Physio Final PDF

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Final Review ...

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Final Exam Topics and Hints General: 1. Focus on themes such as homeostasis, autonomic nervous system, find role of ANS in homeostasis look at Cannon’s postulates etc • Role of ANS: coordinates and integrates blood volume, blood osmolarity, blood pressure, body temperature. 2. Review exams 1-3; use exam keys as learning tools. Topics to review: Basic Topics: Movement across membranes, Osm/Ton, Hormones, Neuro 1. Difference between teleological and mechanistic approaches to physiology • Teleological: describing physiological processes by their purpose rather than their mechanism. o “Why?” • Mechanistic: the ability to explain the mechanism that underlie physiological events o “How?” 2. Movement of molecules across membranes: • Simple vs. mediated transport o Simple: small, nonpolar molecules, goes down concentration gradient. Gases and steroid hormones. o mediated: crosses membrane with the help of a membrane protein. Can be passive or active. • active vs. passive o active: Charged molecule up concentration gradient. Na+/K+ ATPase, H+/K+ ATPase. o Passive: facilitated diffusion. Charged or polar down concentration gradient. Glucose via GLUT and Na via If channels. • 1o active vs. 2o active. o Primary: uses ATP. Charged, down concentration gradient. o Secondary: moves one molecule against concentration gradient by having it follow another that is moving with its concentration gradient. Glucose via Na/glu symport. Polar, up concentration gradient. *3. Characteristics of mediated transport. Be able to draw/interpret graphs, and to apply to renal reabsorption and secretion. SEE SEPARATE PAPER. 4. Body compartments and markers to determine volumes of distribution; be able to determine TBW, ECF, ICF and plasma. DIAGRAM ON SEPARATE PAPER. • Markers: o Evan’s blue: binds to plasma proteins, measures plasma. o Radioactive albumin (RISA): also measures plasma volume. o Inulin: goes everywhere except inside the cells so it measures ECF. Also: sucrose. o Deuterium oxide (D2O): heavy H2O, measures TBW. Another version is tritiated H2O (THO) o Radio chromium: blood volume • Calculations: o Interstitial = ECF – plasma o TBW = ECF + ICF o Volume of compartment = (mL indicator injected * [indicator]) / [compartment] ▪ c1v1 = c2v2 o plasma volume = blood volume * 1-Hct o ECF OSMOLARITY = ICF OSMOLARITY b/c water moves across cell membranes easily.

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5. Osmolarity vs. tonicity: be able to work quantitative problems (s.g. p.13-14 #12, 13, 14 or HW1 or exam 1, p. 5-6 or discussion ex p. 16-17), qualitative chart problems (s.g. p. 13 #10-11), RBC problems (s.g. pg. 9-11). Understand the relevance to IV therapy ( s.g. p. 14 #14 or 16 # 4) STUDY GUIDE PROBLEMS WORKED ON SEPARATE SHEET. Solutes • NaCl—functionally non-penetrating; will not enter cells • Urea—freely penetrating, moving back and forth between ECF and ICF until [urea] equal. (not until amounts are equal!) • Glucose (dextrose) –penetrates cell but once inside is phosphorylated and becomes nonpen • Intracellular solutes—non-penetrating Water • Water will distribute based on the relative concentrations of the nonpenetrating solutes. Water moves to the compartment with the higher concentration of nonpenetrating solutes. • Water distributes evenly across all compartments, so at equilibrium: ECF osmolarity = ICF osmolarity = total body osmolarity • All administered fluids go first into the ECF. • Any time you add a volume to a body, the volume of the total body (and therefore of at least one of its compartments) must increase. • Any time you add a solution to a body, the final osmolarity of the body will depend on the osmolarity of the added solution. • Any time you add solute only (e.g., eat salt), the body osmolarity will increase. All hyposmotic solutions are hypotonic. IVs: Solution

Osmolarit y

Osmolarity Tonicity compared to compared to body = 300 mOsM body cells (300 mOsM)

Effect on ICF

Used to treat

NS

300 mOsM

Iso

iso

~ none

hemorrhage

D5NS

578 mOsM

Hyper

~ iso

~ none

hemorrhage

D5W

278

~ iso

hypo

swells

hypoglycemi a

½ NS

150

Hypo

hypo

swells

Dehydration

D5 ½ NS

428

Hyper

hypo

swells

dehydration

6. Steroid vs. peptide vs. amine hormones. Compare/contrast and then categorize every hormone specifically covered this semester. Review hormone interactions: permissiveness, synergism, antagonism (s.g. p. 19 #3, 4; p. 20 #10 & 11; exam 1 p. 5 #5) *melatonin from tryptophan Peptide

