1
Q
Balance Concept
A
- internal pool: quantity of any particular substance in the ECF
- if quantity is to remain stable within the body, input must be balanced with output
input: ingestion, metabolic consumption
output: excretion, metabolic consumption
2
Q
Maintenance of a Balanced ECF Constituent
A
- input must equal output
- positive balance: exists when input exceeds output
- negative balance: exists when output exceeds input
3
Q
Input and Output
A
- input os substances into plasma is poorly controlled or not controlled; eating habits are variable
- output: compensatory adjustments usually occur on output side by urinary excretion
4
Q
Fluid Balance
A
- water most abundant substance in body
- amounts varies in different kinds of tissues
- content remains fairly constant within an individual
5
Q
Body Water Distribution
A
- extracellular: 33% (1/3) in fluid surrounding the cells
- interstitial fluid (80%) and plasma (20%) - intracellular: 67% (2/3) within the cells
6
Q
Minor ECF components
A
- lymph
- transcellular fluid:
cerebrospinal, intraocular, synovial, pericardial, intrapleural, peritoneal fluids, and digestive juices
7
Q
Barriers Separating Body-Fluid Compartments: Cellular Plasma Membrane
A
- major differences between ECF and ICF is
a) presence of cell proteins in the ICF that cannot permeate the cell membrane to leave the cells
b) unequal distribution of Na and K and their attendant ions - action of membrane-bound Na-K+ATPase pump present in all cells
- Na is primary ECF cation and K+ is primarily found in ICF
8
Q
Barrier Separating Compartments: Blood Vessel Walls
A
- identical in composition (minus plasma proteins in interstitial fluid)
9
Q
ECF Volume and Osmolarity
A
- ECF serves as an intermediary between the cells and the external environment
- body “looks after” the ECF
10
Q
ECF Volume and Osmolarity Factors That are Regulated
A
- ECF Volume: closely regulated to help maintain blood pressure
- maintaining salt balance is very important in long-term regulation of ECF volume - ECF Osmolarity: closely regulated to prevent swelling or shrinking of cells
- maintaining water balance is very important in regulating ECF osmolarity
11
Q
Control ECF Na balance =…
A
Control of ECF volume
12
Q
Salt Balance
A
- very important in regulating ECF volume for long term control of BP
- salt input occurs by ingestion; often not well controlled
- salt balance maintained by outputs in urine; salt also lost in perspiration and in feces
13
Q
Control of Salt
A
- to maintain salt balance, excess salt must be exerted in the urine
- deviations in the ECF volume trigger renal compensatory responses that bring salt balance back into line
- the kidneys accordingly adjust the amount of salt excreted by controlling 2 processes (GFR and tubular reabsorption)
14
Q
Daily Salt Balance
A
ingestion: output= (0.5g) through sweat and feces; controlled excretion in urine (10.0g)
15
Q
Regulated by GFR and Tubular
A
- baroreceptor reflex
- amount Na filtered is equal to the plasma Na concentration times the GFR
- baroreceptor reflex
- DCT is subject to control
- RAAS
* long term regulation of ECF volume and BP
16
Q
Control of ECF Osmolarity
A
- with water balance= control cell shape/volume
- isotonic, hypertonic, and hypotonic
17
Q
Osmolarity
A
- measure of the concentration of individual solute particles dissolved in a fluid
- number of particles, not their nature that is important
- ECF and ICF have same osmolarity despite large chemical differences (no net movement of water)
18
Q
Ions Responsible for ECF and ICF Osmolarity
A
- sodium and its attendant anions account for vast majority of the ECF’s osmotic activity
- in contrast, K+ and its accompanying intracellular anions are responsible for the ICF’s osmotic activity
19
Q
Importance of Regulating ECF Osmolarity
A
- circumstances that result in a loss or gain of free water lead to changes in the ECF osmolarity
1. Deficit of free water in ECF - osmolarity becomes hypertonic (too concentrated) and often associated with dehydration
2. Excess of free water in ECF - osmolarity becomes hypotonic (too dilute) and usually associated with over hydration
20
Q
ECF Hypertonicity and Shrinking Cells
A
- excessive concentration of ECF solutes
- cells tend to shrink
- causes: insufficient water intake, excessive water loss, diabetes Insipidus
21
Q
Hypertonicity Symptoms and Effects
A
- shrinking of brain neutrons: confusion, irritability, delirium, convulsions, coma
- circulatory disturbances: reduction in plasma volume, lowering of BP, circulatory shock
- dry skin, sunken eyeballs, dry tongue
22
Q
ECF Hypotonicity and Swelling Cells
A
- usually excreted in urine
- cells tend to swell
- causes: renal failure who cannot excrete a dilute urine become hypotonic when they consume more water than solutes
