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106 Cards in this Set
- Front
- Back
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What is the most important factor determining muscle force?
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number and size of muscle fibres
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What percentage of Australians have visited a complementary medicine practitioner?
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20%
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What is the Tarcott-Parsons sick role?
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Obligations to see the illness as undesirable, to take all steps to leave the sick role, exemption from normal social role responsibilities, recognition that the patient cannot help being sick
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What causes syncope?
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Abrupt decrease in arterial blood pressure unable to be compensated for.
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What is the most common cause of syncope?
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Vasovagal syndrome
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What are the four main factors that can cause abrupt and large decreases in blood pressure?
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Obstruction to the circulation, transient arrhythmias, neurological disorders, vasovagal syndrome
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Describe how you would assess if the cause of muscle weakness was from an upper motor neuron, lower motor neuron or the muscle itself?
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S1 = magnetic stimulation of motor cortex - if no reponse, it is central cause of weakness
S2 = stimulation of peripheral nerve - if force is above the max voluntary contraction, weakness is central S3 = stimulation of the muscle - if force is above MVC, then the weakness is at the NMJ or central. |
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What makes muscles get bigger?
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Generally, increased muscle synthesis and decreased muscle degradation.
Exercising = 10 mvc/day Diet = high protein just post exercise Hormones = Thyroxine, insuline, steroids, IGF1 |
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What effect does cyclosporin have on muscles and how?
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Cyclosporin is an immunosuppressant which can inhibit the calineurin/NFAT pathway needed for hypertrophy, and thus cause muscle wasting.
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What effect does rapamycin have on muscles and how?
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Rapamycin is an immunosuppressant which inhibits mTOR, a key kinase in hypertrophy.
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What makes muscles smaller?
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Starvation, immobilization, cachexia.
Myostatin (related to TGFB) inhibits hypertrophy. Ubiquitin/proteosome pathway, which tags proteins for destruction/recycling, upregulated in cachexia. |
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What is another name for chronic fatigue syndrome?
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Post-infective fatigue syndrome, due to a common belief that this disease is brought about after infection from a virus.
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What causes the muscle fatigue in chronic fatigue syndrome?
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It appears to be an abnormality of perception of muscle force and effort, rather than an actual decrease in force production.
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What is the definition of chronic fatigue syndrome?
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Chronic, intermittent fatiguability > 6 months, disrupting normal activities.
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What is the impact of depression on survival post MI?
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Increased levels of depression are associated with a steeper decrease in survival post MI over a long period of time. This effect is more marked in depression which initiates after the MI than that which started before the MI
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t/f... smoking is a risk factor for causing depression
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true, smoking is associated with new-onset depression, and is not just something which is seen more commonly in those who are depressed
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What effect does depression have on treatment compliance?
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Depression decreases compliance with treatment, e.g. 1/3 depressed people post MI don't take aspirin.
If depression is treated, compliance improves. |
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Who are the group of people at high risk of CVD who are often not given interventions they need, and why?
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Mentally ill/those with psychological disorder, as many people have a negative perception due to experiences e.g. in the ED.
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What antidepressent should be avoided in CVD?
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Tricyclic antidepressants (TCA) - older style anti-depressants which worsen outcomes, increase mortality in CHD patients.
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What are the 2 things with the strongest evidence for increasing outcomes in patients with depression and CHD?
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Exercise and use of collaborative care
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What is conversion disorder?
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A symptom or deficit of voluntary motor or sensory function suggesting a general medical condition, psychological factors precede the stressor, the symptom can't be fully explained by a general medical condition
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What are the clinical features of conversion disorder?
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Motor symptoms - impaired coordination, balalance, paralysis, weakness, aphonia, seizure
Sensory symptoms - loss of pain sensation, blindness, double vision. Any symptoms do not conform to anatomical pathways or physiological mechanisms. |
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Who are most likely to have a conversion disorder?
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Females, adolescents and young adults, those of lower SES
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What is La belle indifference?
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Little concern about the symptom presenting. Only of value diagnostically in that diagnosis of conversion disorder is less likely if this is not present.
