Physiology

Question 1

Explain the pacemaker potential

Answer 1

Phase 4: resting membrane potential. membrane is -60 mv opening of slow Na channels that give inward current which causes depolarization

Opening of T-type Ca channels with Ca inflow, reaches -40 mV

Phase 0: firing level. closure of slow Na and T Ca channels. Opening of L-type Ca channel giving slow AP response and opening of delayed rectifying K+ channels

Phase 3: repolarization

Opening of delayed rectifying K+ channels, closure of LCa channels and in activation of delayed rectifying K+ channels and activation of slow Na channels restarting a new phase 4

Question 2

Factors affecting rate of discharge of SA node?

Answer 2

Body temp: for every degree 10 heart beats

Autonomic activity:
Sympathetic: tachycardia
Parasympathetic: bradycardia

Catecholamines: adrenal medulla releases adrenaline and noreadrenaline which increases HR

Extracellular K level: hypokalemia is tachycardia and hyper is bradycardia

Ca channel blockers: in activation causes bradychardia

Question 3

What are the factors affecting inotropic state of cardiac myocytes

Answer 3

Positive inotropic:

increasing sympathetic or catecholamines which increases Ca in cells

Glucagon: increases c-AMP in myocytes

Increase ECF Ca which makes more inter the cell

Drugs: digitalis and caffine

Negative inotropic:

Ischemia: hypoxia to cardiac muscle

Increase parasympathetic: release acetylcholine which decreases c-AMP

Adenosine: — c-AMP

Drugs: Ca channel blockers and anesthetic drugs

Question 4

Explain myocyte action potential

Answer 4

Phase 4: RMP

K+ slowly moves out (Ik1) through inward rectifying potassium channels IRK to reach RMP (-90 mV)

Phase 0: Depolarization goes to +20 mv

fast Na channel op and Na influx
IRK close
Fast Na channels close

Phase 1: rapid small initial repolarization

Fast Na are inactivated
transient outward channels op

Phase 2: plateau

L Ca open, inward Ca current
Na and Ca exchanger active
Op of delayed rectifying K

Phase 3: rapid repolarization

Long lasting Ca channels closed
K outward current and then closer of DRK
op of IRK

Question 5

Describe the excitation contraction coupling

Answer 5

Membrane depolarization–> op of L type Ca–> Ca enters below sarcolemma which open ‘ryanodine Ca channel” which cause SR to release Ca

❶ Ca++ binds to Troponin-C → contraction as described for skeletal muscle

❷ Ca++ release decreases when AP ends.

❸ Relaxation: Ca++ is removed from the cytoplasm by:

a. Ca++ pump into SR

b. Ca++ is transported into ECF by:
• Na+ -Ca++ exchanger
• Ca++ pump

Question 6

Describe the venous return curve and describe the factors affecting it

Answer 6

Effect of changes in right atrial pressure on venous return curve: +++ RAP → —- VR —–RAP→+++ VR

Effect of changes in MSFP on venous return curve:

+++ MSFP→ shift of VR curve up & right

—–MSFP→ shift of VR curve down & left

Question 7

What are the mechanisms that help venous return against gravity?

Answer 7

Muscle pump

Venous valves

Thoracic pump: During inspiration it sucks up VR

Heartbeat effect: atrial suction and ventricular suction

Question 8

Define Edema, mention its causes

Answer 8

Abnormal large accumulation of ISF in lower limb

Causes:

Inadequate lymph flow

Decrease osmotic pressure gradient: accumulation of osmotically active substance in the interstitial space

Increased filtration pressure: high venous pressure

Increase capillary permeability

Question 9

What is meant by autoregulation? Explain it’s types

Answer 9

Intrinsic capacity of vascular beds to compensate for moderate changes in perfusion pressure by
changing vascular resistance so that blood flow remains constant

Myogenic autoregulation:

Aim: maintain constant blood flow to an organ in spite of increase in its perfusion pressure

Mechanism: +++ perfusion pressure–> increase in blood flow and makes blood vessels distended which causes Ca to enter and cause VC increasing the resistance.

Metabolic auto-regulation: maintain constant blood flow to organ despite decrease of perfusion pressure

—- perfusion pressure → initial —- in blood flow
→ +++ VD metabolites → relaxation of arterioles & pre-
capillary sphincters → — resistance →+++ blood flow

Question 10

Give an account of the diff vasoactive substances secreted by endothelium.

Answer 10

NO: stimulated by acetylcholine and its action is VD of coronary, cerebral and pulmonary vessels

Endothelin-1: Stimulated by Hypoxia, catecholamines, stress. Inhibited by NO, prostacyclin
VC of veins, renal VC, pulmonary VC and coronary VC, positive chronotropic and inotropic effect

Prostacyclin: Action: VD, decrease platelet aggregation and facilitates NO release.

