big boys Flashcards
what type of tissue and what is the function of fibrous skeleton of the heart? (4)
- dense CT surrounds AV and outflow of vessel valves (semi-lunar valves)
- fuses together and merges with interventricular septum:
i) supports the valves
ii) prevents overstretching of the valves
iii) insertion point of cardiac muscle bundles
iv) electrical insulator between atria and ventricles - gives small delay between atria and ventricles to allow ventricles to fill before ventricles contract
the cardiac muscle fibres form two networks from two different types of fibres.
a) what direction are the atrial fibres like? what about the ventricles?
b) how does this influence how blood moves in each ?
Cardiac muscle fibres form 2 networks via gap junctions at intercalated discs.
There are two types of fibres
- the atria have a circular arrangement to squash the blood down
- the ventricles have a spiralling arrangement to push the blood up and out.
These fibres are, regardless, still separated by the fibrous skeleton of the heart.
explain the direction of conduction throughout the heart
The sino-atrial node is where the conducting system begins: natural pacemaker of the heart and is where electrical conduction will begin and spread across the atria to cause synchronous contraction.
The impulse will pause when it reaches the AV node, in order to ensure the atria have fully contracted.
The atrioventricular bundle connects the atria to the ventricles.
The AV bundle branches conduct the impulses through the interventricular septum, and the purkinjie fibres stimulate both the contractile cells of both ventricles, starting at the apex and moving superiorly
where do you find preganglionic and postganglionic
i) sympathetic neurons
ii) parasympathetic neurons
in the heart?
cardioacceletory centre: medullary reticular formation
preganglionic sympathetic neurons: thoracic spinal cord
postganglionic sympathetic neurons: SA & AV node, & coronary vasuclar smooth muscle
preganglionic parasympathetic neurons: vagus nerve
postganglionic parasympathetic neurons: SA & AV node,
explain how action potentials occur in pacemaker cells
explain how action potentials occur in ventricular cells
what determines the race of firing of cardiac pacemaker cells?
Pacemaker cells in the SA node
- Action potential are initiated by opening of sodium and calcium channels
- After each action potential potassium channels (which open during the action potential) will slowly and spontaneously close.
- This causes a progressive depolarisation (pre-potential or pacemaker potential) which eventually reaches threshold for the Na+ and Ca2+ to open and a new action potential is generated
Ventricular action potentials
Ventricular muscle has an unusual shape of action potential. It starts like a normal nerve action potential with sodium influx, however this is followed by a prolonged depolarisation phase called the plateau. This plateau is due to a late and prolonged entry of calcium into the cell which helps the muscles contract for a much longer time than ordinary skeletal muscle
- **regular, spontaneous action potentials:
- specialK channels open duringAP, butslowly, spontaneously close** (aka funny current)
- causes a progressive depolarisation
- normal K channels are not present
- eventually this pacemaker / prepotential potenential reaches threshold for the Na AP channels to open: new AP generated*
- the rate of firing of pacemaker cells is determined by rate of closure of K channels
explain the mechanism of calcium signalling driving muscle contraction in the heart
- depol of membrane from Na+, through Na+ channels = opens Ca 2+ channels
- Ca2+ move through calciumc channels into cell membrane
- rise in Ca2+ triggers further calcium release from the sarcoplasmic reticulum, via the ryanodine receptor
- calcium associates with troponin C in the sarcomere: calcium & troponin c exposes the myosin binding sites on the actin = allows the myosin to bind to actin
ATP hydrolyses: provides the energy to drive filament sliding
- events terminated by release of Ca2+ from sarcomere (relaxation - diastole), and reuptake into sarcoplasmic reticulum
decribe the mechanism of excitation-contraction coupling happens in SMC
- rise in intracellular calcium can occur by
i) depol of membrane opens Ca2+ channels and calcium enters
OR
ii) agonist induced release of calcium via IP3., through sarcoplasmic reticulum - Calcium binds to calmodulin, which actiavtes an enzyme called myosin light chain kinase (MLCK)
- MLCK activates myosin head by phosphorylating them (ATP -> ADP + Pi, Pi attaches to the head)
- phosphorylation of myosin light chain increase ATP activity and allows myosin head groups to bind to actin & undergo cross-bridge cycling (which initiates contraction)
explain mechanism of RBC interacting with Co2?