Steroid

Catecholamines

Thyroid Hormones

Synthesis and storage

From a.a.s, made in advance, stored in secretory vesicles

Made on demand from precursors, from cholesterol

Modify tyrosine side groups, made in advance, stored in secretory vesicles

Made from 2 tyrosine + iodine, made in advance, precursors stored in secretory vesicles

Release from parent cell

Exocytosis

Simple diffusion

Exocytosis

Simple diffusion

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•

Transport in blood

Dissolved in plasma

Bound to carrier proteins

Dissolved in plasma

Bound to carrier proteins

Half life

Short

Long

Short

Long

Location of receptor

Cell membrane

Usually cytoplasm Cell membrane or nucleus

Response to receptor-ligand binding

Activation of Activation of second messenger genes systems

Activation of Activation of genes second messenger systems

General target response

Modification of existing proteins and induction of new protein synthesis

Induction of new protein synthesis

Modification of existing proteins

Induction of new protein synthesis

Examples from this semester

Trophic hormones from hypo., ADH from post pit, growth hormone, ACTH, insulin, glucagon, gastrin, CCK, IGF, parathyroid hormone, TSH. (majority)

Aldosterone, cortisol, androgens, calciferol, vitamin D, estrogen, progesterone.

Epinephrine, norepineprine, dopamine.

T3, T4

Nucleus

Hormone interactions: how they interact at their target cells (SEE GRAPHS IN JOURNAL) o Synergism: the effect of interacting hormones is MORE THAN additive. ▪ Aka “potentiation” ▪ Ex glucagon, epin, and cortisol all raise blood glucose levels. o Permissiveness: one hormone cannot fully exert its effects unless a second hormone is present. o Antagonistism: two molecules work against each other, one diminishing the effectiveness of the other. ▪ Opposing actions ▪ Can involve receptors/inhibitors or completely different pathways.

7. Hypothalamic/ant. pit. pathway of control; 1o vs. 2o pathologies and how to distinguish them (s.g. p. 20, 7-9 or discussion exercise p. 23-4 or exam 1 p. 4, D #1-4) MAPS ON SEPARATE PAGE • Ant pit is a true endocrine gland • Post pit is an extension of neural brain tissue, secretes neurohormones • Primary pathology: arises in the last endocrine gland of a reflex • Secondary pathology: arises in one of the tissues producing trophic hormones 8. Ligand receptors—general categories and general mechanisms elicited by ligand binding (Fig 6.3 or 6-5) Relate to hormones and NTs studied this semester • Lipophilic signal molecules can diffuse through the membrane (genes, new proteins) o HORMONES o Slower pathway response time • Lipophobic signal molecules can’t diffuse and bind to membrane proteins/receptors on surface o Fast pathway response time o Types of protein receptors: ▪ Receptor channels: gated, alters ion flow. FOR Ach ON SKELETAL MUSCLE NICOTINIC. Not 2nd messenger if it only causes voltage changes. ▪ For the next 3, info must be passed across the membrane ! signal transduction with a second messenger system.

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▪ ▪

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▪ ▪

Receptor enzymes: ligand binding activates an intracellular enzyme. PEPTIDE HORMONES, INSULIN G protein-coupled receptors: ligand binding opens an ion channel or alters enzyme activity. FOR HORMONES (PEPTIDE), GROWTH FACTORS, AND NEUROTRANSMITTERS. MUSCARINIC, ADRENERGIC. Integrin receptors: ligand binding alters the cytoskeleton STEROID HORMONES USUALLY BIND TO RECEPTORS IN CYTOPLASM