Question 11

Explain natriuretic peptides types, synthesis, stimulators and action

Answer 11

a. Atrial natriuretic peptide (ANP) → by atrial myocytes
b. Brain natriuretic peptide (BNP) → by ventricular myocytes & brain.
c. C-type natriuretic peptide (CNP) → endothelial cells, brain, kidney

Secretion is increased by:

❶ Stretch of atrial muscle fibers

❷ +++ Na+ concentration in ECF.

❹ Angiotensin-II.

❸ +++ sympatheticß-adrenoceptors.

❺ Endothelin.

Actions: counters ABP raising affects; decreases blood volume

Question 12

Describe the role of atrial baroreceptors in arterial blood pressure regulation

Answer 12

Found in left and right atrium as well as pulmonary vessels.

Stimulation:
❶ Distension of atrial walls.
❷ +++ blood volume → +++ their discharge.
❸ — blood volume (hemorrhage) → — their discharge.

Stimulation leads to VD and increase HR

Prevents accumulation of blood in atria and pulmonary vessels.

Question 13

Describe the role of peripheral chemoreceptors in arterial blood pressure

Answer 13

found in carotid and aortic bodies,

Stimulation:

❶ Primarily concerned with respiratory regulation

❷ Marked — in ABP → — blood flow in carotid, aortic bodies → hypoxia → +++ of peripheral chemoreceptors

Response: +++ Peripheral chemoreceptor → tachycardia and VC to increase ABP

Question 14

Describe the role of the kidney in regulation of arterial pressure

Answer 14

Basic and most important mechanism for long-term regulation of ABP:

a) +++ ABP → +++ renal excretion of Na+& water → pressure natriuresis → — – ECF volume & ABP. Pressure natriuresis continues until — ABP to normal level.

b) — ABP (hemorrhage) → — renal Na+ & H2O excretion → minimize the —- of ABP.

II- Renin-angiotensin-aldosterone system:

❶ — ABP → +++ rennin → angiotensin II → long-term regulation of ABP through:

a) — Na+ and water excretion by the kidneys.

b) +++ aldosterone → +++ Na+& H2O reabsorption → +++ ECF volume → +++ ABP

❷ +++ ABP → — angiotensin II & aldosterone → +++ Na+& H2O excretion → — ECF volume → —- ABP back to normal.

Question 15

Describe rapid compensatory reaction to hemorrhage.

Answer 15

❶ — ABP → — arterial baroreceptors
❷ — blood volume → — atrial volume receptors
❸ — blood flow rate → +++ peripheral chemoreceptors

VC of skin, renal vessels and arterioles and veins
increase HR and inotropic state of heart

Release of catecholamines like adrenaline

Angiotensin II: VC, thirst sensation

ADH: increase water retention 1

Question 16

Describe the long term compensatory reaction to hemorrhage

Answer 16

Correction of plasma volume: tissue fluid shift, thirst sensation aldosterone (for Na and H2O reabsorption and ADH secretion to decrease water waste.

Correction of plasma proteins

Correction of RBC by increasing erythropoietin

Question 17

Regulation of coronary vascular resistance

Answer 17

Myogenic autoregulation

Metabolic regulation: high exercise makes coronary VD and increase coronary flow to match.

endothelial regulation:
VD substances like NO
VC like endothelin

Sympathetic and parasympathetic: cause VC and VD

Question 18

Define intra-pleural pressure value causes and importance

Answer 18

normal expiration: -3 Normal inspiration: -6
forced inspiration: -40 Forced expiration: +50

Function of IPP: helps lung expansion and VR

Causes of the negativity of IPP

Recoil tendency of the lungs due: elastic tissue and surface tension of alveoli

Expansion tendency of chest wall due: Elasticity of muscles tendons of chest

Question 19

Discuss nature/ functions of surfactant/ causes of surfactant deficiency

Answer 19

Formed of lecithin

it decreases surface tension by

① Facilitate lung expansion during inspiration (↓effort)

② Prevent alveolar collapse during expiration

③ Prevent pulmonary edema

Question 20

Causes of surfactant deficiency

Answer 20

① Respiratory distress syndrome

• in premature infant →↓ Surfactant →↑ surface tension → lung collapse

②Long term inhalation of 100% 02 or use of pump oxygenator in cardiac surgery

③ Obstruction of branch of pulmonary artery

④ Heavy smokers

⑤ Hypothyroidism

⑥ Hypocorticism

⑦ Hyperinsulinsm:

Question 21

List factors affecting airflow in respiratory passage

Answer 21

Physical factors:

negative intrapleural pressure: During inspiration → more negative intrapleural pressure → more airways distention →↓ airway resistance.

