CR EOYS2 Flashcards

1
Q

what is the thoraco-abdominal pump that is a drive of venous return of blood? [1]

A

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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2
Q

what is starlings law of the heart?

A
  • 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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3
Q

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?

A
  • *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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4
Q

what is isometric contraction of the ventricles?

A

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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5
Q

what is JVP? what are the 3 waves of it

A

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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6
Q

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

A

Heart sounds:

  • *LUBB / SI:** after QRS
  • *DUPP / S2:** after T phase
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7
Q

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

A

Heart sounds:

  • *LUBB / SI:** after QRS
  • *DUPP / S2:** after T phase
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8
Q

Q

what is the Windkessel effect?

A

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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9
Q

how do you calculate pulse pressure? [1]

A

difference between pressure of artery in systole and diastole

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10
Q

Which two factors influence the work of the heart? [2]

A
  1. Diameter of arterioles (main)
  2. Viscosity of blood
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11
Q

what influences viscosity of blood? (4)

A

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

  1. 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.

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12
Q

what is stucture of Haemoglobin A?

what is structure of fetal Hb?

strucutre of myoglobin?

A

Hb A = 2a, 2b subunits

Fetal Hb = 2a, 2g (gamma): fetal 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

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13
Q

Q

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

A

A

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

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14
Q

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

A

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)
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15
Q

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

A

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)
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16
Q

which are receptors detect change in BP? for neural control !

where located? [2]

barorecptors nerve fibres [2] travels up the brain and syanpse where? [1]

A

change detected by baroreceptors:

  • *- carotid sinu**s in the internal carotid artery (just above the bifurcation of carotid arteries)
  • *- aortic sinus**

travel up via CN IX or CN X & synapse at nucleus of solitary tract (NTS)

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17
Q

Q

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

A

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
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18
Q

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

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
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19
Q

what is average GFR for both kidneys for healthy adult?

A

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

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20
Q

which cells detect changes in GFR? where located/

A

macula densa;

juxtaglomerular apparatus

21
Q

how does excersie decrease hypertension? (long term)

A

causes release of NO - vasodilator

22
Q

when does Clearance = GFR?

A

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

23
Q

how do u measure clearance?

A
24
Q

which part of nephron controls blood pressure?

A

juxtaglomerular apparatus

25
Q

loop of henle is responsible for filtering what % of Na and H20, from urine -> blood?

A

20% Na

15% H20

26
Q

what would u use furosemide for? (2)

A

Furosemide removes excess water in the body: blocks NaKCC channel

indications:

  • oedema
  • resistant hypertension
27
Q

Diabetes insipidus is caused by what?

A

Diabetes insipidus; damage to the hypothalamus or posterior pituitary leading to loss of ADH secretion. Result high volume of dilute urine.

28
Q

where do u find the cells that release ANP ? what stimulus do they cause

what is their effect? where does the effect occur!

A

Specialised muscle cells: right atrium and inferior vena cava.

In response to stretch (indicating increased preload) these cells release atrial natriuretic peptide (ANP)

ANP decreases Na+ reabsorption in the distal tubule and collecting duct of the kidney.

29
Q

where do u find the cells that release ANP ? what stimulus do they cause

what is their effect? where does the effect occur!

A

Specialised muscle cells: right atrium and inferior vena cava.

In response to stretch (indicating increased preload) these cells release atrial natriuretic peptide (ANP)

ANP decreases Na+ reabsorption in the distal tubule and collecting duct of the kidney.

30
Q

what would u use furosemide for? (2)

A

Furosemide removes excess water in the body: blocks NaKCC channel

indications:

  • oedema
  • resistant hypertension
31
Q

which part of nephron controls blood pressure?

A

juxtaglomerular apparatus

32
Q

what would u use furosemide for? (2)

A

Furosemide removes excess water in the body: blocks NaKCC channel

indications:

  • oedema
  • resistant hypertension
33
Q

Diabetes insipidus is caused by what?

A

Diabetes insipidus; damage to the hypothalamus or posterior pituitary leading to loss of ADH secretion. Result high volume of dilute urine.

34
Q

how do thiazide diuretics work?
what is an AE of these?

A

Thiazide diuretics like bendroflumethiazide (Aprinox) inhibit reabsorption of sodium and chloride ions from the distal convoluted tubules in the kidneys by blocking a Na+/Cl− cotransporter.

One important adverse effect of long-term thiazide use is loss of potassium resulting in hypokalaemia.

35
Q

* how do u calculate net filtration pressure? *

A

NFP = (HPc - HPif) - (OPc - OPif)

36
Q

what are distinguishing features of the spleen? (2)

A

no cortex or medulla

has red and white pulp

37
Q

what are Epithelial reticular cells? where do u find?

A

Epithelial reticular cells, or epithelioreticular cells (ERC) are a structure in both the cortex and medulla of the thymus.

Make sure that no T cells are allowed to survive which could attack the body’s own cells

38
Q

Q

where in a lymph node would you find:

a) B cells
b) T cells
c) immature B cells

A

A

The nodes are covered by a capsule of dense connective tissue, and have find lymphocytes

  • cortex (under the capsule) - lymphoid follices: B cells
  • *- deep cortex:** T cells
  • medulla: B cells (immature)
39
Q

what are Hasssals corpsucles?
function?
location?

A

hassals corpuscles: concentric layers of flattened reticular epithelial cells filled with keratohyalin granules and keratin.

activate dendritic cells

only found in thymus

40
Q

where does the intercostal neurovascular bundle lie in relation to intercostal muscles?

A

between internal and innermost IC muscles

41
Q

what are the names and locations of the pleural recesses? [2]

A
  1. costadiaphragmatic: located between the costal pleurae and diaphragmatic pleura
  2. costomedialstinal: located betweeen the costal pleurae and the mediastinal pleurae, behind the sternum
42
Q

what does the eustachian tube connect?

A

eustachian tube: connects the middle ear cavity to the nasopharynx

43
Q

what do the vocal cords attach to i) anteriorly ii) posteriorly? [2]

A

anterior: thyroid cartilage
posterior: artyenoids

44
Q

which artery branches off the obturator artery? [1]

A

internal common iliac -> obturator artery -> (passes through the obturator foramen) acetabular branch

acetabular supplies the hip joint

45
Q

how do you managed treatment for hypertension depending on patient populations race and age?

A

under 55 = ACE

black / afro carribean = Ca2+ channel blockers

46
Q

what are effects of RAAS system? [4]

A

differing effects depending on where it binds:

  • *i) proximal tubule**: Increases Na+ reabsorbtion, which increases blood flow, which increases BP
  • *ii) adrenal cortex:** increases aldosterone, which causes increase Na+ reabsorbtion in distal tubule, increase bloodflow and BP
  • *iii) systemic arterioles**: binds to GPCR = artriolar vasoconstriction = increases BP
  • *iv) brain:** stimules release of ADH = increase Na reabsorbtion
47
Q

what are the three mechanisms that RAAS system might be activated? [3]

A
  1. sympathetic nerve activation (via B-adrenoreceptors)
  2. renal artery hypotension
  3. decreased sodium delivery to the distal tubules of the kidney
48
Q

what is the green?

A

costodiaphragmatic recess :)