**9. Compare/contrast autonomic vs. somatic nervous system. C/C parasymp vs. symp. (s.g. p. 26 # 6) Make a chart of adrenergic vs. cholinergic receptors and the targets on which they are present.(s.g. p. 43 #4) • Autonomic: not under voluntary control. o divided into sympathetic (fight or flight, excitatory) and parasympathetic (rest and digest, inhibitory) • Somatic: voluntary control of skeletal muscles. Excitatory only (muscle contracts) • SEE CHARTS IN STUDY GUIDE PG 4, PICTURE ON SEPARATE PAGE • Adrenergic receptors: NE/E on target cell , postganglion, symp, alpha (NE on arterioles and veins), beta 1 (NE and E on heart) and beta 2 (E on arterioles) • Cholinergic receptors: nicotinic (Ach, preganglion, both symp and para) and muscarinic (Ach, target cell, postganglion, para) ! *10. Membrane potential: how established; increase vs. decrease potential difference • Resting membrane potential determined primarily by K+ concentration gradient and the cell’s resting permeability to K, Na, and Cl. See SG pg 4 • Relating to exam 3 material: o Cl- follows electrical gradient created by Na transport during reabsorption 11. Homeostasis: definition, response vs. feedback loops; reflex vs. local control. How does reflex vs. local control apply to CV, respiratory, renal, and digestive? • Definition: ability of the environment to maintain a relatively constant internal environment. • Feedback loop: information about a response that is sent back to the IC o Negative feedback is homeostatic (response opposes or removes the signal), positive is not • Response loop: control pathway that begins with the stimulus and ends with the response. o Feedback loops modulate the response loops • Reflex control: long distance homeostatic control in which the decision that a response is needed is made away from the cell or tissue o Involves nervous system (efferent = muscles and glands, “efferent neuron”) and endocrine system (efferent = hormone), colored boxes in maps o Has response loop and feedback loop • Local control: homeostatic control that takes place strictly at the tissue or cell by using paracrine or autocrine signals o [O2] in a tissue decreases ! blood vessels sense low O2 !secrete paracrine signal (CO2, lactic acid) ! muscles relax ! vessel dilates ! more blood and O2 come to the area • CV (ch 14, 15): o Hormones travel in the blood to their targets o Reflex: Autonomic neurotransmitters alter heart rate (symp/NE on B1 receptors of autorhythmic cells to inc HR or para/Ach on muscarinic receptors of auto cells to dec HR), vasoconstriction/dilation o Local: heart ecitation/contraction • Respiratory (17, 18) o See local control example

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o o o

• •

Regulation of pHby controlling CO2 lvels Control of ventilation (conscious or unconscious), Constriction of bronchioles by hormone/nervous system, this is local if controlled by histmine or CO2 (paracrines) Renal (19, 20) o Control of pH, osM, ECF volume, BP Digestive (21) o Regulate mass balance, secretion of digestive enzymes, cephalic reflex

12. Cannon’s postulates, particularly as applies to cardio. • The nervous system has a role in preserving the “fitness” (conditions for normal function) of the internal environment. o coordinates and integrates blood volume, blood osmolarity, blood pressure, body temperature. • Some systems are under tonic control. o Like volume control o Neural regulation of diameter of blood vessels (increased signal rate ! dec. diameter) • Some systems under antagonistic control. o Symp nerves increase HR, para nerves decrease HR • One chemical signal can have different effects in different tissues. o Epin constricts or dilates blood vessels depending on alpha or B adrenergic receptors. * largely integrated with exam 3 material (chapters 18, 19, 20, and 22) **integrated with exam 2 material (see exam 2 review doc) Cardio & Respiratory! 1. Relate Flow = ΔP/R to CV and to respiratory. What creates the pressure gradient in each? Where is resistance regulated? (s.g. p. 43 #3) • Flow rate: Q, volume that passes a point per unit time, HOW MUCH • Blood/ gasses flow b/c they move down pressure gradients • P can change without a change in volume • CV: heart creates high pressure when it contracts. Blood flows from this area of high P to blood vessels (low P). as it moves, pressure is lost b/c of friction, P falls as distance from heart inc. R is also related to vessel diameter and length and viscosity (area relates to velocity) o R regulated by baroreceptor reflex (Symp output inc/dec !NE inc/dec !alpha receptor on arterioles ! vasoconstriction/dilation ! inc/dec R) • Respiratory: air is less viscous and compressible ! high flow, low pressure o Mvmt of the thorax during breathing causes alternating conditions of high/low P in lungs. Changes in vol of the chest cavity due to contracting muscles cause the pressure gradients. o R is low because shorter vessels and larger area in pulmonary arterioles o R is regulated by diameter of airways. ▪ Upper: physical obstruction (ex mucus) ▪ Bronchioles: constriction (para neurons – muscarinic receptors, histamine)/dilation (CO2, Epin on B2 receptors). Cardiovascular

Respiratory

site of variable resistance

arterioles

bronchioles

site of highest resistance

Aorta

trachea

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location of pacemaker

SA node

Medulla oblongata

Neural control of resistance

sympathetic (inc. art. Resist)

para (inc. bronchiolar resistance)

