Phys final

Reticulocytes

immature RBCs

main Plasma proteins

albumin, fibrinogen, immunoglobins

albumin

plasma protein that drives osmotic pressure

Platlets

cellular fragments that come off of megakaryotes to aid platlet plug formation/coagulation

basophils

have granules with histamine (inflammation/allergies) and heparin (anticoagulant)

Blood cell formation

Lt-HSC → St-HSC → committed stem cells → specific cells

cytokine

cell-stimulating factor that helps differentiate blood cells

Erythropoiesis

production of RBCs in the red bone marrow when when stimulated by erythropoietin (released when blood O2 drops)

Anemia

decrease O2 delivery due to blood loss, RBC destruction, or decrease RBC production

polycythemia

an increase in hematocrit from sustained hypoxia/doping leading to increase blood viscosity, vascular resistance, and blood pressure

Fibrinogen

plasma protein that interacts with blood to increase viscosity

platelet plug formation

adhesion → activation → aggregation

intrinsic coagulation pathway

Factor XII → XIIa when exposed to platelets or a negative surface (collagen)

extrinsic coagulation pathway

Factor VII → VIIa when exposed to thromboplastin

final common coagulation pathway

Factor Xa + Va + Ca+ + phospholipids → prothrombinase

Thrombin

converts fibrinogen into fibrin which then traps blood cells (clot)

tissue plasminogen activator

activates plasminogen into plasmin which then breaks down clots

fibrinolysis

breakdown of clots via plasmin

Neutrophils

migrate to tissue to become macrophages

Phagocytosis

adherence→ destruction → respiratory burst

macrophages

destroy foreign material via phagocytosis

NK cells

non -specific killer cells that kill cells without a “self marker” and also enhance inflammatory response

antimicrobial proteins

interferons and compliment proteins

compliment proteins

form the membrane attack complex (insert pores in pathogens leading to cell lysis), promotes opsonization, amplify immune response

Interferons

released by infected cells and bind to neighbor cells to block viral reproduction, activates macrophages and NK cells

APCs

engulf and present foreign particles to T cells via MHC II proteins

1. dendritic cells

2. macrophages

3. B cells

MHC proteins

display self-antigens and present foreign antigens to T cells

• MHC 1 - hold endogenous antigens and display to CD8 cells

• MHC 2 - present to CD4 cells

Antibodies

binds to specific antigens to form antigen-antibody complex which inactivates and tags antigens for destruction for innate defenses

actions of antigen-antibody complex

1. neutralization (cover binding sites)

2. agglutination (clumps antigens)

3. precipitation (insoluble complex forms precipitate)

4. complement fixation

compliment fixation

antibodies bound to cells expose the compliment binding site leading to a change shape → cell lysis, enhance inflammation, opsonization

active humoral immunity

B cells encounter an antigen and produce antibodies

passive humoral immunity

antibodies acquired from and extrinsic source (serum injection/ moms blood through placental barrier)

CD receptors

assist cell-to-cell interactions

• CD4 → MHC II

• CD8 → MHC I

Humoral immunity

antigen activated B cells → plasma cells → antibodies

CD4 cells

create memory cells and differentiate into Th cells

CD8 cells

create memory cells and differentiate into Tc cells

Th cells

• release cytokines → stimulate innate immune system

• stimulate CD8 cells

• stimulate B cells

Tc cells

kill cells by releasing perforins (create pores) and granyzymes (enter cell and stimulate apoptosis)

pressure flow relationship

there is a critical closing pressure of the vessels that must be overcome to allow blood flow

pressure resistance relationship

as resistance decreases driving pressure increases in a logarithmic curve

(veins are much more compliant than arteries)

compliance of vessels

the ability expand to hold a larger volume and therefore have less change in transmural pressure

Law of LaPlace

the equilibrium between collapsing force (tension) and the blowout force (transmural pressure) depends on vessel radius

Heart depolarization

SA node → atrial muscle → internodal pathways → AV node → bundle branches → purkinje fibers → verticular muscles

Phases of heart depolarization

0. depolarizing upstroke - slow with Ca2+ (pacemakers), fast with Ca2+ and Na+ (contractile cells)

1. rapid repolarization (contractile cells) - inactivation of Ca2+ and Na+ currents

2. Plateau phase of ventricular muscle - continued Ca2+ and Na+ influx to lengthen refractory period

3. repolarization - outward K+ current

4. Diastolic potential - stable RMP (contractile cells), pacemaker potential (pacemakers)

Modulation of pacemakers

1. decrease steepness of pacemaker potential

2. more negative diastolic pressure

3. more positive threshold

ECG Waves

• P wave - atrial depolarization

• QRS - ventricle depolarization

• T - ventricle repolarization

Cardiac cycle flow

Pulmonary veins/Vena cava → L/R Atrium → mitral/tricuspid valve open (AV) → L/R Atrium → Aortic/Pulmonary SLV open → outflow

Phases of cardiac cycle

ventricular filling→ isovolumetric contraction → ventricular ejection → isovolumetric relaxation

