyramidal descending tracts originate from?
What types of cells are present?
What is the NT?

A

Precentral gyrus in the primary motor cortex
Large Betz cells → large diameter corticospinal axons
Glutamate

273
Q

What is the most common area of the brain for stroke?

Why?

A

Internal capsule in corona radiata
Blood supply comes from branch of MCA
Vessel comes off at right angle, fat can deposit/high BP can push and cause aneurysm

274
Q

What is the average postural sway?

How does it change as you get older?

A

A-P 7mm

Gets larger

275
Q

What can stroke mimic? (5 S’)

A 
S: SYNCOPE
S: SEIZURES
S: SEPSIS
S: SPACE OCCUPYING LESION
S: SOMATISATION
276
Q

What is transient global amnesia? (TGA)

A

Sudden disorder of memory
For a period (some hours), X memorise any
current info (anterograde amnesia)
Oft X recall events of past few days/weeks (retrograde amnesia)

277
Q

What age group does TGA affect?

A

Middle aged or elderly

278
Q

What is horripilation?

A

Erection of hairs on skin due to cold/fear/excitement

279
Q

What is reverse stress relaxation in immediate compensation for shock?

A

Veins shrink around reduced blood volume

Helps maintain venous pressure\venous return (starts after ~10 min, takes an hour or so to develop fully)

Science to Clinical Practice 1 (5 decks)

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