::) Flashcards by patrick ellis

in cardiac wall - which is the OUTER and INNER layer?

what cells compromise the myocardium?

inner: endocardium - inside is blood / heart chamber
outer: epicardium

Myocardium: Comprised of cardiac myocytes, interlinked with intercalated discs with gap junctions on them. These myocytes are supported by fibro-collagenous tissue with extensive vascularisation

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which cardiac layer are purkinje fibres in?

a) epicardium
b) myocardium
c) endocardium
d) subendocardium?

which cardiac layer are purkinje fibres in?

a) epicardium
b) myocardium
c) endocardium
d) subendocardium

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what are the three layers that make up the heart valves?

– Fibrosa: forms the core of the valve -DIC.

– Spongiosa: LCT on atrial side (loose collagen/elastic fibres), as shock absorber. has bubble morphology (looks like a sponge)

– Ventricularis: Adjacent to ventricular surface of the valve. DCT with elastic fibres. Forms the chordae tendineae (fibrous cords covered with endothelium).

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purkinje fibres conduct depolaristion of heart. they’re sepcialised myocytes. How are they different to normal myocytes found in the myocardium?(4)

are larger than cardiac muscle fibres
have central pale staining with most of the common red staining shown in the periphery of the cell. - no T-Tubule system and
connect with each other via desmosomes and gap junctions rather NO intercalated discs.

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where do u find discontinous capillaries? why ?

what does this describe: ‘contractible cells wrapped around the endothelial cells’ - what is their function?

thymus & spleen - to allow leukocytes to leave !

= pericytes -> produce fibroblasts

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what are valves made from

valves: are semilunar projections of tunica intima into the lumen of the vessel. A

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where do you find each of the following:

a) fenestrated capillaries
b) continous capillaries
c) discontinous capillaries

a) fenestrated capillaries: extensive molecular exchange with the blood such as the small intestine, endocrine glands and the kidney.
b) continous capillaries: muscle & nerve tissue
c) discontinous capillaries: liver, thymus and spleen - that allows proteins, or even blood cells to pass through.

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what is pressure in sysetmic and pulmonary circ? at normal levls

systemic circ:
a) normal: 120 /80 mmHg

pulmonary circ:
a) normal: 25/8 mmHg

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what is starlings law of the heart?

ventricular contractile force is proproportional to end diastolic volume (aka ventricle will pump out however much blood is delivered to it by atria - more blood: more strongly pumped)
if more blood is delivered: ventricle expands to a greater diameter & contracts more strongly

why?

at low EDV: there is less overlap of cross bridges (of actin and myosin): weak contraction
at high EDV: more overlap of cross bridges stronger contraction
ncreasing the overlap of active region of A & M increases the force of contraction

BUT limit to starlings law:

If the preload is too great and the ventricle expands beyond a certain volume, the mechanism fails: ventricle contracts more weakly
this is a tipping point: beyong which heart failure starts to occur

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what is cardiac output? - what is it a product of?

and what is stroke volume? what is SV in normal, healthy person?

what is end diastolic volume? what is end systolic volume? why different?

how do u work out stroke volume from EDV and ESV?

*cardiac output:** is the amount of blood pumped by the heart minute (litres / min)
product of heart rate (HR) and stroke volume (SV)

stroke volume: volume of blood ejected during ventricular contraction or for each stroke of the heart. usually 70ml

*EDV** is the filled volume of the ventricle prior to contraction
*ESV** is the residual volume of blood remaining in the ventricle after ejection (not all gets ejected)

stroke volume = EDV - ESV (e.g EDV: 120 ml - ESV: 50 ml =70ml)

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what is isometric contraction of the ventricles?

Isometric contraction is when the pressure is rising in the ventricles, yet not enough for the aortic/pulmonary valves to be pushed open.

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what are the lubb and dupp heart sounds caused by? aka?

lubb: closure of AV valves followed by the opening of the aortic and pulmonary artery valves is the first heart sound. This is known as S1.
dupp: closure of the aortic and pulmonary artery valves followed by the opening of the AV valves is the second heat sound, known as S2

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what are s3 and s4 sounds? which pops more likely to hear?

what botth caused by?

*S3:
** faint low-pitched sound is heard in about 1/3 of the way through diastole in many children and young adults.
period of rapid ventricular filling and is due to turbulent flow during the filling
a sign of serious heart damage, possibly damaged heart valves.
*s4:**
*-** sometimes heard immediately before the first heart sound.
It is due to turbulent flow in the ventricle and rarely occurs in normal adults.

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what is JVP? what are the 3 waves of it

the jugular venous pulse: right atrium contracts a back pressure that occurs in the jugular vein

There are three peaks in the venous pulse: a, c, and v:

a pulse is due to atrial contraction just before the tricuspid valve closes
c wave is due to pressure rising in the atrium just after the tricuspid valve closes before the valve bulges back into the atrium,
v wave corresponds to venous filling when the tricuspid valve is closed

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Venous return to the heart is mediated by which three main factors?

