BRS MOCK 8 - cells of nervous, psychiatry, intro to heart Flashcards
4 types of neurones
Unipolar, pseudounipolar, bipolar and multipolar.
Examples of multipolar neurones?
Pyramidal cell, purkinje cell and golgi cell.
Where are purkinje and golgi cells found?
Cerebellum.
What neurotransmitter do purkinje and golgi cells release?
GABA
Function of dendrites?
Receive signals from other neurones.
Oligodendrocyte function?
Myelinate neurones.
Most abundant cell type in CNS?
Astrocyte.
Astrocyte function?
Homeostasis of neuronal external environment.
What are microglia?
Neuronal macrophages.
What are ependyma?
CNS epithelial cells.
Membrane potential resting potential difference?
-70mV.
What restores the membrane potential?
Na+K- ATPase restores the ion gradients.
What are the small gaps in myelin called?
Nodes of ranvier.
How does myelin prevent action potential from spreading?
High resistance and low capacitance.
Na+ K+ ion ratio for Na+K+ ATPase?
3 sodium ions out and 2 potassium ions in.
How does Na+K+ATPase work?
Three sodium ions and ATP bind to pump. Upon phosphorylation of pump sodium ions are transported through protein. Two potassium ions bind to pump, release of phosphate reverts channel to original form and potassium is released on the inside on the membrane.
Neurotransmitter release is an example of what type of communication?
Paracrine. Can also act on same neurone in this case would be autocrine.
Synapses are organised into 4 types. What are the 4 types?
Axodendritic, axosomatic, axoaxonic and dendrodentritic.
What occurs when acetylcholine binds to receptors on skeletal muscle?
Change in end plate potential.
What is the release mechanism of neurotransmitter called?
Quantal release.
How does botulism disrupt neuromuscular junction?
Stops release of acetylcholine from presynaptic terminal.
How does myasthenia gravis disrupt neuromuscular junction?
Antibodies disrupt acetyl choline receptor on post synaptic terminal.
How does lambert eaton myasthenic syndrome disrupt neuromuscular junction?
Antibodies directed at voltage gated calcium ion channels.
How would you treat OCD?
Cognitive behaviour therapy. Clomipramine.
Anxiety symptoms?
Feeling of fear. Palpitations. Sweating.
OCD symptoms?
Ego-dystonic thoughts
Repetitive, circular ruminations
Compulsions
Core symptoms of depression?
Low mood, loss of energy, loss of enjoyment.
Depression treatment?
Antidepressants, cognitive behavioural therapy, social prescribing of exercise.
Mania symptoms?
Elated mood, Over-energized, Little need for sleep, Over-spending.
Schizophrenia symptoms?
Hallucination, delusion, Abnormal Behaviour such as disorganised behavior such as wandering aimlessly, mumbling or laughing to self.
Schizophrenia treatment?
Antipsychotics
Psychological therapies
Family therapy
Arts therapies
Example of depressogenic stressors?
Bullying and chronic illness.
What is negative reinforcement?
Encouragement of certain behaviors by removing a negative stimuli.
What can habit formation lead to?
Compulsion.
What leads to addiction?
Repeated negative reinforcement, in the context of persistent states of suffering.
How do substances cause addiction?
Direct action on neural circuits for motivation and reward-seeking.
Types of psychosis?
Schizophrenia, Mania.
Psychosis key symptoms
Hallucinations,
Delusions
Thought Disorder
Schizophrenia positive symptoms?
Hallucinations
Delusions
Schizophrenia negative symptoms?
Anhedonia
Apathy
Schizophrenia disorganised symptoms?
Thought disorder
Disorganised speech
What is see on a PET scan of a schizophrenia patient?
Excess of striatal dopamine
What increases your risk of developing schizophrenia by a lot?
If both parents have schizophrenia. Strong genetic component.
What is working memory?
You use this to store information for short periods and contextualise the present moment.
Class of antipsychotics?
Antidopaminergic.
How is social support provided for psychosis?
Housing, benefits
Support with budgeting /employment.
What increases by a lot in schizophrenia patients?
Violence.
What results in negative reinforcement in OCD?
Distress reducing mechanisms like washing, counting that give temporary relief from intrusive thoughts.
Symptoms of eating disorder?
Restriction of diet
Episodes of laxative abuse
Excessive exercise
Explain the electrical activity in the heart?
