Physiology Flashcards

1
Q

1.Normal renal blood flow
2.?percentage of cardiac output
3. ml/100g/min

A
  1. 1.2L/ min
  2. 20-25% CO
  3. around 420ml/100g/min
    this varies from resource to resource but aroud 350-450 in general.
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2
Q

which measure is the best measure of LV contractility?

A

Ejection fraction
EF is less influenced by preload//afterload as other measures (LVEDP, LVEDV, LVESP, SV)

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3
Q

what does ST elevation in II, III, AVF suggest?

Which vessel is occluded

A

inferior MI
inferior left ventricle is supplied by RCA in 90% of individuals therefore inferior MI is likely due to RCA occlusion

LAD supplies anterior wall of LV
LCA supplies lateral and posterior of LV

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4
Q

During vigorous exercise what changes occur to enhance oxygen delivery to skeletal muscles.

A

1.relaxation of skeletal muscle precapillary sphincters increases blood fllow & O2 delivery 20-30 fold

  1. increased CO increases delivery 5-10 fold
  2. increased o2 offloading from Hb (2-3 fold)
  3. increased PaO2 gradient (<2fold)
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5
Q

pH of venous blood is only slightly lower than arterial blood despite addition of large amounts of CO2- why?

A

The Haldane effect, which describes the increased capacity for deoxyhaemoglobin to carry CO2, as carbaminohaemoglobin & to buffer H+ ions generated from dissociation of carbonic acid. (Isohydric buffering)

plasma proteins and dissolution of CO2 play a minor role in CO2 transport

Carbonic Anhydrase plays a major role but cannot buffer pH changes caused by addition of CO2

Definition of the Haldane Effect
The Haldane effect states that:

Deoxygenation of hemoglobin increases its ability to carry CO₂ and H⁺ (as carbamino compounds and bicarbonate, respectively).
Conversely, oxygenation of hemoglobin reduces its capacity to carry CO₂ and H⁺, facilitating the release of CO₂ in the lungs.
This effect helps optimize CO₂ transport and release in the body.

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6
Q

Which rhythms are at risk of asystole

A

-ventricular pause >3secs
-Recent Asystole
-Complete HB with broad QRS
-Mobitz II (regular PR interval, occasional dropped QRS)

(Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node) where as Mobitz I is often due to suppression at AV node due to reversible causes (drugs, reversible ischaemia)

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7
Q

What is the average circulating blood volume?

A

around 5L
75ml/kg

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8
Q

What is the alveolar gas equation for working out alveolar oxygen tension (PAO2)

A

PAO2=[FiO2 x(Patm-PaH2O)] -PaCO2/ R

Where R is respiratory quotient (amount of CO2 produced (200ml/min) divided by amount of O2 consumed (250ml/min).
The value with a normal diet is 0.8
PAO2= PiO2 - PaCO2/ R
PiO2 = FiO2 - (PB-PaH2O)
e.g 0.21- (100kPa -6.3kPA)
because partial pressure exerted by water vapour at body temp is around 6.3kPa

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9
Q

Tell me about surfactant, type 1 and type 2 cells

A

produced by type 2 alveolar cells (pneumocytes) which are granular modified epithelial cells that contain microvilli. they are immature in infants.

surfactant is a lipoprotein complex that releases surface tension in lungs preventing collapse. it also contains proteins, lipids etc

Type 1 cells cover 95% surface area of alveoli, are 1 cell thick & responsible for gas exchange in lungs.

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10
Q

What is the direction of the spread of the excitatory wave in the heart?

A

From the endocardial surface outwards

This corresponds with the position of the neural network.

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11
Q

What effect does carotid sinus massage work & what effect does it have on ventricular contraction?

A

Carotid sinus massage increases pressure, mimicking high bp. The baroreceptors stretch and sen signals via glossopharyngeal nerve (CN IX) to nucleus of solitary tract in medulla of the brainstem.

In response, the brain increases PS output via the vagus nerve (CN X) which slows firing of SA node, reducing HR (negative chronotropy)#

-Can be used in narrow complex tachycardias to treat reentrant tachycardias.
-CI carotdid stenosis/plaque, recent TIA/stroke, carotid hypersensitivity syndrome

With a slower HR, ventricles have more time to fill during diastole, increasing the end-diastolic volume.
This increases the force of ventricular contraction through improved preload.
FRANK-STARLING mechanism: increased EDV stretches myocardial fibres, optimising overlap of actin and myosing filaments, which enhances force of contraction during subsequent systole

This is accompanied by a reduced rate and increased filling time.