Lateral tension: During inspiration as alveoli expand → exerts lateral traction on small airways →↓ airway resistance.

Nervous: sympathetic and parasympathetic

Chemical factors: cause bronchodilation like hitamine

Question 22

Define dead space, type significance?

Answer 22

❶ Anatomical Dead Space: volume of air in the conducting zone = 150 ml

❷ Physiological dead space = anatomical dead space + alveolar dead space. in normal both are the same

Significance:

❶ Difference in composition between inspired, alveolar and expired air: Alveolar air contain less PO2 and more CO2 than inspired/expired

❷ Differences in alveolar ventilation in various breathing patterns: in shallow rapid there is low
ventilation causing hypoxia. In deep becomes high alveolar ventilation

Protective function: humification and warming of inspired air. Removal of foreign particles from air.

Question 23

Explain causes of regional difference in alveolar ventilation-perfusion

Answer 23

VA/Q = 0.8.

Both alveolar ventilation and perfusion ↓ from lung base toward apex

At apex, perfusion is poor compared to ventilation

At base, perfusion is high compared to ventilation

Cause of the regional difference:

Under the effect of its weight, the lung drop → widen
pleural space more at lung apex
Intra pleural pressure is more negative at apex than base

Cause of regional difference in perfusion is due to the effect of gravity.

Question 24

Discuss variation of ventilation and perfusion in chronic bronchitis.

Answer 24

At ideal ventilation and perfusion: Arterial PO2 slightly < alveolar PO2 due to venous admixture

At normal perfusion, no ventilation (in bronchial obstruction): VA/Q is 0, capillaries can’t be oxygenated

At normal ventilation, no perfusion (pulmonary embolism) VA/Q is infinite. No gas exchange.

Question 25

Mention causes of hemoglobin O2 dissociation curve/significance.

Answer 25

Relationship between PO2 and % HbO2 saturation is S shaped

Plateau part: PO2 from 100 to 60 mmHg the saturation is relatively constant, doesn’t go below 90%. Importance at high altitudes allow easy saturation even if O2 tension is low

Steep part: At 60 mmHg, desaturation is very rapid. At 40 mmHg 27% of O2 is taken by tissue. At 20 mmHg curve becomes vertical.

Question 26

Name factors that shift curve to the right

Answer 26

Means ↓ Hb affinity to O2 = less O2 bound to Hb

↑ temperature

↑ PCO2

↑ H+ (↓PH)

muscular exercise

↑ (2.3 DBG)

Question 27

Factors that shift curve to the left

Answer 27

Means ↑ Hb affinity to O2 = more O2 bound to Hb

❶ ↓ temperature

❷ ↓ PCO2

❸ ↓ H+ (↑ PH)

❹ ↓ 2,3 DBG

❺ Carbon monoxide

❻ ↓ fetal hemoglobin

Question 28

Chloride shift phenomenon

Answer 28

At tissues; CO2 diffuse from tissue to blood according to pressure gradient. CO2 gets converted into HCO3- which causes an electric charge. Chloride diffuses from plasma to RBCs so it can neutralize this charge.

At the lungs: Low CO2 tension, HCO3 shifted from plasma to RBC’s and Chloride returns to plasma.

Question 29

Describe the site and stimuli of central chemoreceptors.

Answer 29

Site: under ventral surface of medulla

Stimulus:

↑H+ (primary stimulus)

 H+ in CSF & brain interstitial fluid: the only direct stimulus

 H+ in blood: has no effect on stimulating central chemoreceptor

b) ↑ PCO2 in blood

 indirect effect as CO2 crosses BBB

 CO2+H2O → H2CO3→ HCO3- + H+ (acidifying CSF)

 Small change in arterial PCO2→ results in large changes in CSF pH

Question 30

Describe site, innervation, stimuli of Peripheral chemoreceptors:

Answer 30

Site: carotid bodies and aortic bodies

They monitor only PO2

Stimulus:
↓ Oxygen tension (hypoxia) most potent stimulus. At PO2 60 doubles ventilation, PO2 100 no effect on ventilation and at 20 inhibit RC.

H+ concentration:
Metabolic acidosis: stimulate ventilation
Metabolic alkalosis: inhibit ventilation

CO2 tension: when increase it stimulates ventilation

Question 31

Why hypoxia is a weaker stimulus for respiration than CO2 excess?

Answer 31

↓ PO2 from 100-60 mmHg has a minimal effect on Hb O2 saturation

Stimulatory effect of ↓ PO2 from 100 to 60 mmHg → not affect ventilation

↓ PO2 has Stimulatory effect on peripheral chemoreceptors & inhibitory effects on RC