Physiology 1: Final Review Flashcards
cAMP Second Messenger System: Gs, Gi, Adenylate cyclase
Gs stimulate, Gi inhibit adenyl cyclase.
IP3 and DAG Second Messenger System: PLC
PLC membrane bound converts PIP2 into IP3 and DAG. IP3 moves to ER and helps release Ca++ store. DAG remains in membrane and activate PKC, this phosphorylates proteins and causes Ca++ influx
cGMP Secondary Messenger Systems
Membrane bound guanylate yclase helps form cGMP from GTP. NO activates soluble types of guanylate cyclase and increase cGMP. cGMP acts on ion channels (phospohdiesterases) and activates cGMP-dependent protein kinase.
Ca/Calmodulin complex
activates NO synthase which creates NO from argentine.
NO Synthetase
NO formed by breakdown or Arginine. NO acts on soluble guanylate cyclase.
Cholinergic Receptors: Nicotinic vs Muscarinic; #’s, types, means of action (channel vs. G-protein)
Nicotinic: N1 - skeletal muscle, N2 - ganglia. Form pore across membrane, ACh binding causes pores to open.
Muscarinic: M1,3,5 - activate PLC using Gq = increase in intracellular Ca++. M2,4 - inhibit adenylate cyclase using Gi.
Adrenergic receptors: alpha and beta receptors
Beta receptors stimulate adenylate cyclase to produce cAMP and activate PKA.
Alpha1 receptors increase IP3 and DAG or activate Ca-channels using Gq.
Alpha2 receptors inhibit adenylate cyclase by Gi.
Resting Membrane Potentials: Nerves and Muscles
-70mv Nerves, -90mv Muscles
Nernst Equation
E= (61/charge)log([ion]out/[ion]in)
Describe how the P Na/K ration affect membrane potential in a typical cell:
Higher Ratio = more Na and less negative membrane potential, easier to excite
Lower Ratio = more K and more negative membrane potential, less easy to excite
Gastrin
Increases stomach motility
Increases force of contractions
Relaxes pyloric sphincter = gastric emptying
Secreted in pyloric stomach
Motilin
Increases force of stomach contractions
Migrating Motor Complex (MMC)
GIP - Gastic Inhibiting Protein
Decreases gastric motility
Secreted in response to fats in duodenum
CCK
Secreted in small intestine
Decreases stomach motility
Increases gallbladder contractility
Results in EMZYME rich pancreatic secretions
Secretin
Decreases GI track motility
Secreted in response to acid
Results in AQUEUS pancreatic secretions rich in BiCarb
Saliva; relation to plasma, qualities
Hypotonic to plasma, proline rich = antibacterial, amalyases for starch digestion, PNS-vasodilation-increase blood flow
Parasympathetic action on GI track
ACh & Substance P = increased contractions
VIP & NO = decreased contractions
Sympathetic action on GI track
NE = inhibits ACh = blocks Alpha2 receptors, results in vasoconstriction
Nicotinic Receptors
N1: skeletal muscle, blocked by curare
N2: ganglia, blocked by hexomethonium
Muscarinic Receptors
M1 - glands M2 - heart/smooth muscle M3 - smooth muscle/glands M4 - unknown M5 - unknown
M1,3,5 - active PLC vía Gq = increase intracellular Ca++
M2,4 - inhibit adenyl cyclase via Gi
Alpha Receptors
Stimulated: Epi, NE.
Agonist: Phenylepherine
A1; post-junctional, Increase IP3 & DAG via Gq
A2; pre/post-junctional, decrease adenylate cyclase via Gi
Beta Receptors
Stimulated: Epi, NE
Agonist: Iso
B1; heart/kidneys
B2; elsewhere
B3; fat cells
All: increase adenyl cyclase, cAMP, activate PKA
Single Unit vs. Multiple Unit Smooth Muscle
Single Unit: many gap junctions, sparse innervation, slow wave potentials with spontaneous, graded oscillation in membrane potential, plasticity, and stretch induced contraction.
Multiunit: less gap junctions, higher innervation ratios, stable membrane potentials without spontaneous depolarization.
Economy and Efficiency of Smooth Muscle
Lower efficiency in smooth muscle due to 2 ATP requirement for light chain phosphorylation.
Economy is higher because ATP use is low when maintaining contraction force (latch state).
Cardiac Conduction System; locations, path, speed
SA node: primary, fast
AV node: secondary, slower, delay for ventricular filling
Bundle of His: last, ventricular spread, relatively quick
What is preload, other names?
