Physiology Flashcards
Explain the pacemaker potential
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
Factors affecting rate of discharge of SA node?
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
What are the factors affecting inotropic state of cardiac myocytes
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
Explain myocyte action potential
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
Describe the excitation contraction coupling
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
Describe the venous return curve and describe the factors affecting it
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
What are the mechanisms that help venous return against gravity?
Muscle pump
Venous valves
Thoracic pump: During inspiration it sucks up VR
Heartbeat effect: atrial suction and ventricular suction
Define Edema, mention its causes
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
What is meant by autoregulation? Explain it’s types
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
Give an account of the diff vasoactive substances secreted by endothelium.
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.
Explain natriuretic peptides types, synthesis, stimulators and action
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
Describe the role of atrial baroreceptors in arterial blood pressure regulation
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.
Describe the role of peripheral chemoreceptors in arterial blood pressure
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
Describe the role of the kidney in regulation of arterial pressure
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.
Describe rapid compensatory reaction to hemorrhage.
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
Describe the long term compensatory reaction to hemorrhage
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
Regulation of coronary vascular resistance
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
Define intra-pleural pressure value causes and importance
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
Discuss nature/ functions of surfactant/ causes of surfactant deficiency
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
Causes of surfactant deficiency
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:
List factors affecting airflow in respiratory passage
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
Define dead space, type significance?
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.
Explain causes of regional difference in alveolar ventilation-perfusion
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.
Discuss variation of ventilation and perfusion in chronic bronchitis.
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.