One way valves in the veins

Muscular pumps

Thoraco-abdominal pump. During inspiration, pressures in the thoracic cavity are reduced, pulling blood into the inferior vena cava. On exhalation, thoracic pressure increases and this blood is forced into the right atrium

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when doe S1 and S2 heart sounds corresspond to on ECG?

Heart sounds:

*LUBB / SI:** after QRS
*DUPP / S2:** after T phase

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what is the Windkessel effect?

The walls of the aorta and elastic arteries distend when the blood pressure rises during systole and recoil when the blood pressure falls during diastole. There is a thus net storage of blood during systole which discharges during diastole.

Without this distension and recoil they would easily become damaged when the pressure rises, and their ability to accommodate the rapid blood flow is beneficial for keep pressure high

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how

Pulse pressure is the difference between systole and diastole. As arteries are elastic, pulse pressure normally decreases slightly from aorta to brachial artery

Mean arterial pressure (MAP) is calculated as diastolic plus 1/3 pulse pressure

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what happens to diastolic and systolic pressure when have stiff arteries?

what effect does this have on LV afterload and myocardial oxyegen demand?

there is a decrease in diastolic pressure (& increase in systolic presure)

These changes in pressure components increase LV afterload and myocardial oxygen demand

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how much ml per minute of blood does the following need?

brain, heart & kidneys?

what % do these three take up of overall cardiac output?

Your BRAIN needs about 700 ml per minute of blood (14-15% resting Cardiac Output)

Your HEART needs about 200 ml per minute of blood (4% resting cardiac output)

Your KIDNEYS take about 1250 ml/min (25% resting cardiac output)

These three organs take up about 40-45% C.O at rest.

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Which two factors influence the work of the heart? !

Diameter of arterioles (main)
Viscosity of blood

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what influences viscosity of blood? (4)

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blood viscosity depends on:
1. (mainly) on the haematocrit (proportion of red cells in blood, normally ~45%

2. On the mechanical properties (mainly the deformability) of the red cells:
If the cells are too large or malformed (e.g. as in sickle cell disease) they clog up the capillary and oxygen delivery is compromised

3. red blood cell aggregation

4. plasma viscosity.

what is polycythaemia? what is absolute polycythaemia? what is relative polycythaemia?

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Polycythaemia is a disease state in which the haematocrit increases. It can be due to an excessive production of red blood cells, absolute polycythaemia, or to a decrease in the volume of plasma, relative polycythaemia

what are immature RBC called?
what stain used?
how do RBC make ATP - what does mean for pH?

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reticulocytes
methylene blue
RBC produce ATP by glycolysis (glucose -> pyruvate -> lactic acid)
due to lactic acid = low pH

which glucose transporter do RBC use? what do rbcs become oxidised to ?

RBC use **Glut1**: faciliated diffussion. not regulated by insulin RBC become oxidsed by o2 -\> **methaemoglobin (oxidised haemoglobin)**

what is stucture of Haemoglobin A? what is structure of fetal Hb? strucutre of myoglobin?

Hb A = **2a, 2b subunits** Fetal Hb = **2a, 2g (gamma): f**etal haemoglobin has a higher affinity for oxygen than the adult haemoglobin, and thus can remove it from the placental blood at the lower partial pressure. myoglobin = **a single subunit**

which molecule is being described here: 'When beta subunits start to ....., it binds the beta subunits more tightly, moves into the centre of the Haemoglobin and increases the rate of oxygen release. 'enhances the ability of RBC’s to release oxygen in hypoxic tissues'

**2,3 DPG (2,3- di phosphoglycerate)** is a small separate molecule bound loosely to the Hb molecule. When beta subunits start to deoxygenate, 2,3 DPG binds the beta subunits more tightly, moves into the centre of the Haemoglobin and increases the rate of oxygen release. 2,3 DPG (2,3- di phosphoglycerate) is critical in making S shape of ox saturation curve Thus, it enhances the ability of RBC’s to release oxygen in hypoxic tissues.

why might a cold limb become hypoxic, even if well perfused? what is effect of lowering pH with regards to ppO2/

**lowering temperature** shifts **oxygen saturation curve to the left.** Hb releases oxygen less readily l**owering pH sh**ifts to the **right** (increases pp02)

what is the name for when myoglobin is relesed from damaged muscle tissue?

When myoglobin is released from damaged muscle tissue, the process is called **_rhabdomyolysis_**. The released myoglobin is filtered by the kidneys but is **toxic to the renal tubular epithelium** and so may cause acute renal failure

which hormone is haematocrit contolled by?

**EPO**

in sympathetic NS, what type of myelination are the preganglionic neurones and postganglionic neurons?

preganglionic neurones: **Type Ab axons - small myelination** postganglionic neurons: **Type C axons - unmyelinated**

explain how sympathetic NS causes vasoconstricntion?

The **postganglionic** neurone releases **noradrenaline** on to the **arterial smooth muscle** to make it contract via an action on **alpha 1 adrenoceptors.**

which sympathetic pre-ganglionic neurones DO NOT stop at ganglia and go directly to a gland? which sympathetic post ganglionic fibre does NOT release noradrenaline? what does it release instead?

