Renal Physiology Flashcards
(128 cards)
1
Q
Functions of the kidneys
A
overall function: maintain homeostasis
2
Q
how do the kidneys maintain homeostasis
A
- blood (plasma) in equilibrium with the ECF
- controlling blood composition (amount of electrolytes, water) will control the composition to the ECF
- regulates electrolytes ( NA K Cl Ca and PO34)
- control the release of ions into the urine (some you want to keep and some you dont)
- proper ecf (ion) helps maintain proper plasma volume (osmotic pressure)
- regulate water balance in the body, through water conservation from, or release into the urine
- maintain pH by controlling H and HCo3 release into urine
- excrete metabolic waste products (filters the blood, anything released and not used)
- excrete foreign compounds from the body (such as drugs and chemicals)
- secrete hormones : erthropoietin and renin
- metabolism - convert vitamine D into its actin form
3
Q
where are the kidneys located
A
2 kidneys retroperitoneal, stuck to the body wall not free in abdomen
- towards the back of the body
4
Q
kidney anatomy
A
- out cortex region and inner medulla region
- very large renal artery and vein enter renal hilus area
- ureter is collecting tube that takes urine to the bladder
- nephron is the functional unit of the kidney
5
Q
variation in mammalian kidneys
A
- equine with heart shaped right and near bean shaped left kidneys
- bovine kidneys with lobulated cortex but fused medulla
- canine bean shaped kidneys with fused cortex and medulla (no sepparation of cortex and medulla)
6
Q
the nephron
A
- two parts
- vascular - blood containing portion
- tubular - urine containing portion
7
Q
blood flow to the kidney path
A
- 20% of cardiac output goes to kidneys
- path - renal artery - branches to smaller arteries - afferent arteriole (arrives) - glomerulus (site of filtration and leaky capillaries
- filtration - efferent arteriole (exsists capsule) - peritubular capillaries (vasa recta) - renal vein
8
Q
filtrate flow through the kidneys
A
- tubular flow
- path - bowmans capsule collects the filtrate from glomerulus (leaking) - proximal tubule - loop of hele (descending and ascending parts - distale tubule - collecting duct
9
Q
the two types of nephrons
A
- collecting ducts from all nephrons pass though the medulla
- the cortical nephrons are located within the cortex with the loop of henle (L of H) dipping slightly into the medulla
- the juxtamedullary nephrons have their bowmans capsule in the cortex, but their L of H extends deeply into the medulla
10
Q
urine formation 3 processes
A
- filtration
- tubular reabsorbtion
- tubular secretion
11
Q
step 1: glomerular filtration
A
- the sieve = 3 layers
1. endothelium
2. basement membrane
3. podocyte
12
Q
what is filtered out of the glomerulus
A
- plamsa
- electrolytes
- small peptide (like toxins)
13
Q
what is not filtered and stays in the blood
A
- most plasma proteins (albumin, globulins usually too large to pass through)
- red and white blood cells, platelets (too large)
- negatively charged compounds have more difficulty being filtered - repelled by negatively charged glomerulus basement memebrane
14
Q
filtration forces
A
- capillary blood pressure - favours filtration
- pressure pushing plasma into bowmans capsule
- pressure controlled by the diameter of afferent and efferent arterioles
- afferent arteriole diameter > efferent diameter:
- backlog of blood in the glomerulus
increases capillary blood pressure
15
Q
plasma colloid osmotic pressure
A
- opposes filtration of plasma
- plamsa proteins are too large for filtration
- osmotic pressure force of non filtered protein pulls plasma back into glomerulus from bowmans capsule
16
Q
bowmans capsule hydrostatic pressure
A
- opposes filtration of plasma
- backflow pressure that pushes plasma out of bowmans capsule back into the glomerulus - rushes in water, identifies to much pressure, and immediately goes back out
17
Q
net filtration pressure
A
- capillary blood pressure
- plasma colliod osmotic pressure
- hydrostatic pressure
- decreases osmotic pressure = decreases filtration rate
18
Q
GFR
A
- golmerular filtration rate
- rate of filtration production in the glomerulus
- net filtration pressure x Kf
- Kf filtration coefficient - how much surface is avaliable for filtering in the glomerulus, hoe permeable the membrane (how holy/leaky the membrane is)
- filtration pressure increases, GFR increases
19
Q