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What are some reasons for no medical cause being found for a symptom/s?
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False negative, didn't consider the right test, there is no test for the disease yet, psychological cause for the symptoms
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Why do you have to be careful about giving a diagnosis of conversion disorder?
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Other possible treatable diseases must be excluded, as it is common to find out that someone diagnosed with conversion disorder actually had an organic illness or another type of psychiatric illness. It is not just a diagnosis of exclusion.
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What % adults presenting to GP complain of tiredness?
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20%
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What are common causes of tiredness?
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depression, diabetes, hypothyroidism, viral infections and post-viral syndromes, OSA, anaemia (stress/sleeplessnes??)
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What should be the minimum requirements of a physical examination of someone presenting with tiredness?
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vitals, jaundice, CVS examination, liver and spleen palpation, lymph nod examination.
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What is the aetiology of chronic fatigue syndrome?
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it is not known, perhaps post viral effects of brucellosis, EBV, coxsackie infection. believed to be a mixture of physical and psychological causes
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What is the name of the disease caused by reactivated of varicella zoster (chicken pox) virus?
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shingles
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What is the acute disease that precedes Burkitt's lymphoma?
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glandular fever, by the EBV
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What are the non-specific symptoms that can be induced in a chronic viaral infection?
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fatigue, muscle ache, low grade fecer
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How should the power balance be in a doctor-patient interation?
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Begins with the power markedly unbalanced in favour of the doctor and should end with a restoration of power to the patient
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What are the issues associated with treating family and friends, as a doctor?
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While they trust you, they may find it difficult to accept your authority when you give advice, they may also appeal to your special relationship to allow you to make special judgements which may not accord with your own perceptions of the right action, distortion of facts due to different language, breaking bad news often is done with false hopes
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What is autonomy?
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The right of self-determination in giving consent
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t/f... in obtaining consent for a procedure, small risks of major harm and large risks of minor harm should be disclosed to patients
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false, large risks of minor harm and small risks of major harm should be disclosed to patients
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t/f... a valid consent must always be given in emergency, even if it can only be provided by family or friends
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false, it is presumed that an unconscious (usually the state of those brought into ED?) patient in a life threatening situation would have consented to treatment
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t/f... a consent form signed from the patient is proof of informed consent
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false, this is only proof that they have signed the paper, not that they have understood the information and given informed consent
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t/f... the mean pressure in the cerebral arteries is essentially the same as in systemic arteries
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true
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t/f... the cerebral blood flow is very sensitive to changes in mean arterial pressure, causing it to vary in accordance with the MAP change
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false, the CBF remains relatively constant over a wide range of mean arterial pressures (60-150mmHg)
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How does the cerebral blood flow remain relatively constant in the face of changing MAP?
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local vasoconstriction when MAP increases, dilation when MAP drops,
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t/f... as soon as the cerebral blood flow drops, brain tissue will have a significant reduction in oxygen supply to the brain
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false, there is a partial compensation where oxygen extraction is increased. When it drops below the ability of this mechanism to compensate, then hypoxia ensues.
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What causes vasodilation in cerebral arteries?
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H+ and adenosine released in the metabolism of neurons with increased activity (possibly NO too)
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t/f... cerebral blood flow is very sensitive to changes in concentration of CO2 in the blood
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true, if CO2 decreases e.g. hyperventilation, then the blood becomes less acidic, so cerebral vasculature becomes more constricted, which reduces CBF, which can lead to unconsioucness
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How do glial cells play a roll in cerebral blood flow alterations?
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active neruons release NT which cause Ca+ build up in glial cells (astrocyte) which then releases PGL/vasodilators. Glial cells are found in close association with cerebral blood vessels
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What is Phase 0 of the cardiac action potential?
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Rapid depolarisation (vertical line) when membrane potential reaches the threshold, associated with a large influx of Na (rapid Na current in)
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What is Phase 1 of the cardiac action potential?