Sympathetic innervation to the **adrenal medulla** is via myelinated pre-synaptic fibres, mainly from the T10 to L1 spinal cord segments. ## Footnote **sweat glands: secrete Ach on muscarinic R**

exercise causes what effects (think SNS and adrenaline innervation)

stimulates: - **brainstem:** respiratory centre to **increase rate AND depth of breathing** - **adrenaline: -** relaxes SM around lung airways - bronchodilation - liver and non active muscles to release glucose - stimulates lipolysis: FA for fuel * *- SNS & adrenaline:** increases **HR** and **force of contraction**

what are role of alpha 1 and alpha 2 adrenoreceptors? what are the roles of B1, B2 & B3 adrenoreceptors?

**alpha 1:** located on vasuclar SM. causes vasoconstriction. NT: noradrenaline. excitatory **alpha 2:** located .. inhibits the release of noradrenaline via negative feedback loop. NT: noradrenaline. inhbitoary: * *Beta 1 receptor:** location: heart function: increase force and rate of contraction of myocardium **Beta 2 receptor** location: bronchial smooth muscle function: primarily relaxes ^ further functions: (Decreased motility of the GI tract; Lipolysis in adipose tissue; Relaxation of detrusor urinae muscle of bladder wall; Glycogenolysis and gluconeogenesis; Stimulation of insulin secretions ; Thickened secretions from saliva; Inhibition of histamine release from mast cells) **Beta 3 receptor - unclear function** location: adipose tissue cells function: stimulates lipolysis

what effect do alpha 1, beta 1 and beta 2 (2) adrenoreceptors have in exercise?

**alpha 1 receptors:** constrict vessels in the non-active muscles and gut and so redistribute the blood to the active exercising muscles. **beta 1 receptors**: increase the rate and force of cardiac contraction and thus increase cardiac output * *beta 2 receptors:** i) relax bronchial smooth muscle to decrease airway resistance and increase oxygen uptake. ii) increase glucose supply to exercising muscle by glycogenolysis (breakdown of glycogen) and gluconeogenesis (formation of glucose)

how does stress influence sympathetic NS? how does prolonged stress damage your ability to cope with stress?

- causes cortisol to be released - causes increase in adrenaline and noradrenaline synthesis - If cortisol production is lowered the sympathetic nervous system becomes progressively weaker

which are receptors detect change in BP? for neural control ! where located? barorecptors nerve fibres travels up the brain and syanpse where?

change detected by **baroreceptors:** - **carotid sinus** in the **internal carotid arter**y (just above the bifurcation of carotid arteries) - **aortic sinus** travel up via CN IX or CN X & synapse at **nucleus of solitary tract (NTS)**

where in the medulla is the NTS located? what does the NTS connect to ? (2) - which one of these is linked to parasympathetic output and sympathetic output?

The Nucleus of the solitary tract (NTS) lies near the **dorsal surface of the medulla** NTS connects to: - the **vasomotor centre** in the **rostral medulla: _sympathetic output_** - **nucleus ambiguus** in the **nearby lateral medulla: _parasympathetic output_**

BP is detected in the carotid and aortic sinus, afferent nerve fibres come via CNIX and CNX to the NTS centre in brain. Describe the efferent nerve fibre outflow and effect if: a) BP is too low (3) b) BP is too high (2)

a) BP is too low: - NTS, **via the vasomotor centre,** activates SNS: **noradrenaline acts on alpha 1 adrenoreceptors** on vascular smooth muscle = **vasoconstriction** - increase in HR - raises CO - constriction of veins b) BP is too high: - NTS, via the **nucleus amibguus,** actvates PNS: **SAN** inhibiting muscarinic receptors to cause **hyperpolarisation** of the cardiac muscle cells and therefore **slow the heart down** - vasomotor centre inhibited

carotid massage increases WHICH output (para or sym)?

**increases vagal output**

how does excersie decrease hypertension? (long term)

causes release of NO - vasodilates

whats in the carotid body?

**chemoreceptors - pa02**

where do the renal arteries llie on abdominal aorta? and in relation to which other artery?

inferior to superior mesenteric artery L1/2

name for the arteries that terminate in kidey glomerulus?

arcuate glomerulus

urine drains out of dct into what? (2)

into calyxes -\> renal pelvis -\> ureter

what is average GFR for both kidneys for healthy adult?

The total amount of fluid filtered through ALL the glomeruli in BOTH kidneys in a fit adult is about **120-125 ml/min.**

what happens to filtration pressure & GFR if afferent arterioles contract / relax?

- if afferent arterioles contrict: l**owers filtration pressure & GFR** - if afferent arterioles relax: **increases filtration pressure & GFR**

which cells detect changes in GFR? where located/

macula densa in JGA

what is clearance?

GFR is measured by the CLEARANCE of a selected material. **It is the effective volume of plasma completely ‘cleared’ of a substance per minute** Clearance is measured in units of litres/minute

when does Clearance = GFR?

when substance in blood is removed at same rate as water passes through glomeruli: Clearance = GFR

what happens to GFR value if kidneys are damaged?

Generally **GFR will decrease** although RPF may be normal. Measurement of GFR is an essential test of kidney health.

how do u measure clearance?

::) Flashcards

(53 cards)