control of GFR
A
- net filtration pressure = plasma colloid pressure and bowmans capsule hydrostatic pressure are not easily regulated
- capillary BP is altered by changing afferent arteriole diameter - can be modified
20
Q
autoregulation
A
- kidneys try to maiantain constant blood flow to the glomerulus
- easiest way : change afferent arteriole diameter
21
Q
two primary autoregulation mechanisms
A
- myogenic control
- tubuloglonerular feedback (juxtaglomerular apparatus)
22
Q
myogenic control
A
- stretch mechanism in smooth muscle
- if glomerulus pressure is too high, afferent artery constricts to reduce pressure (decrease blood flow to glomerulous)
- if glomerulus presrue is too low, afferent artery dilates - to increase pressure (increasing blood flow to glomerulus)
23
Q
tubuloglomerular feedback
A
- juxtoglomerular apparatus
- ## detects Na Cl to increase the tubular flow
24
Q
what is BP is too low
A
- tubular flow lower than expected
- low salt detected at macular densa
- could indicate low GFR (kidney) or renal flow (systemic)
- release chemicals that cause vasodilation of afferent arteriole
25
extrinsic nervous control
- cause : plasma volume is decreased (hemorrhaging ) - arterial BP drops and triggers baroreceptor reflex
- compensation for plasma loss : retain more fluid via reduced urinary output
- at the nephron level there is two mechanisms in control
- afferent arteriol is constricted from SNS - less glomarular pressure - decreases GFR
- SNS signal - mesangial cells around glomerular capillaries to contract - Kf leakiness of capilary decreases - GFR decreases
- together lower GFR saves water for plasma not urine
26
Autoregulation
1. myogenic stretch mechanisms = smooth muscle
- if glomerular pressure is too high, afferent arteriole constricts (decrease flow)
- if glomerular is too low, afferent arteriole dilates (flow increases
- juxtoglomerular apparatus - macula densa(tubule), granular cells (arteriole)
27
sympathetic innervation
- direct vasoconstriction of afferent arteriole
- decrease leakiness of glomerulus endothelium
28
step 2: Tubular reabsorption
- filtration through glomerular capillaries largely indiscriminate (depending on charge and size)
- filtrates include waste, but also nutrients, electrolytes and other substances that the body cant afford to lose to the urine (AA, glucose)
- humans produce more filtrate than urine is produced
- fluid and solutes are reabsorbed in the tubular portion of the nephron (highly selective process)
29
how do solutes pass through tubule cells
through tight junctions between cells (transcellular)
- water can sometimes pass between cells (paracellular) (through leaky tight junctions in some regions)
30
sodium reabsorption
- takes sodium from filtrate back into blood
- sodium allows for the sodium to move across 5 layers
- active transport
- Na cotransporter : when Na moves from filtrate to tubular cell, it takes other molecules with it (glucose AA and phosphate)
- Na/H transporter : important for acid/base balance
31
proximal tubule
- most filtered sodium is reabsorbed here (65%)
- Na co transport: glucose, AA and phosphate
- passive reabsorption: chloride(electrical gradient)
- water (osmotic pull)
- urea,K (osmotic pull)
- all are secondary active transport (dependent on energy requiring Na transport)
32
where is the rest of the Na reabsorbed
- lesser amounts of Na reabsorbed in:
- loop of henle and distal tubule/ collecting duct (under hormonal control: aldosterone, ANP)
33
RAAS
- renin angiotensin - aldosterone system
34
what is the goal of RAAs
- to increase Na retention, increase water retention and increase BP
35
step one of RAAs
- renin released from the JGA in response to 1 of 3 triggers
1. low Na detected by macula densa cells
2. low BP in afferent arterioles
3. sympathetic NS stimulation
36
ANP
atrial Nutriuretic peptide (released when BP is too high)
- dont want low sodium, lots of water in a state of high BP - ANP will circulate and stops RAAs from increasing BP
37
step 2 of RAAS
- activation of angiotensin 1
- lots of angiotensinogen are circulating in the blood
- renin cuts a part of it (but it doesnt do anything until it gets to the lungs)
38
step 3 of RAAS
- activation of angiotensin II
- lungs: contain a lot of ACE (angiotensin converting enzymes ) - some in kidneys too
- in the lungs : angiotensin I turns to angiotensin II
39
effects of angiotensin II on kidneys
