physiology part1
Post on 23-Jan-2018
51 Views
Preview:
TRANSCRIPT
PHYSIOLOGY
FLUID DISTRIBUTION
• The body in divided in two compartment, and extracelular and intracelular compartment separeted by the membranes
• Membrane = Barrier
• About 60% of the body mass is water
• Relationship ICF/ECF: 2/3:1/3
• Na+ stay ousite the extracellular compartment can cross the cell membrane
• ECF is divided in ISF and vascular membrane separeted by capillarymembrane• ISF: Interstitial FLUID
• Vascular Volumen: Proteins (Albumin cant cross the capillary membrane
OSMOSIS• mOsm/kg: concentration of particles per Kg of solvent
• Osmolarity = Osmolality
• Glucose effective osmole
• Effective osmole: Solute which cant cross the membrane is effectivecausing the movement of water
• In DM glucose cant cross
• GLUT 1 is a receptor for glucose in Red blood cells (RBC)
• GLUT 4 in adipose tissue and muscle
• Effecitve osmole for the vascular compartment: Albumbin
OSMOSIS
EXTRACELLULAR SOLUTES
• Na+: 140
• K+: 4
• Cl: 104
• HCO3- : 24
• Measured in mEq/L; mmol/L; mM
BUN: 15
Cr: 1
Glucose: 80
Measured in mg/dl and mg%
Osmolar GAP
•𝐸𝑠𝑡𝑖𝑚𝑎𝑡𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦 = 2 𝑁𝑎 + +𝐺𝑙𝑢𝑐𝑜𝑠𝑒
18+
𝐵𝑈𝑁
2.8
•𝐸𝑠𝑡𝑖𝑚𝑎𝑡𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦 = 2 𝑁𝑎 + +𝐺𝑙𝑢𝑐𝑜𝑠𝑒
20+
15
3
•𝐸𝑠𝑡𝑖𝑚𝑎𝑡𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦 = 2 140 + +80
20+
30
3
• Estimated osmolality: 280 + 4 + 5= 289
OSMOLAR GAP
• Osmolar Gap: Difference in stimated and measured osmolarity. Measure should be more than 15 above stimated
• Result of Clinical vignette
• 𝐸𝑠𝑡𝑖𝑚𝑎𝑡𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦 = 2 150 +100
20+
30
3= 315
Plasma osmolarity of paciente: 320
Osmolarity measured of the paciente: 315
• Osmolar gap: 320 – 315 = 15
Darrow – Yannet Diagram
•Excersice are in the book (pag 8)
•Two big player for volumen regulation are: •Aldosterone
•Anti-Diuretic Hormone (ADH; also called AVP
• Primary factors regulating Renin
1. Perfusion pressure to the kidney (PP)
2. Sympathetic stimulation (Beta-1 receptor) – Renin ↑
3. Na+ delivery to the macula densa (Nephron)
• Primary factors regulating Aldostenore
1. Plasma (angiotensin II) stimulates release (RAAS) NEGATIVE FEEDBACK SYSTEM
2. Plasma K+ stimulates release
• Primary factors regulating ADH (AVP)
1. Plasma osmolarity stimulates
2. Blood volumen/pressure (inversely related)
RAAS
↓PP – Renin ↑↑PP – Renin ↓
↓[𝑵𝒂+] – Renin ↑↑[𝑵𝒂+] – Renin ↓
↑Oms - ↑ AVP
↓Oms - ↓ AVP
↓BD ↔ ↑AVP
↑BD ↔ ↓AVP
ExamplesVolumen Distribution Regulation Clinical
↓ ECF BP ↓ Loss of hypotonic fluidDehydrationSweating and respiration)Hypotonic urine (diabetes insípida)↓ ADH could be cause
↓ ICF RAAS ↑
↑ OSM AVP ↑
Volumen Distribution Regulation Explaination Clinical
↑ ECF BP ↑Add more osmolewhich stay in Extracellularvolumen
Excessive salt intakeHypertonic salineHypertonci manitolInitial effect of hyperglycemia
↓ ICF RAAS ↓
↑ OSM AVP ↑/↓/↔
Volumen Distribution Regulation Explaination Clinical
↑ ECF BP ↔
Add more wáter so it drops osmolarity
Primary polidipsia hypotonicsalineSIADHIncreased ADH could be thecause
↑ ICF RAAS ↓
↓ OSM AVP ↓
Volumen Distribution Regulation Explaination Clinical
↑ ECF BP ↑
Add more equal solute(osmole) and water
Infusion of isotonic fluid such as saline (entire ECF expands)Infusion of solution with colloids (dextran, plasma with proteins) expands plasma portion of ECFPathology: Increased Aldosterone, Primaryaldosteronism (Conn's síndrome)
No change ICF RAAS ↓
No change OSM AVP ↓
Volumen Distribution Regulation Explaination Clinical
↓ ECF BP ↓
Loss more osmolesDecreased of AldosteroneAddison's disease
↑ ICF RAAS ↑
↓ OSM AVP ↑/↓/↔
Flu
id F
lux Hydrostatic Pressure (P)
Filtration (+)
𝑃𝑐Flow
Venous Pressure
Blood Volumen
𝜋𝐼𝐹 Osmotic forces in the intersticial
Osmotic/Oncotic pressure (π)
Absorption (-)
πcOsmoles = Plasma protein
Any solute that doesnt croos themembrane is gonna pull wáter