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12
Q

Which phase of the cardiac cycle shortens most during exercise?

A

Diastole shortens during exercise to allow sufficient time to contact and eject blood effectively.

This is an issue in tachycardia or daistolic dysfunction because the heart may struggle to fill adequately. e.g HF with preserves ejection fraction-ventricles struglge to realx, leading to inadequate perfusion during diastole. Diastole shortens excessively in SVT, fast AF particulalry if stiff ventricles or valvular disease

coronary perfusion occurs during diastole. Coronary arteries supply myocardium and originate from the aortic root just above the aortic valve

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13
Q

What is the effect of de-innervation of the heart on heart rate?

A

Significant increase in heart rate due to reduced vagal tone

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14
Q

what causes contraction of bronchial smooth muscle?

What causes relaxation

A

contraction:
-sulphur dioxide (irritating to airways and can lead to release of pro-inflammatory cytokines and leukotrienes (potent bronchoconstrictors). Can also stimulate arachidonic acid pathway leading to release of prostaglandins and leukotrienes.
-acetylcholine (hence anticholinergics that block acetylcholine at muscarinic receptors lead to bronchodilation) .
-leukotrienes.

relaxation of bronchial smooth muscle:
-VIP (broncho & /vasodilate), effects due to increase NO, cyclic GMP) VIP and NO are co-transmitters
-Epinephrine: beta 2 agonist (beta 2 receptor stimulation leads to relaxation of bronchial smooth muscle mainly through increase in cAMP- helps in fight or flight)
-
-

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15
Q

1 effect of beta 2 adrenergic receptor stimulation:

  1. Name two non specific beta blockers
A
  1. beta 2 stimulation:
    -bronchodilation
    -vasodilation of skeletal muscle increasing blood flow during fight or flight
    -glycogenolysis (breakdown of glycogen)
    -uterine relaxation
    -relaxation of smooth muscle- GI tract and bladder
  2. non specific beta blockers: Propranolol, timolol
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16
Q

1.effect of beta 1 adrenergic receptor stimulation

  1. Name the specific beta1 blockers
A

beta 1 receptor are primarily found in the heart.
stimulation increases HR(chronotropy), conduction speed (dromotropy), contractility (inotropy)

specific beta 1 blockers: atenolol, bisoprolol, metoprolol, esmolol (short acting)

17
Q

tell me about lung compliance

A

determined by plotting a sigmoid pressure-volume curve graph of pressure(x) against volume (y).

relationship between pressure and volume is linear in the middle range (during tidal volumes)

compliance is decreased at low and high volumes, pulm oedema, and pulm fibrosis

compliance increases with age

Normal compliance(Cl) of a lung= 200ml/cmH2O (range 100-400)

total static compliance (Ct) includes compliance of chest wall (Ccw) that is also 200ml/cmH2O

summation of elastance =1/compliance

Ct= CI + Ccw

The dynamic compliance is inversely proportional to the frequency of ventilation & refers to compliance during normal air flow. change in volume is divided by change in airway pressure (whereas it is divided by change in intrapulmonary and intrapleural pressure in static)

Static compliance= change in volume/change in pressure.
refers to compliance when there is no air flow (end-insp/end exp when flow has temporarily stopped) - influencd by lung elasticity, surface tension, and stiffness of chest wall.
increased compliance can occur with emphysema where lungs can overexpand but may not recoil properly.
reduced compliance

18
Q

magnesium
1. is it intracellular or extracellar
2. normal blood levels
3. effect on calcuiu
4. clinical uses
5. effect of hypermagnaesia on reflexes

A

largely an intracellular cation, mainly in bone & skeletal muscle
1% is extracellular
normal plasma levels 0.75-1.05 mmol/l
anatgonises actions of calcium

use in pre-eclampia as anticonvulsant
relaxes vascular smooth muscle, causing vasodilation thus lowering bp

effective tocolytic (helps reduce uterine contractions)
-decreases ACh release at NMJ thus neuromuscular function is weakened.

increased magnesium levels reduce deep tendon reflexes gradually until absent.
Tendon reflexes are used at bedside as a measurement of hypermagnaesia.