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partial repolarisation - when Na influx ceases and there is a transient outward current of K+ flows (fast K1 current out)
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What is Phase 2 of the cardiac AP?
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Plateau - influx of Ca and efflux of K (slow Ca current in with slow K current out)
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What is Phase 3 of the cardiac AP?
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Repolarisation - inward Ca flow ceases and K outward flow dominates (slow K current)
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What is Phase 4 of the cardiac AP?
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Pacemaker potential - gradual depolarisation occurring during diastole (fast K1 current)
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What is an 'early after-depolarisation', in the context of arrhythmias?
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Occurs in Phase 3 of the cardiac AP when abnormal Ca influx leads to more Na in/Ca out and membrane depolarisation = ectopic beat
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What is a 'delayed after-depolarisation', in the context of arrhythmias?
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Occurs in Phase 4 of cardiac AP, abnormal Ca in leads to more Na in/Ca out and membrane depolarisation = ectopic beat
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What is ectopic pacemaker activity?
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When another tissue besides AVN, SAN or HP system takes on pacemaker activty = arrhythmical. Induced by ischaemic damage inducing partial depolarisation, or increased SNS in phase 4 of cardiac activity
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What is Heart block?
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fibosis/ischaemic damage to conducting system, may cause atria and ventricles to beat independently
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What are Class I antiarrhythmic drug characteristics?
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Drugs that block voltage-sensitive Na channels in open or inactivated states, causing a reduction in the phase 0 slope and AP peak (a-reduce AP duration, decrease ERP, b- decrease ERP weakly c-strongly reduce peak only) e.g. quinidine, lidocaine, flecainide
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What are Class II antiarrhythmic drugs characteristics?
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Beta antagonists (reduce HR and conduction) e.g. metoprolol
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What are Class III antiarrhythmic drugs characteristics?
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Drugs that prolong AP by Potassium Channel Blockade (delay phase 3), increase AP duration and ERP. e.g. amiodarone
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What are Class IV antiarrhythmic drugs characteristics?
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Calcium channel antagonists (reduce rate and conduction), non-dihydropyridines. e.g. verapamil
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When is blood pressure at its highest during the day?
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morning
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When is blood pressure at its lowest during the day?
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night time, when asleep
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t/f... increased perfusion pressure to the kidney increases urine output
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true
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What occurs in your cardiovascular system when you eat a lot of salt?
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Increase in fluid = increase arterial BP = decrease RAAS = decrease Na/water retention (excreted = decreased fluid = decreased arterial BP
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t/f equilibrium MAP is little affected by salt intake
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tre, provided RAAS is working normally
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How does the SNS affect long term level of blood pressure?
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1) directly, by increasing renal vascular resistance/Na absorption 2) indirectly, through the release of renin from the kidney or catecholamines from the adrenal medulla
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What nerve do the baroreceptor impulses from the aortic arch travel up?
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Vagus
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What nerve do the baroreceptor impulses from the carotid sinus travel up?
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Carotid sinus nerve (part of glossopharyngeal)
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What causes activation of the baroreceptor reflex?
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vascular stretch and deformation induced by arterial pressure enhance firing
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t/f... the carotid baroreceptors are more sensitive to changes in BP than the aortic baroreceptors are
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true
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How might baroreceptor sensitivity decrease?
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In chronic hypertension, the carotid sinus becomes stiffer and less deformable as a result of the high arterial pressure, and sensitivity decreases.
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What causes the eliciting of pain in angina pectoris?
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chemoreceptors with SNS fibres are in the heart, and are activated by myocardial ischaemia, transmitting the pain.
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t/f... it is normal to hear a murmur in a new born
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true, as the ductus arteriosis constricts when the blood flow is reversed, turbulent flow is produced which can be hear as a murmur
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What mechanisms could increase long term level of renal sympathetic nerve activity?
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1)chronic resetting of baroreceptor reflex 2)inputs from other peripheral receptors 3) circulating hormones acting on circumventricular organs in brain 4) other changes in brain mechanisms controlling sympathetic outflow
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How do chemoreceptors in the carotid body cause a sustained increased in renal SNS activation?