𝑃𝐼𝐹 Hydrostatic pressure in theinterstitial
𝑃𝑐 :Hydrostatic pressure in the capillary𝜋𝐼𝐹 Oncotic pressure of the instertitial
πc:Oncotic pressure in the capillary𝑃𝐼𝐹 Hydrostatic pressure in the interstitial
Filtration and Absortion – Fluid Flux
Hydrosteatic pressure (P)
• Pc promotes Filtration (+) meanspushing water out also means gradient
1. Hydrostatic pressure in the Capillary• Regulated by 3 things
1. FLOW (Regulated at arteiole)
2. VENOUS PRESSURE (directly related)
3. BLOOD VOLUMEN (Greater the volumen greater thepressure
2. Oncotic pressure in the interstitial
Oncotic pressure (π)
• Oncotic promotes Absorption (-)• Oulling water to the capillary
1. Oncotic pressure in the capillary• Osmoles in the capillary that pull water
out (Albumin)
2. Hydrostatic pressure in the intertitial
STARLING EQUATION• Qf: filtration
• k: filtration coeficiente• Relates to permeability
• If the capillary is more permeable increased the filtration• ↑ permaebility = ↑ Filtration
• Lymphatics: Regulate• 𝜋𝐼𝐹 Oncotic pressure in the interstitial
• 𝑃𝐼𝐹 (Hydrotastic pressure in theintertitial)
Exercise
• Calculate Net pressure
Pc: 25 mm Hg
PIF: 2 mm Hg
πc: 20 mm Hg
π IF: 1 mm Hg
Calculate Net pressure
(Pc + π IF ) – (πc – PIF)
(25+1) – (20 + 2)
R: 4
Primary causes of edema
• Increased Pc: • Flow: vasodilation• Venous pressure: Venous obstruction, heart failure• Blood volumen: (Na+ retention) Heart failure
• Increased π IF : Hypothyroid – Myxedema
• Decreaed vascular oncotic pressure: Liver; Kidney
• Increased Capillary permeability: Inflammatory response (TNF-Alpha; histamine; bradykinin
• Lymphedema: Filarial (W. Broncofti); bacterial lymphangitis (streptococci); trauma, surgery, tumor
PITTING EDMA
NO PITTING EDMA
CLINICAL VIGNETTE
• If TNF (Tumor necrosis factor) and BK (Bradykinin) are increased• Increased permeability
↑ FLOW
↑ PC (Hydrostatic Pressure in the capillary
↑ FILTRATION
Which decreased PTC (precapillary arteriolar tone) and PNE (Pre-capillary noepinephrine contration/release
PULMONARY EDEMA
Most common form of pulmonary edema
• Cardiogenic (elevated PC)
• In this condition the patient is not injecting blood(Right heart start to fail blood is going to back up)• Increased left atrial pressure
• Increased venous pressure which in turn increasedcapillary pressure
• Initially increased lymph Flow reduces interstitialproteins and is protective
• First clinical sign is ORTHOPNEA (disnea whensupine), which can be relieved SITTING UPRIGHT
PURMONARY EDEMA
↑Left atrial pressure
↑Venouspressure
↑Capillarypressure
PULMONARY EDEMA
• Non-cardiogenic (increasedpermeability)• Adult respiratory distress síndrome
(ARDS)
• Due to direct injury of the alveolar epithelium or after a primary injury tothe capillary endothelium
• Clinical signs are severe disnea ofrapid onset, hipoxemia and diffusepulmonary inflitrates leading torespiratory failure
Most common causes
SEPSIS
Most important
Bacterialpneumonia
Trauma
Gastricaspitation
PULMONARY EDEMA
•Non-cardiogenic•Fluid accumulation as a result of the loss of epithelialintegrity
•Presence of protein containing fluid in the alveoliinactivates surfactant causing reduced lungcompliance
•Pulmonary wegde pressure is normal or low
VOLUMEN MEASUREMENTS
• INDICATOR-DILUTION
• Volumen of distrinution in pharmacology
• 𝑉 =𝐴
𝐶
Properties of Tracer
Introduced into a vascular compartment and distribute untilthey reach a barrier they can’tpenétrate.
• Two major barrier are• Capillary membrane
• Cell membrane
Plasma: Doesnt cross capillary (e.galbumin)
ECF: Cross capillary but not the cellmembrane (e.g., mannitor, sodium, sucrose)
Total body water: Permeable tocapillary and cell membrane (waterand urea)
Volume measurement of compartments• Blood volumen: RBC volumen + plasma
• Blood volumen = 𝑃𝑙𝑎𝑠𝑚𝑎 𝑉𝑜𝑙𝑢𝑚𝑒
1 −𝐻𝑒𝑚𝑎𝑡𝑜𝑐𝑟𝑖𝑡
Example
Ht:50mg (0.50)
Plasma volumen = 3L𝐵𝑙𝑜𝑜𝑑 𝑉𝑜𝑙𝑢𝑚𝑒𝑛 =
3𝐿
1 − 0.5= 6𝐿
top related