19
Q

Explain the Frank-Starling mechanism

A

When the ventricles are filled with more blood during diastole (increased end-diastolic volume, EDV), the cardiac muscle fibers are stretched more.
This stretch optimizes the alignment of actin and myosin filaments within the muscle cells, leading to a stronger force of contraction during systole.
As a result, the stroke volume (amount of blood ejected with each heartbeat) increases to match the increased venous return.
In simpler terms:

More blood in = stronger contraction = more blood out.

20
Q

define pharmacodynamics

A

What the drug does to the body

effects of drugs on the body and the mechanisms through which these effects occur.

21
Q

define the following drug interactions & give examples:

  1. Summation
  2. Synergism
  3. Potentiation
  4. Antagonism
A
  1. summation =drugs are additive in effect
    eg benzos & propofol, N2o & volatiles
  2. synergism- greater effect than additive
    e.g propfol and remi, clonidine and opioids.
  3. potentiation: one increases the effect of the other
    e.g Non-depolarising NMBs and MgSO4, probenacid prevents renal excretion of penicillin
  4. Antagonism- opposing effect of drugs
    eg flumezanil with benzos, neostigmine and non-depolarising NMBs

reactions can be direct e.g flumezanil reversing benzos, morphine and nalaxone

or indirect e.g neostigmine and ND NMBs, adrenaline and enoximone

22
Q

Tell me about enoximone

A

phosphodiesterase III inhibitor which (as well as adrenaline) by inhibiting PDE III prevents breakdown of cAMP thus increasing the levels of cAMP in cardiac and vascular smooth muscle cells.

increased cAMP enhances calcium influx, improving myocardial contractility (positive inotropy).

in vascular smooth muscle, elevated cAMP causes vasodilation, reduced SVR & PVR. vasodilation decreases venous return and preload (& afterload) thus reducing the workload of the heart.
-> increased SV, CO.
-> decreased pulmonary capillary wedge pressure, reflecting reduced congestion in heart failure.

Adrenaline achieves this by binding to G-protein receptors.

23
Q

1.define pharmacokinetics
2. define absorption

A

1.what the body does to the drug
2. absorption: movement of drug from site of administration into the plasma (no necessary for all drugs eg topicals for derm conditions, bronchodilators for asthma.
by definition IV is completely absorbed and non is lost (100% bioavailability)

24
Q

define first pass metabolism

give examples of drug with high first pass metabolism

what happens with IM drugs

A

first pass metabolism is where an orally administered drug is metabolised by the liver via the portal system prior to reaching the systemic circulation.

Drugs with high first pass metabolism (thus reducing bioavailability): morphine, midazolam, lidocaine, aspirin, GTN

IM avoids first pass metabolism as they allow direct absorption into the systemic circulation.

25
Q

what is the equation for bioavailability

whats the difference between absolute and relative BA

A

F is the fraction of an administered drug that reaches the systemic circulation intact and is therefore available to act at the site of action.

bioavailability (F)= AUC (PO)/ AUC (IV)

absolute BA is the equation above.

relative BA is calculated for drugs unable to be given IV and compares formulations eg capsule vs tablet

26
Q

tell me about osmolality in the blood
what is the equation

A

A raised osmolality with hyponatraemia, suggests the patient may have hyperglycaemia (as in diabetes mellitus). This can also be seen with hyperglycinaemia, as can occur post transurethral resection of the prostate (TURP).
Serum osmolality can also be calculated using the following simple equation:-

Calculated osmolarity = 2 (Na+) + Glucose/18 + Urea/2.8 (all in mmol/L)

The difference between the measured osmolality and the calculated is known as the osmolal gap and is normally less than 10 mOsm/kg.

A raised osmolal gap provides evidence of the presence of another osmotically active substance, for example ethanol, methanol, isopropyl alcohol or ethylene glycol. Note however that a normal osmolal gap does not exclude ethylene glycol toxicity..
Urine osmolality is used in the differential diagnosis of hyper- and hyponatraemia and in investigating abnormalities of ADH action (suspected SIADH or diabetes insipidus).

An osmolar/osmolal gap (difference between measured and expected) >10 can be caused by toxic alcohols (e.g., ethanol, methanol, ethylene glycol, isopropyl alcohol*), mannitol, and lorazepam infusions (which contain propylene glycol).

*Isopropyl alcohol causes a large osmolar gap but does not cause an anion gap metabolic acidosis.