Term
| 4 types of lymphnodes. where they are and what they indicate? |
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Definition
1.Cervical nodes-in nech-swelling can indicate pharyngitis(strep) or lymphoma
2.Axillary nodes-in armpit-swelling can indicate breast cancer,lymphoma,bubonic plague
3.inguinal nodes-in groin-various tick-borne infections(lyme,tularemia,rocky mtn spotted fever)
4.mesenteric nodes-anoung viscra-GI infections(amebic dysentery) |
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Term
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Definition
1.thymus-serves as the site of early maturation of t-lymphocytes-lg in young kids shrinks post-adolescence
2.tonsils-are lag cervical lymph nodes-help protect from pharyngeal infections
a)palatine tonsils-in oropharynx-above base of tongue
b)pharyngeal tonsils(adenoids)-in nasopharynx near openings of Eustachian tubes
3.spleen-reservoir for blood cells of various types including erythrocytes,lymphocytes, and monocytes
-w/tramatic blood loss-it contracts and forces cells into circulation |
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Term
| since cardiac output is a product of -------*------------ it can be changed by changing -------- -----. |
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Definition
Heart Rate
Stroke Volume
either
one |
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Term
| What two things control heart rate? |
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Definition
| nervous and hormonal control |
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Term
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Definition
-autonomic innervation of SA node,AV node, and myocardium
-sympathetic input ot the SA node is via the chain ganglia of the sympathetic trunk. The endings secrete norepinephrine(Beta-adrenergic receptors) effect of input is to increase HR by hypopolarizing the cells of the SA node (closer to threshold so it fires sooner)
-sympathetic input to the AV node increases it's conductance also increases rate(decreases delay)
-sympathetic input to the myocardium decreases the time in systole which also increaes HR
-parasympathic input of the SA node is via the vagus nerves(#10) the endings are cholinergic-is to decrease HR by hyperpolarizeing the cells of the SA node-further from threshold-firing delayed
-both sympathetic and parasympatheic systems are continuously active-ratio of symp/parasymp impulses to SA node will set the actual rate |
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Term
| What is athelic bradycardia? |
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Definition
| abnormally low resting HR due to regualr aerobic exercise your cardiovascualar increases and the cardiovas system can meet the body's demands w/ a lower resting HR |
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Term
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Definition
| -is thru secretion by adrenal medulla-release of epinephrine in "fight or flight" response causes a dramatic increase in HR and contraction strength. |
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Term
| intrinsic control of contraction strength |
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Definition
| -involves the "frank-starling law of heart"=states that ventricular contratction strength is directly proportional to the end diastolic volume therefore EDV increases contraction strength increases |
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Term
| extrinsic control of contraction strength |
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Definition
-nervous and hormonal
-sympathetic stim increases contraction strength along w/ HR
-adrenal sec. also increases contraction strength throughout sympathetico-adrenal stim has 2 effects on the heart
1.positive chronotropic effect-increases HR
2.positive inotropic effect-increases contraction strength |
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Term
| What are the 4 primary factors involved what the rate of venous return to the heart? |
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Definition
1.difference in pressure(deltaP)=between the venules and heart-determines the gradient for flow
-pressure at the venules is about 10mm Hg-pressure at the heart is about 0mm Hg therefore (Delta P) is 10 mm Hg
2.sympathetic innervation to the veins-causes arent very muscular but it can help w/ return a little
3.skeletal muscle pump-when the skeletal nuscles contract the squeeze near by veins and that forces the blood along-valves in the veins prevent backflow so it must flow toward the heart(when standing blood must counter gravity)
4.negative pressure w/in the thoracic cavity on inspiration-decreased pressure at the heart-thus increased gradient for return |
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Term
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Definition
1.CHF-blood pooling in veins decrease return in capillaries b/c of back pressure
2.corticosteriod therapy-electrolyte imbalances resulting draw fluid into tissues
3.decrease in PP production-due to starvation,liver damage,etc-decrease oncotic pressure for return
4.increase in PP's in tissues-ex.b/c of contusions or microanglopathy etc.
5.chronic hypertenstion-increase the filtration pressue
6.hypersec. of corticosteriods-ex. cushing's syndrome-rel. to electrolyte imbalances
7.hormonal changes w/ menstral cycle
8.renal failure-decreases fluid elimation
9.blockage of lymphatics-ex:breast cancer,lymphoma,elephantiasis,etc. |
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Term
| Kidney regulation of blood volume |
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Definition
-the kidney's filter about 180 liters of fluid per day from flood.