Primary pacemaker signal is generated in the SAN. Electrical signals is transmitted across the myocardium of atrium along the internodal tracts. Slowing down of electrical signal at AV node. Transmission of electrical signals along bundle of his down intravetrincular septum to apex of heart. Transmission of electrical signals along the purkinje fibers cause contraction of ventricles.
What cause the P wave in ECG?
Electrical signals transmitting across the myocardium of atrium along the internodal tracts.
What causes the P-R interval?
Slowing down of electrical signal at AV node.
Where are t tubules found?
Along each z line of every myofibril.
What mechanism triggers heart contraction?
Calcium induced calcium release.
Explain calcium induced calcium release?
Depolarisation occurs on the surface of a cardiomyocyte via sodium channels. Depolarisation opens voltage gated L-type calcium channels on the surface and in the T-tubules allowing calcium to enter the cell. Calcium acts as a ligand and binds to the ryanodine receptor on the sarcoplasmic reticulum and activates it. This triggers calcium release from sarcoplasmic reticulum which further increases calcium availability in the cell. Calcium release from SR results in contraction of myofilaments. As the contraction ends calcium is pumped back into the sarcoplasmic reticulum by SR Ca2+ ATPase (active transport). Calcium that entered the cell via the L-type calcium channel diffused out via the surface level Na+/Ca2+ exchanger; restoring calcium balance.
What does stretching do to the muscle?
More stretch. Increase in passive force. More powerful contraction.
How do you measure preload in the heart?
End diastolic pressure, End diastolic volume and right atrial pressure.
When is preload increased in the heart?
Hypervolemia, regurgitation of aortic and pulmonary valve (leaky heart valves - don’t close fully), heart failure.
How is afterload measured?
Diastolic blood pressure. End systolic volume.
When is afterload increased in the heart?
Hypertension and vasoconstriction.
Why is high afterload in a heart bad?
Reduced stroke volume. More cardiac workload.
What is starling’s law and why is it important?
Increased diastolic fibre length increases ventricular contraction. At equilibrium cardiac output exactly balances the augmented venous return.
What are the theories to why increase the length of a fibre increases level of contraction?
More stretching of muscle fibres leads to decreased myofilament lattice spacing and so more likely to form myofilament cross bridges. More force for the same amount of activating calcium.
Longer sarcomere lengths increase affinity of troponin C for Ca2+ due to conformational change in protein. Less Ca2+ required for same force.
What is law of laplace?
Wall tension = (pressure in vessel x radius of vessel) / wall thickness
How does the left ventricle walls experience similar tension to right ventricles?
Left ventricles have a low radius of curvature (radius) and a higher pressure.
Why do failing hearts have increased wall stress?
The ventricles become dilated.
When would you have a 4th heart sound?
During atrial systole. In patients with congestive heart failure, pulmonary embolism or tricuspid incompetence (regurgitation).
When is the P wave on ECG?
Atrial systole.
When is S1 sound produced?
Isovolumetric contraction.
When is the QRS complex produced?
Isovolumetric contraction.
When is the T wave produced?
Reduced ejection.
When is the dichrotic notch present?
Isovolumetric relaxation.
When would you have a 3rd heart sound?
During rapid passive filling in patients with severe hypertension or mitral incompetence.
Another name for reduced passive filling?
Diastasis.
Explain how noradrenaline or adrenaline can cause changes in cardiac contractility?
Noradrenaline or adrenaline bind to beta 1 or beta 2 receptors. This triggers a g protein to activate adenylyl cyclase. Adenylyl cyclase converts ATP to cAMP (cyclic adenosine monophosphate). cAMP activates PKA (protein kinase A). PKA phosphorylates the L-type calcium channel and the ryanodine receptor. This leads to more calcium entry and calcium release. More calcium delivery to myofilaments results in more force produced. PKA also phosphorylates SRCa2+ATPase allowing for more take up of calcium to prepare for next contraction.
Why can very high tachycardia be a problem?
Can result in low diastolic filling time resulting in a lower EDV. This results in a lower stroke volume.
What is ESPVR?
Maximal pressure developed by the LV at any given volume and is a measure of cardiac contractility.
What does an increase in contractibility result in?
Increased ESPVR gradient.
Why does an increase in afterload (arterial pressure) during exercise not result in an overall decrease in stroke volume?
Increase in contractibility and increase in preload (increase in venous return) offsets increase in afterload (arterial pressure). Overall there is a net increase in stroke volume.