Starlings law

increased venous return → increased myocardial stretch → increased stroke volume

Factors affecting heart cardiac output

• heart rate (filling time)

• preload (starling law)

• afterload (background aortic pressure)

preload

the end-diastolic volume

afterload

pressure needed to open semilunar valve

Atrial baroreflex

increase blood pressure → stretch HP baroreceptors → decreased sympathetic stimulation → vasodilation → decrease BP

or

decrease BP → decrease stretch HP baroreceptor → increase sympathetic stim → vasoconstriction → increase BP

high pressure baroreceptors

• located in carotid sinus/aortic arch

• detect changes in atrial pressure

• dominates unloading

low pressure baroreceptors

• located in atrium

• detect stretch → increase cardiac output

• dominate loading

Respiratory sinus arrhythmia

correlation of breathing with heart rate due to bainbridge reflex

bainbridge reflex

increase venous return → increased pressure in atrium → increased stretch → increased sympathetic tone via vagus nerve → increased HR

cardiac response to exercise

mechanical

• pumping muscle → increase venous return → increased SV/CO

chemical

• increased metabolism → decrease pH → vasodilation → increased flow

partial pressures at different spots

Air

• PO2 - 160

• PCO2 - 0.3

Lungs

• PO2 - 104

• PCO2 - 40

Tissue

• PO2 - 40

• PCO2 - 45

daltons law

total pressure is the sum of gas partial pressure

Henrys law

concentration of dissolved has correlates to partial pressure of that gas

Lung vacuum

elastic recoil of lungs opposes the recoil of the chest wall to create a relative negative pressure → drawing air in

Insparation

Respiratory muscles contract → increased thoracic cavity volume → decreased thoracic cavity pressure → vacuum → air flow in

respiratory muscle

primary - diaphragm and intercostals

secondary - scalenes, neck and back, upper airway

Quiet expiration

elastic recoil of lungs / muscles relax → decrease thoracic volume → increase thoracic pressure → air flows out

Active expiration

abs, intercostals, and neck/back muscle forcefully contract to push air out

Atelectasis

punctured lung → Pip = Patm → no vacuum → alveoli collapse

fixed by increasing transpulmonary pressure

transpulmonary pressure

Ptp = Pa - Pip

alveolar surface tension

water on alveoli creates a collapsing force

surfactant

produced by alveolar type II cells to break the surface tension and allow alveoli to inflate

Infant respiratory distress syndrome

no surfactant → increased surface tension → lungs collapse

O2 transport in blood

1. dissolved in plasma

2. bound to hemoglobin

CO2 transport in blood

1. dissolved in plasma (minimal)

2. bound to hemoglobin (minimal)

3. Bicarbonate (majority)

Bohr effect

increased metabolic rate → increased temperature, CO2, H+, 2-3 DPG

Haladane effect

Hemoglobins ability to carry O2 in the blood is dependent upon O2

Fick’s law

rate of diffusion is affected by

1. molecular weight of gas (negative)

2. solubility of the gas (positive)

3. area of membrane (positive)

4. thickness of membrane (negative)

Factors affecting gas exchange

• diffusion capacity (fick’s law)

• partial pressure difference

• transit time

Fick principle

VO2 = CO x (a-v difference)

Diffusion equilibrium

when P_artieriole = P_blood

happens 1/3 down the capillary

Minute ventilation

V_E = (V_Tidal - V_{Dead Space)} x Respiratory rate

characteristics of pulmonary circulation

• low resistance

• low pressure

• high compliance

  • increase arterial pressure → decreased resistance

V/Q matching

• the balance of ventilation and perfusion

• If V is too high → alveolar air approaching atmospheric air

• If Q is too high → alveolar air approaches venous air

Alveolar dead space ventilation

• ventilation without perfusion

• no blood flow to alveoli → ventilation increases

• lungs compensated with bronchoconstriction and reduced surfactant → ventilation decrease

pulmonary shunt

• perfusion without ventilation

• Blood passes from right to left heart without becoming oxygenated

• lungs compensate by shunting (redirecting) blood away from unventilated alveoli

Apnea

• the cessation of breathing

• occurs when sleeping if CO₂ drops blow apneic threshold

central respiratory chemoreceptors

• located in the brainstem

• detect brain tissue PCO₂/H⁺

• control 70% of ventilation

peripheral respiratory chemoreceptors

• located in carotid and aortic bodies

• detect blood O₂/CO₂

• control 30% of ventilation

Dorsal respiratory group

detect lung stretch/peripheral chemoreceptors and send the signal to the VRG

Ventral respiratory group

• rhythm generating/integrating center

• sets eupena (breaths/minute)

• VRG → phrenic/intercostal nerves → inspiratory muscles

Pontine respiratory center

• influence/modify the activity pf the medullary (timing) centers

• influence the inspiration/expiration transition

response to increased arterial PCO₂

increased arterial PCO₂ → CRC/PRC detect → medullary respiratory centers → respiratory muscles → increase ventilation