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If chronically hypoxic, the chemoreceptors firing rate increases, which leads to increased stimulation of the SNS to vasoconstrict renal arterioles
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How does obesity and its interaction with leptin lead to a long term increase in renal SNS activity?
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Leptin,when released by adipocytes, decreases appetite and increases SNS activity. Obese people with higher number of adipocytes have higher levels of leptin, which desensitises its satiating effects, but still induces the SNS activation which can lead to hypertension.
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What is Leptin?
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A protein hormone encoded by ob gene and released by adipocytes which increases satiation/decreases appetite, and increases SNS activity.
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What effect does renal denervation have on the BP of HT patients?
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decreases BP, decreasing HT
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t/f... increasing renal arterial presssure increases renal output of salt and water
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true, exponential increase?
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Explain how an increase in BP can effect renal function?
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An increased blood pressure increases how much the Na/water intake/output must increase beyond normal intake to reach an equilibrium
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How can the Mean Arterial Pressue required for the kidney to reach an in/output equilibrium be raised above normal?
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If the renal function curve somehow shifts to the right, or there is a great increase in the intake of Na and water.
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What is obesity defined as?
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body fat >25% in men and >35% in women, BMI >30 kg/m2
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What % Australian adults are overweight?
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60%
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What % Australian children are overweight?
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20%
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What % Australian adults are obese?
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20%
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What % of Australian children are obese?
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5%
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What is the BP in a pre-hypertensive patient?
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120-140/80-89 mmHg
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What is the BP in stage I hypertension?
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140-159/90-99 mmHg
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What is the BP in stage II HT?
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160-179/100-109 mmHg
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What is the BP in stage III HT?
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>180/110 mmHg
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t/f... obesity increases the likelihood of being hypertensive
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true
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t/f... HT from diet induced obesity can be reversed with SNS blockade
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true, this has been found in animal studies
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What are the features of metabolic syndrome?
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syndrome X - HT, central obesisty, Insulin resistance, dyslipidaemia, hyperuricaemia, polycystic ovaries, prothrombotc and elevated glucose
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What can cause atherogenic dyslipidaemia?
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Increased serum triglycerides, apoB, LDL, reduced HDL
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What factors are implicated in development of metabolic syndrome?
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NEFAs, CRP, PAI-1, Adiponectin, Leptin, resistin
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What are the chronic effects of HT?
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LV hypertrophy, CHF, aneurysm, stroke, renal failure
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What type ofcardiac hypertrophy is associated with obesity when not Hypertensive?
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Increased intravascular volume, therefore eccentric LVH from volume overload
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What type of cardiac hypertrophy is associated with hypertension when not obese but lean?
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Concentric LVH from pressure overload
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What type of cardiac hypertrophy occurs in a HT obese patient?
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Volume and pressure overload = concentric and eccentric hypertrophy = synergistically bad, higher incidence of heart failure
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What is syndrome Z?
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syndrome X with OSA (central obesity, insulin resistance etc) therefore the patient is ALWAYS hypertensive, even at night when usually BP should be lower
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t/f... the greater the number of hypopneoa/apnoea events in a night , the greater the eccentric hypertrophy of the heart
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true
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t/f... the greater the number of hypopneoa/apnoea events in a night , the greater the prevalence of low ejection fraction
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true
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t/f... ACE inhibitors and Angiotensin II receptor antagonists have the same efficacy in reducing BP in HT patients
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true
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What are some medications which can increase BP?
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corticosteroids, clozapine, cyclosporin (anti-inflam), NSAIDS, OCP, complementary meds
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What are the guidelines for uncomplicated HT drug treatment?
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Start on lowest recommended dose in the following order, switching class if not well tolerated - ACEI/ARB, dihydropyridine Ca channel blockers, thiazide diuretcs (if >65)
If minimal response, add a second agent from the same class, if still minimal response, increase dose |
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t/f... gout is contrainidcated in thiazide use
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true
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What % patients need to be on 2 or more drugs to control their BP?
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50-75%
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