Preload is the load/length on the muscle at rest before the onset of contraction = also equals the end diastolic volume or pressure.
What is after load, other names?
Afterload is the load the muscle is contracting against after the onset of a contraction = resistance to the ejection of blood.
Intrinsic Respiration
How cells handle and utilize oxygen
Extrinsic Respiration
How 02 is delivered from the external environment to cells
Special considerations of bronchial circulation
This circulation is supplied from the left ventricle but in this blood a “venous admixture” / “right to left shunt” occurs as deoxygenated venous blood mixes with oxygenated pulmonary venous blood returning to left heart.
Lung sounds; crackles, wheezing, rhonchi
Crackles: inspiration sound due to airways popping open or air flowing through fluid. Fine are high pitched, more intense, shorter duration. Coarse are lower, less intense and longer duration (associated with CHF and pneumonia).
Wheezing: labored breathing with inspiration and expiration, associated with airway compression.
Rhonchi: low pitched, snoring quality, inspiration and expiration due to secretions.
Effects on Ventilation; airway resistance, airway compliance
Increased resistance decreases flow
Increased compliance results in less structural support of lungs during expiration, lungs collapse increasing resistance and trapping air in the lungs.
Decreased compliance requires larger inflation pressure to move same amount of air.
Clinical hypoventilation, associated factors
PaCO2>40, accompanied by low PAO2.
Means patin is not losing CO2 waste efficiently and also not getting enough O2 into tissue.
A-a difference, average value, what it means.
A-a is the difference between Aveolar and arterial partial pressure of oxygen. Normally between 5-20 mmHg. Increased difference means poor O2 exchange in capillaries.
Possible causes: V/Q mismatching, Right to Left Shunt, diffusion impairment.
Obstructive diseases; definition, effect on lab values, examples
Trouble getting air out.
Normal TLC
Low FEV1.0/FVC ratio (should be >0.7)
Asthma; increase activity of airway smooth muscles.
COPD; chronic bronchitis due to inflammation and edema of airway walls increasing resistance obstructing emptying of lungs.
Restrictive diseases; definition, effect on lab values
Trouble getting air in.
Reduced TLC
Normal or Increased FEV1.0/FVC
Interstitial fibrosis; dyspnea worsening on exertion, clubbing and cyanosis, due to chronic infections causing infiltration of immune cells into causes scarring in alveolar walls = decreased lung compliance.
Heart sounds; S1, S2, which valves open/close with each sound.
S1: Mitral and Tricuspid closure, beginning of systole
S2: Aortic and Pulmonic valve closure, beginning of diastole.
S2 Splitting: Aortic closure 1st, Pulmonic closure 2nd
Valve Sequence
M Close, T Close, P Open, A Open, A Close, P Close, T Open, M Open
BER; stomach, duodénum, jéjunum
Stomach: 3/min
Duodénum: 12/min
Jejunum: 9/min
Swallowing Phases
- Oral or Voluntary Phase - separates food bolus
- Pharyngeal Phase: soft palate moved upwards, UES relaxes, peristalsis pushes food down, coordinated by “Swallowing Center” - vagus nerve
- Esophageal Phase - primary and secondary peristalsis.
Esophageal Sphincters
UES - at swallowing pressure drops allowing bolus into esophagus
LES: tonically contracted, relaxation is mediated by a vagovagal reflex known as “receptive relaxation”.
Phases of Ventricular Systole
Isovolumetric contraction
Rapid ejection
Reduced ejection
Phases of Ventricular Diastole
Protodiastole Isovolumetric relaxation Rapid filling Diastasis Atrial Systole
MMC Phases
1: slow waves with little activity
2: irregular action potentials and increasing contractions
3: intense activity
4: rapid decline in activity
Which stomach region secretes what?
Cardiac: Mucus
Fundic: Acid
Pyloric: Mucus and Gastrin
Which stomach cells secrete which substances?
Epithelium: mucus and alkaline fluid
Parietal Cells: HCL and Intrinsic Factor
Chief/Pepetic Cells: Pepsinogen
Neck Cells: Mucus
What stimulates pepsinogen secretion?
Histamine, ACh, Gastrin, Secretin
What secretes Intrinsic Factor and what stimulates it’s secretion?
Parietal cells secrete IF and is also stimulated by histamine, ACh, Gastrin, Secretin.