-most of this is reabsorbed as the filtrate passes down the kidney tubules leaving 1-2 liters per day to be excreted as urine
-kidneys control your body h2O volume thru mechanisms affecting the rate of reabsorption
-2 hormones are involved
1.ADH-prod. in hypolthalamus-stored and rel. from post pituitary
2.aldosterone-prod. by sonz glamerulosa of adrenal cortex |
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Term
| the kidney hormone ADH can work alone or in tandem w/aldosterone to regulate blood volume |
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Definition
-ALONE-is governed by the plasma osmolality when osmolality rises(dehydration)this is detected by osmoreceptors in the hypothalamus and the trigger ADH rel. which increases H2O retension by the kidneys thus diluting the plasma-osmolality decreasing as the BP and blood pressure increase
-IN TANDEM-is governed by the BP entering the kidneys-the mechanism is NOT direct several steps are required
1.low BP entering the kidney triggers release of renin from the juxtaglomerular apparatus
2.renin(enzyme)-converts angiotensinogen(plamsa protein) to angiotension I
3.angiotension gonverting enzyme(ACE)-converts Angiotensin I to angiotension II ACE is produced in many tissues(primairly in the lungs)
4.angiotension II accts to increase BP-2 ways
-causes vasoconstriction
-triggers rel. of aldosterone-it increases NaCl retension in kidney-as osmolaity increases-triggers ADH rel.-Increases H2O retension-inceases blood vol. and BP |
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Term
| Thus blood vol. and BP ------ in both situations(w/ADH alone or together w/ aldosterone) but w/ ADH alone overall osomolaity ----------- whereas w/ ADH and aldosterone together overall osomolaity is ------ --------. |
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Definition
increase
decreases
rel.
stable |
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Term
| Vascular resistance and blood flow |
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Definition
-flow of blood thru the vessels is by bulk flow so it dep. on the pressure gradient(ie delta p-difference in pressure alone the vessels)
-average arterial pressure is about 100 mL Hg pressure at the heart is about 0 mm Hg therefore the overall delta P=100mm Hg |
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Term
| blood flow is ----------- proportional to resistance(ie drag against vessel walls=R) therefore blood flow =? |
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Definition
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Term
| 3 major factors that affect vascular resistance and blood flow? |
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Definition
1.length of vessels
2.viscosity of bloof
3.radius of the vessels-major factor affecting the changes in resistance for regulatory purposes
-radius of vessels is routinely adjusted to adjust blood flow to various organs as the activity state changes. this is controlled by precapillary sphincters in the walls of the artrioles leading in. |
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Term
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Definition
| diverting blood from one are of the body to another |
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Term
| Extrinsic factors affecting flow |
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Definition
1.sympathetic cholinergic stimulation(ie. using acetylcholine causes vasodilation to skeletal muscles)
2.sympathetic adrenergic stimulation (ie norepinephrine)causes vasoconstriction in other organs(ex.skin or GI tract)
3.parasympathetic innervation-is always cholinergic and always vasodilates-only in a few sites(ex:exturnal genitalia,GI tract)-appetite responses |
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Term
| Intrinsic factors affecting flow |
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Definition
1.decreased tissue O2 context(ex:w/exercise)-causes vasodilation and increases blood flow to compensate
2.increaes tissure CO2 content(ex:w/exercise)-causes vasodialtion and increased blood flow to flush the excess CO23.decrease tissue pH-can result from increase CO2 or build up of lactic acid (as w/anaerobic metabolism in muscles during exercise)-also causes vasodilation
4.intrinsic vasodilation-response to decrease arterial pressure-isexp. important in brain where blood flow is under autoregulation-flow to the brain must be maintained |
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Term
| blood flow to skeletal muscles |
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Definition
-demands vary w/ activity
-at rest the muscles recieve about 15-25% of Cardiac Output in heave exercise can increase to 80-85% of CO
-is regulated by precapillary sphincters in the arterioles leading into the muscles |