- can occur in healthy people when water is rapidly ingested and kidney’s do not respond quickly enough
- when excess water is retained in body due to inappropriate secretion of vasopressin
23
Q
Hypotonicity Symptoms and Effects
A
- swelling of brain cells: confusion, lethargy, headache, dizziness, vomiting, drowsiness, convulsions, coma, death
- weakness (swelling of muscle cells)
- circulatory disturbances (hypertension and edema)
- excess free water= water intoxication
24
Q
H2O Input and Output
A
Input: drinking liquids, eating solid foods, metabolically produced water
output: insensible loss= lungs, non sweating skin; and sensible loss= sweating, faces, urine excretion (controlled to keep balance, 1500)
25
Water Balance and Vasopressin (ADH)
- water excretion controlled in collecting ducts and tubules of neoprene
- partially dissociated from solutes
- water distributes in ICF and ECF
- restore ECF osmolarity
26
Hypothalamic Osmoreceptors
- located near vasopressin-secreting cells and thirst centre
- excitatory input for both vasopressin secretion and thirst
- monitor osmolarity of fluid surrounding them
- if osmolarity increases, need for water conservation increases- stimulating vasopressin release and thirst
27
Vasopressin Release
- produced by hypothalamus (stretch-sensitive neutrons)
- stored and released from posterior pituitary gland
- released on command from hypothalamus (also location of thirst centre)
28
Role of Left Atrial Volume Receptors
- monitor pressure of blood flowing through (reflects ECF volume)
- upon detection of major reduction in arterial pressure, receptors stimulate vasopressin secretion and thirst
- upon detection of elevated arterial pressure, vasopressin and thirst are both inhibited
29
Role of Angiotensin 2
- stimulates vasopressin secretion and thirst when renin-angiotensin-aldosterone mechanism is activated to conserve sodium
30
Regulatory Factors that Do Not Link to Vasopressin and Thirst
- dryness of mouth stimulates thirst but not vasopressin
- oral metering: some animals rapidly drink only enough water to satisfy water deficit; mechanisms is less effective in humans
- nonphysiological influences on fluid intake: fluid intake often influenced by habit and sociological factors
31
Acid-Base Balance
- refers to precise regulation of free H+ concentration in body fluids
- acids liberate hydrogen ions: group of H+ containing substances that dissociate in solution to release free H+ and anions
- bases accept hydrogen ions: substances that can combine with free H+ and remove it from solution
32
pH
- designation used to express that concentration of H+
| - pH 7= neutral
33
Acidosis and Alkalosis in Body
- arterial pH less than 6.8 or greater than 8.0 is not compatible with life
- acidosis= blood pH falls below 7.35
- alkalosis= blood pH is above 7.45
34
Consequences of Fluctuations in pH
- changes in excitability of nerve and muscle cells
- marked influence on enzyme activity
- changes influence K+ levels in body
35
Sources of H+ in the Body
- carbonic acid formation
- inorganic nutrients produced during breakdown of nutrients
- organic acids resulting from intermediary metabolism
36
Sources of H+ Gain
- generation of H+ from CO2
- production of nonvolatile acids from the metabolism of proteins and organic molecules
- gain of H+ due to loss of HCOs- in diarrhea or other non gastric GI fluids
- gain of H+ due to loos of HCO3- in urine
37
Sources of H+ Loss
- utilization of H+ in the metabolism of various organic anions
- loss of H+ in vomitus and urine
- hyperventilation
38
Lines of Denfense Against pH Changes
- chemical buffer systems
- respiratory mechanisms of pH control
- kidneys- renal mechanism of pH of control
39
Chemical Buffer Systems
- minimize changes in pH by binding with or yielding free H+
| - first line of defense
40
Chemical Buffer Systems
1. H2CO3, HCO3- buffer system
- primary ECF buffer for non carbonic acids
2. Protein buffer system
- primary ICF buffer, also buffers ECF
3. Hemoglobin buffer system
- primary buffer against carbonic acid changes
4. Phosphate buffer system
- important urinary buffer, also buffers ICF
- Na2HPO4 + H+ - NaH2PO4 + Na+
41
Henderson- Hasselbalch Equation
```
pH = pK + log[HCO3=]/[H2CO3]
- H2CO3 directly reflects dissolved CO2- [CO2] via CA action
- for H2CO3, pK= 6.1
- pK is constant
* if ratio > 20, more alkaline
if ratio
```
42
Plasma pH is set by Carbonic Acid System
- plentiful H2CO3 and HCO3-
| - regulated by kidneys (HCO3-) and Respiratory system (CO2)
43
Chemical Buffers
- rapid response to excess or loss of H+
- H+ removed from solution, thus no effect on acidity
- excess is not eliminated
- buffering has a capacity
- ultimately, changes in H+ regulated by respiratory and kidney systems
44
Respiratory system
- second line of defence again changes in pH
- acts at a moderate speed (chemical first)