- The RBCs convert the CO2 to bicarbonate via carbonic anhydrase
- Most of the bicarbonate that is formed is expelled into the plasma and carried in the venous blood to the lungs.
- As bicarbonate diffuses out, chloride ions diffuse into the red blood cells to maintain electrical neutrality (the chloride shift)
- In the lungs, bicarbonate enters the RBCs and is converted back into C02, then released into the alveoli. Chloride leaves the red cell to balance the electrical charge of the bicarbonate leaving the cell
ALSO: BUT LESS IMPORTANT
- C02 is also carried to the lungs in the form of carbaminohaemoglobin.
- in lungs, the high partial pressure of oxygen and low pH displaces the CO2 from haemoglobin and oxyhaemoglobin is formed
what is a consequence of exercising muscles having vasodilation?
how does the body get around to solving this?
- vasodilation in the active muscles reduces total peripheral resistance and would, if not compensated for, cause a drop in blood pressure.
SO
- at the start of exercise the sympathetic outflow increases.
- This produces a general vasoconstriction in the non-exercising muscles and the digestive tract
- The result is that the decrease in vascular resistance in the exercising muscles is compensated by an increase in vascular resistance in the nonactive muscles
explain the mechanism that occurs if GFR is too low
and high :)
- *GFR too low**
- Cells in the macula densa of the JGA detect the concentration of sodium in the distal tubular fluid
- If Na+ levels are low, shows that GFR is too low
- The macula densa releases local chemical factors which relax the smooth muscle in the proximal tubule
- this increases the filtration pressure and GFR.
- *GFR too high**
- Cells in the macula densa of the JGA detect the concentration of sodium in the distal tubular fluid
- If Na+ levels are high, shows that GFR is too high
- The macula densa releases local chemical factors which constrict the smooth muscle in the proximal tubule
- *- decreases filtration pressure and GFR**
explain what occurs at the loop of Henle / what is absorbed etc
a) descending loop of Henle?
b) ascedning loop of Henle?
c) distal tubule?
d) collecting duct?
- *As the fluid descends DLH:**
- water moves out (via aquaporins), which makes the fluid more and more concentrated because it is in equilibrium with the high concentration in the extracellular fluid in the renal medulla.
- *fluid moves up the ALH:**
- the thick ascending wall is impermeable to water
- Na+ & Cl- are pumped out of tube into extracellular space: active transport by ATP-ase
- makes the fluid v. dilute (most of Na / Cl has been removed)
- *fluid moves to distal tubule:**
- aldosterone acts to increase Na reabsorbtion (and other materials)
- *fluid moves to collecting duct:**
- fluid passes down from here to ureter and ladders
- CD has aquaporins that are opened by ADH
- if channels are open: water is reabsorbed & urine is same osmolarity as renal medullary fluid
- if channels are closed: water not reabsorbed & dilute urine produced
what is the location, function and mechanism of action for the NKCC2 channels?
NKCC2 (Na-K-Cl cotransporter channel
- location: thick ascending limb of the loop of Henle
- function: to get Na / Cl out of the ascending limb and into extracellular fluid
- *- mechanism of action:**
i) luminal walls of the epithelial cells allows sodium, potassium & chloride ions to move passively together down their concentration gradient into the cells that make thick ascending limb
ii) then, sodium is actively transported out into extracellular space by Na/K ATP-ase
iii) Cl- moves passively with the sodium
iv) most of K+ ions diffuse back into the lumen via K ion channels
which pump assists the NKCC2 pump?