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Term
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Definition
-at rest(adult Heart) recieves about 80 mL/min
-in heavy exercise-this can increase up to 5X(400 mL/min)
-NOTE:w/ advanced CAD from arteriosclerosis or atheroscierosis the coronary arteries may be unable to dilate to meet increased demands resulting in angina and possible MI at onset of heavy exercise
Tx:coronary vasodilators ex:Ca channel blockers EX: cardizen nitrates Ex:nitroglycerine,isosorbide dinitrate |
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Term
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Definition
| -blood flow to the brain is under autoregulation-adult brain recieves a rel. constant flow of about 750 mL/min regardless of activity or state of consciousness |
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Term
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Definition
-Blood flow to the skin is routinely adjusted as a thermoregulatory mechanism
-w/hyperthermia-flow to skin increases to radiate off excess heat
-w/hypothermia-flow to skin decreases to conserve heat in body core |
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Term
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Definition
| -flow varies w/ activity-entrance of chyme causes vasodilation and increased flow to aid absorption |
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Term
| Blood flow to exturnal genitalia |
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Definition
| -flow increases a/ sexual stimulation |
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Term
| Changes in blood pressure is regualted by both? |
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Definition
nervous ad hormonal mechanisms
-hormonal reg-involved the actions of ADH and aldosterone on the kidney
-nervous reg-major mechanism involves the baroreceptor reflex[at the onset of exercise-fasodil. to the skeletal muscles causeds increased blood flow(blood is dumped into muscles) causes a decrease in BP. This is sensed by baroreceptors(press. rec.)in aorta and carotid sinus-they signal the cardiovascular tenter in the hypothalamus-it in turn signals the cardiac and vasomotor centers in the medulla oblongata. They raise sympathetic activity-decrease parasym. activity.
result:increased HR and contraction strength-peripheral vasocon. (GI tract)-increased BP to compensate |
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Term
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Definition
1.physical characteristics
1)temp-is about 38 deg.C at heart(100.4 F)
2)viscosity-is about 5
3)pH-is about 7.4
4)osmolality-about 290 milliosmols
2.Plasma Componets-is mostly H2O-also
1)dissolved salts(ions=electrolytes) ex:Na,Cl,K,Ca,Mg,PO4,H,HCO3
2)Dissolved nutrients-glucose,soulable amino acids,H2O sol. vitamins(B&C)
3)Dissolved Wastes-NH3 and urea
4)Dissolved gases-N2,CO2,O2
5)soluable hormones-catecholamines
7)Plasma Proteins-make up 7-9% of total plasma volume-account for its hight viscosity-3 CLASSES
1.albumins-are 60-80% of total PP's-function primarly to produce colloid osmotic pressure-prod. in liver
2.Globulins-3 types-alpha,beta globulins-prod. in liver-function as carrieers fro hydrophobic molecules-gamma globulins-produced by lymphocytes-are antibodies-func. in immuity
3.fibrinogens-prod. by liver and they function in clotting |
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Term
| 3 major categories for blood cells |
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Definition
1.erythrocytes-by far the most numerous-are about 4.3-5.8 million/mm cubed of blood-each RBC is a biconcave disc
-mature RBC's have no nuclei or mitochondria-is an adaptation to increase the #'S carried-increaeing O2 transport in turn increaed metabolism
-decreases lifespane of RBC last just 120 days in circulation
-production is erythropoiesis-occurs in the myeloid tissue-worn out RBC's are destoryed in the liver and spleen
2.leukocytes-are far fewer than RBC's about 5-9 thousand/mm cubed
-function in immune responses
3.thrombocytes(platelets)-are sctually cell fragments-arise from the breakup of megakaryocytes
-have no nuclei or mitochondria but still are capable of ameboid movements-are involved in the clotting reaction. last just 5-9 days in circulation
-platelet prod. is thromobopoiesis-occurs in myeloid tissue. are destroyed by liver and spleen about 130-300000 platelets/mm cubed of blood |
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Term
| 2 major categories and subcat. of WBC's |
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Definition
1.gl=ranular leukocytes-have lg. granules in cytoplasm and irregular lobulated nuclei-3 TYPES DEP. ON STAINING
1)EOSINOPHILS-GRANULES STAIN PINKISH-ORANGE IN EOSIN -ARE INVOLVED W/ MANY PARASITIC INFECTIONS/ ETC.