- regulates pH by controlling rate of CO2 removal
45
Effect of Arterial PCO2 on Ventilation
- peripheral:
- CO2-derived H+ detection
- normally less important
46
Effect of Arterial pH on Ventilation
- peripheral - H+ detection:
| - important when H+ from other sources
47
Non- Respiratory Change
- non-respiratory cause of arterial pH change:
- peripheral chemoreceptors alter ventilation but central chemoreceptors act against changes
- partially successful- 50-75% toward normal
- if pH changes due to respiratory failures, system cannot contribute- other chemical buffers and renal mechanism
48
The Kidneys and H+ Excretion
- third line of defence against change in hydrogen ion concentration
- kidneys require hours to days to compensate for changes in body-fluid pH
- control pH of body fluids by adjusting H+ excretion, HCO3- reabsorption/excretion, ammonia secretion
49
Kidneys
- respiratory system can deal with carbonic acid only
- H+ from any acid source by kidneys: Lactic, sulphuric (catabolism of proteins), Phosphoric (catabolism of proteins)
- H+ secreted into tubular fluid PT, DT and CT:
- very little H+ filtrate-plasma pH=7.4, urine pH=6
50
Control of the Rate of Tubular H+ secretion
increase plasma (H+)
- increase H+ secretion, increase H+ excretion, decrease plasma H+= alleviates
- increase HCO3 conservation, decrease HCO3 excretion, increase plasma HCO3= buffers
51
Kidneys and H+
- HCO3 reabsorption is an active process- but no carrier or pump for HCO3
- HCO3 reabsorption depends on tubular secretion of H+ which combines in lumen with filtered HCO3
- H+ secretion linked to HCO3 handling
- HCO3 excretion in urine increases H+ in plasma, as if H+ added to plasma
- HCO3 addition to plasma lowers H+ in plasma, as if H+ removed from plasma
52
HCO3 Reabsorption and H+ Secretion
- CA on luminal membranes
- all HCO3 is "reabsorbed"
- H+ "recycled"
- more H+ secreted than HCO3 filtered:
- all HCO3 reabsorbed
- most secreted H+ used to form CO2
- excess is excreted = rate of non carbonic acid H+ production
53
Hydrogen Ion Secretion and Excretion with the Addition of New HCO3 to the Plasma
- in H+ excess, new HCOs- is generated (a net gain)
- when H+ combines with a buffer other than HCO3, addition of new HCO3
- filtered HPO4
- raises plasma HCO3 and alkalinizes it
54
Kidneys and Acidosis
- when plasma H+ is raised, more secreted
- less HCO3 filtered (used in plasma buffering)
- less HCOs in tubular fluid
- H+ excreted in urine: more acidic; phosphate
- new HCO3 generated to buffer excess H+
55
Kidneys and Alkalosis
- H+ secretion decreases as filtered load of HCO3 is increased (less H+ to combine with)
- HCO3- cannot be reabsorbed without H+ secretion:
- increased HCO3 excreted in urine; alkaline urine
56
Urinary Fluid Buffors
- free tubular H+ cannot rise too high:
- max pH 4.5
- concentration gradient for pumps and carriers too great
- requires buffering to reduce free H+
- filtered phosphate:
excess from diet in tubular fluid
- if capacity exceeded, other sources needed to resist pH fall
- ammonium
57
Ammonium
- meteabolism of glutamine to produce ammonium (NH4)
- NH4+ transported out of cell and excreted
- HCO- generated
58
Acid-Base Imbalances
- kidneys can deal with changes from either respiratory dysfunction or metabolic disturbances
- vary H+ secretion from any source
- variably conserve or excrete HCO3 depending on acid-base balance
- can arise from either respiratory dysfunction or metabolic disturbances
- deviations divided into four general categories: respiratory acidosis and alkalosis, and metabolic acidosis and alkalosis
59
Alkaline and Acidic Imbalances
- if ratio > 20, more alkaline
- resp. alkalosis- decrease CO2
- metabolic alkalosis- increase HCO3-
- if ratio
60
Acidosis
- respiratory acidosis:
- increase in CO2 ex. hypoventilation
- therefore rep. cannot respond to correct
- compensate by increasing plasma HCO3= from normal levels by kidney conservation and new HCO3
- metabolic acidosis:
- decrease HCO3- ex. diarrhea and exercise
- compensate by lungs blow off H+- generating CO2
- compensate by kidneys excrete more H+ and conserve more HCO3-
61
Alkalosis
- resp. alkalosis:
- decrease ex. fever and anxiety
- kidneys compensate by conserving H+ and excreting more HCO3-
- metabolic alkalosis:
- decrease HCO3- ex. vomiting
- compensate by reduced ventilation- retain more CO2 generating more H+
- compensate by excess HCO3- excreted by kidneys and conserve H+ in kidneys
Human Physiology 2
flashcards
Decks in class (10)
# Cards
-
Ch. Eight: Vascular Physiology65
-
Ch. Nine: Blood56
-
Ch. Ten: Body Defences57
-
Ch. Eleven: Respiratory System83
-
Ch. Twelve: Urinary System71
-
Ch.Thirteen: Acid-Base61
-
Ch. Fourteen: Digestive System81
-
Ch. Sixteen: Peripheral Endocrine Glands49
-
Chapter 5: Principle of Endocrinology34
-
Ch. Seventeen: Reproductive System48