explain how xix
Renal Outer Medullary potassium channel or ROMK (royal orders make knights)
- K+ out of the tubule cells into the lumen (where fluid is)
- generates postive voltage: 10mV in tubular lumen
- creates an overall voltage difference of 80mV between tubular lumen and tubular cell
- this voltage difference helps propel sodium via NCKK2 transporter into tubular cells
explain the 4 reasons why oedema might occur xo
- *1. increased capillary hyrdostatic pressure**
- venous pressures become elevated (e.g. through gravitational forces / heart failure)
- this reduces the hydrostatic pressure gradient
- reduces reabsorbtion from interstitial fluid back into capillary
- *2. decrease in plasma oncotic pressure**
- decreases the pressure driving fluid back into capillary
- reduces reabsorbtion
- *3. increased capillary permeability**
- allows more water to leave cap
- also reduces the oncotic pressure different by allowing protein to leave the vessel more easily
4. lymphatic obstruction
what can cause:
- increased capillary hydrostatic pressure?
- decrease in plasma oncotic pressure:?
- increased capillary permeability: ?
- secondary lymphoedema:
- increased capillary hydrostatic pressure: heart failure
- decrease in plasma oncotic pressure: hypoproteinemia (less proteins in blood). e.g. malnutririon (Kwashiorkor) or liver disease
- increased capillary permeability: vascular damage (burns / trauma / inflammation)
- secondary lymphoedema: surgery, elephantiasis - worm infection, tissue injury
explain the different phases of cardiac (myocardium) excitation occurs
- *Phase 4: The resting phase**
- resting potential: −90 mV due to a constant outward leak of K+ through inward rectifier channels.
- *- Na+ and Ca2**+ channels are closed at resting TMP.
- *Phase 0: Depolarization**
- An action potential triggered in a neighbouring cardiomyocyte or pacemaker cell causes the TMP to rise above −90 mV.
- Fast Na+ channels start to open one by one and Na+ leaks into the cell, further raising the TMP.
- TMP approaches −70mV, the threshold potential in cardiomyocytes, i.e. the point at which enough fast Na+ channels have opened to generate a self-sustaining inward Na+ current.
- The large Na+ current rapidly depolarizes the TMP to 0 mV and slightly above 0 mV for a transient period of time called the overshoot; fast Na+ channels close (recall that fast Na+ channels are time-dependent).
- L-type (“long-opening”) Ca2+ channels open when the TMP is greater than −40 mV and cause a small but steady influx of Ca2+ down its concentration gradient.
Phase 1: Early repolarization
TMP is now slightly positive.
Some K+ channels open briefly and an outward flow of K+ returns the TMP to approximately 0 mV.
Phase 2: The plateau phase
L-type Ca2+ channels are still open and there is a small, constant inward current of Ca2+. This becomes significant in the excitation-contraction coupling process.
K+ leaks out down its concentration gradient through delayed rectifier K+ channels.
These two countercurrents are electrically balanced, and the TMP is maintained at a plateau just below 0 mV throughout phase 2.
Phase 3: Repolarization
Ca2+ channels are gradually inactivated.
Persistent outflow of K+, now exceeding Ca2+ inflow, brings TMP back towards resting potential of −90 mV to prepare the cell for a new cycle of depolarization.
how do action pacemaker cells, like the SA node and AV node create different action potentials compared to cardiomyocytes?
at cell in SAN Node:
- Na/K pump: 3 Na out/ 2 in. creates -5mV outside cell,
- K+ leaks out of the cell
- Ca2+ leaks into cell
- Na leaks into the cell
= creates a wondering baseline of positive increase in charge, until reaches -40mv:
- more Ca2+ channels open and come into cell, depolarisng the cell.
when reaches +20mV
more K+ channels open: repolarise the cell
repeat process.
explain the conduction signal of the heart [3]
SA Node: releases electrical stimuli at a regular rate
Each stimulus passes through the myocardial cells of the atria creating a wave of contraction which spreads rapidly through both atria.
The electrical stimulus from the SA node eventually reaches the AV node and is delayed briefly so that the contracting atria have enough time to pump all the blood into the ventricles
Electrical stimulus passes through the AV node and Bundle of His into the Bundle branches and Purkinje fibres
Causes the ventricles to contract