2)BASOPHILS-GRANULES STAIN BLUUE IN BASIC STAIN-ARE INV. W/ ALLERGIC AND INFLAMMATORY RXNS
3)NEUTROPHILS-GRANULES DONT STAIN IN EITHER-ARE ONE CLASS OF PHAGOCYTIC WBC'S=POLYMORPHONUCLEOCYTES
2.agranular leukocytes-w/o lg. granules-nuclei are cresent shaped or spherical
1)LYMPHOCYTES-SMALL(RBC SIZE)W/ SPHERICAL NUCLEI AND LITTLE CYTOPLASM
2)MONOCYTES-LG. (2-3x rbc)W/ CRESCENT NUCLEI AND LOSTS OF CYTOPLASM(PHAGOCYTIC)
**leukopoiesis is WBC production-occurs in 2 sites
-myeloid tissue-prod. granular leuk's
-lymphoid tissue-prod. agranular leuk's areise in the myeloid tissue early in life
----last from .5 day up to 1 year or more dep on type |
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Term
| Hemopoiesis(blood cell production) |
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Definition
-all blood cells arise from a single stem cell type(=hemocytoblast)
hemopoiesis occurs at 2 sites in adults
1.myeloid tissue-forms erythrocytes,granular leukocytes,thrombocytes
2.lymphoid tissue-form agranular leukocytes(arise early in life in myeloid tissue-migrate to lymphoid tissues in childhood) |
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Term
| Hemostasis(halting blood loss) |
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Definition
-when a vessel is injured mechanisms are activated to reduce blood loss. initally, platelets are attracted tot he injury site and they adhere from a "platelet plug"=initial plug
-the platelets then dump their contents in the "relase rxn" they release
1.vasoconstricters-reduce local BF(serotonin) Ex.thromboxiane A(prostaglandin)
2.ADP-attracts more platelets and add to the platelet clot.
3.phospholipids-inv. w/ the "clotting cascade"(=a series of rxns resulting in the prod. of fibrin fibers to trap RBC's and add to the clot) |
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Term
| intrinsic pathway to fibrin formation |
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Definition
=actived from w/i the blood
-fac X(active)+phospholipids+Ca+FAc V=converts prothrombin to Thrombin=fibrinogen=fibrin
-defective fac IX caused hemophilia B
-defective fac VIII causes hemphilia A |
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Term
| extrinisic pathways to fibrin formation |
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Definition
=accelerated clotting w/ more serious injuries
-tissue thrombolastin(fac III) is rel. from damaged tissues=activeates fac VIII
-Fac VII(active)+phosophlipids+Ca=activates Fac V
-from here it follows the intrinsic pathway |
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Term
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Definition
inhibit the clotting process
1.heparin-an intrinsic anticoagulant-used in therapy and clinical work
2.citrate ion-used extensively clinically
3.EDTA-also used extensively clinically
4.Couniarins-ex:coumadin-used in therapy,rat poison,cheap artificial vanilla
5.Aspirin-used as a prophylactic agent in post MI patients to reduce the risk of recurrence |
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Term
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Definition
-break up a clot after healing
-can be used in MI or CVA patients to restore BF(w/caution)
1.streptokinase-bacterial enzyme that dissolves clots[since its a foreign molcule-can only use it one w/i about 5 year b/c of immune response]
2.Tissue Plasmoinogen Activator(TPA)-is a intrinsic clot dissolver is released from healed tissue-converts plasminogen to plasimin dissolved clot-can use it repeatly-COST ALOT |
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Term
Immunity
-provides protection against?
-also inv. with? |
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Definition
-1.foreign pathogens entering the body
2.action of venoms and toxins
3."rogue cells" escaping the normal growth controls
1.transplant rejection
2.allergic responses
3.autoimmune "diseases" |
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Term
| defenses against foreign invaders |
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Definition
1.skin-the dead suface is a barrier to most pathogens also the skin produces antimicrobial secretionsex:lysozyme=enzyme that lyses bacteria
2.digestive tract-high acidity of the stomach is a barrier to most pathogens also competitive exclusion by the "friendly" bacterial flora in intestine keeps pathogens out
3.respiratory tract-the ciliated epith. sweeps out bacteria etc.-also the alveoli contain alveolar macrophages that engulf bacteria.etc.
4.Urogenital tract-high acidity of the urine is a barrier to most pathogens(not all Ex:Niesseria)also the acidity of vaginal secretions is a barrier |
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Term
| if pathogens get past outler barriers then the immune system takes over=2 major categories of immune mechanisms |
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Definition
-non-specific immunity
-specific immunity |
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