muscle type of pump

cardiac

skeletal

CNS control center

medulla

medulla and pons

effect of low interstitial oxygen

vasodilation

vasoconstriction

2. Organize CV info under mean arterial pressure (MAP) map. SEE SEPARATE PAGE • basic anatomy of heart: o Heart: ▪ Valves ensure only one direction ▪ Central wall divider: septum • Right side: receives blood from tissues and sends it to lungs for oxygenation • Left side: receives newly oxygenated blood from lungs and pumps it to tissues ▪ Atrium: receives blood returning to heart from blood vessels ▪ Ventricle: pumps blood out into the blood vessels o Vessels: ▪ Away = arteries, toward heart = veins ▪ Capillaries: where the oxygen leaves the blood for the tissues, change from red to blue, switch from arterial to venous side of circulation ▪ Pulmonary circulation: right side to lungs and back to left side ▪ Systemic circulation: carry from left side to tissues and back to right side • path of conduction through it: o SA node depolarizes o Internodal pathways o AV node o AV bundle o Bundle branches o Purkinje fibers o Ventricular muscle • autorhythmic vs. contractile APs: o Autorhythmic myocardial cells: where the signal for contraction originates. Noncontractile myocardium (only 1%). Can generate APs spontaneously. Unstable membrane potential called a pacemaker potential, which is due to If channels that allow net influx of positive charge. Steep depolarization due to Ca2+ influx, repolarization due to K+ efflux. o Myocardial contractile cells: AP’s have a rapid depolarization phase created by Na+ influx and a steep repolarization phase due to K+ influx. The AP also has a plateau created by Ca2+ influx. Striated muscle. Gap junctions allow waves of depolarization to spread rapidly. Comparison of Action Potentials:

Membrane Potential

SKELETAL MUSCLE

CONTRACTILE MYOCARDIUM

AUTORHYTHMIC MYOCARDIUM

Stable at -70 mV

Stable at -90

Unstable pacemaker potential; usually starts at -60 mV

6!

Events leading to threshold potential

Net Na+ entry through Ach operated channels

Depolarization enters via gap junctions

Net Na entry through If channels, reinforced by Ca entry

Rising phase of AP

Na+ entry

Na entry

Ca2+ entry

Repolarization phase

Rapid, caused by K+ efflux

Extended plateau by Ca2+ entry; rapid phase by K efflux

Rapid, caused by K+ efflux

Hyperpolarization

Due to excessive K+ efflux at high K+ permeability when K+ channels close. Leak of K and Na restores potential to resting state

None

Normally none but Ach and para. can slow depol by hyperpol.

Duration of AP

Short: 1-2 msec

Extended: 200+ msec

Variable; generally 150+ msec

Refractory period

Generally brief

Long b/c resetting of Na+ channel gates delayed until end of AP

None

•

•

• •

ECG: see SG for wave/problems • waves: o P wave: depol of the atria o QRS complex: the next trio of waves, progressive wave of ventricular depol o T wave: repol of the ventricles • calculate heart rate given beats within particular interval, or length of R-R interval o often records at 25 mm/sec • recognize partial vs. complete heart block, fibrillation, tachycardia, bradycardia pg 495 o complete: the conduction of electrical signals from atria to ventricle through AV node is disrupted so ventricles go with their fastest pacemaker which is much slower , often too slow to maintain adequate blood flow o fibrillation: arrythmia where SA node has lost control of pacemaking calculations of HR, CO, MAP: o MAP = diastolic P + 1/3 (systolic P – diastolic P) o Closer to dis than syst bc dias lasts twice as long as systole o Prop to CO x Resistance o CO = HR x stroke volume pressure-volume curve: see SG pg 5 baroreceptor reflex (PG 532, HW2): SEE JOURNAL

! 3. Fight/flight reflex—know how Epi from adrenal medulla reinforces effects of Norepi, and also causes vasodilation in certain tissues • see symp section of baroreceptor reflex for NE effects (vasoconstriction) • E from adrenal medulla travels through blood and binds with alpha receptors, reinforcing vasoconstriction (not as responsive to E as NE though) (constrict to push blood from non essentials like GI tract to vital organs) • E also binds to B2 receptors to cause vasodilation in heart, muscle, liver, tissues (muscles needed to fight) 4. Be able to relate all aspects of respiratory physiology to the 4 processes of external respiration (Fig. 17.1) E.g. HbO2 curve fits under transport in blood • Exchange of air btwn atm and lungs (ventilation) – airways

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• • •

Exchange of O2 and CO2 btwn lungs and blood - alveoli Transport of O2 and CO2 by blood – pulmonary/systemic circulation Exchange of gases btwn blood and cells - cellular respiration

5. Relate process of ventilation to Fig. 17.9 (17-11. What muscles are involved in quiet vs. deep inspiration or expiration? Know intrapulmonary (or intra-aveolar) pressure vs. intrapleural. What is the transpulmonary pressure gradient? What happens to it in pneumothorax? • See SG page 6 #10 • Quiet inspiration: diaphragm, external intercostals, scalenes • Deep/forced breathing: o Inspiration: also uses sternocleidomastoids o Expiration: also uses internal intercostals and abdominal muscles! 6. Work of breathing: difference between compliance and elastance; factors that affect compliance; factors that affect resistance of the air...