- mainly : vasoconstriction and Na reabsorbtion
- vasocontriction leads to decreased filtration (more water retention for the body
- salt retention leads to increase water absorption in the proximal tubule
40
effects of angiotensin II elsewhere
- CV effects : vasoconstriction - increases blood pressure
- neural effects - signal to the hypothalamus - increases thirst and increases water intake - this increases plasma volume, increasing BP
- neural effects: signal to the pituitary gland - increases ADH - which will increase water retention in the kidneys - increases plasma volume and increases blood pressure
- SNS - increases noradrenaline - increases cardiac output - increases blood pressure
41
step 4 of RAAS signalling
- angiotensin II stimulates the release of aldosterone by the adrenal glands
- in the collection ducts: aldosterone acts on the principle cells to increase the reabsorption of urinary Na
- aldosterone also increase Na/K pump. by reabsorbing more Na, we are excreting more K - lower K levels in the blood
42
control of sodium reabsorption: aldosterone
- causes Na reabsorption in distal tubule and collecting ducts
- increase gene expression of Na channels, Na/K pumps
- trigger : when blood pressure is too low - increase Na reabsorption will increase blood pressure
- results in more K excretion
43
atrial naturietic peptide (ANP)
- hormone secreted by cardiac smooth muscle
- trigger: released when BP too high
- decrease Na reabsorption in the distal nephron (more Na in urine, less in plasma ) creating more water in urine
- dilates afferent arteriole (increase GFR = increase in filtration = increases urine production - creating more urine
- overall the effect counteracts RAAS = decreasing BP
44
reabsorption
other solutes reabsorbed at various locations at various locations of the tubule depending on hormones, body needs (PO34, Ca 2)
- waste products (creatine) are not reabsorbed (except urea)
45
maximum tubular transport
- can only bring in so many molecules
- limited number of transporters for solutes
- if tubular [solute] is greater then transport capacity = not all solutes can be reabsorbed from the tubule (lost in urine)
- Tm = the max amount of solute that can be reabsorbed
- filtrate solute load = plasma [solute] x GFR
- renal threshold = max plasma [solute] that can still be completely reaborbed from the filtrate
- clinic relevance : diabetes mellitus
46
diabetes mellitus
- inadequate control of blood glucose levels
tm for glucose is 1.75mmol/min
in a healthy person =
- normal plasma concentration: 5mmol/glucose
- filtered load = 5 mol/L x0.125L/min = 0.625 mol/min (lower threshold)
diabetic person =
- plasma concentration : 15 mol/L
- filtered load = 15 mmol/L = higher then the threshold
- glucose is lost to urine = sweet smell
47
tubular secretion
- some waste products cannot be filtered at the glomerulus because:
1. they are too large to pass through
2. bound to proteins that are too large
3. negatively charged, so repelled by negative charge on basement membrane
how do we remove them? secrete them into the tubule (after the glomerulus) from the peritubular capillaries
48
where does tubular secretion take place
- H secreted along most of nephrons ( to control blood pH, useful in acidosis)
- K always reabsorbed in proximal tubule, but variable secretion in distal nephrons (aldosterone)
- decrease blood pressure causes aldosterone release to conserve Na (K is accidently lost = hypokalemia)
49
acidosis
- switch H instead of K in Na/K pump - accidental K retention (hyperkalemia)
50
renal clearance
measure of how much plasma volume is cleaned of a certain solute per unit of time
- measured as flow (mL/min)
- not amount of solute recovered
- clearance measures the effet of urine excretion on the remaining plasma
clearance = [solute in urine] x urine flow / [solute in plasma]
51
concentrating urine
- small volume of yellow urine vs large volume of clear urine
- kidneys not producing the same type of urine all the time
- benefit: allows mammals to live in wide variety of habitates and environmental conditions
52
water reabsorbtion is passive
- depends on osmolarity of surrounding areas:
- water moves passively from areas of low osmolarity to areas of high osmolarity
- osmotic gradient in ECF of kidney
- cortex is isotonic = similar to plasma
- medullary progressively more hypertonic
- requires energy to maintain concentration gradient
53
loop of henle
- decending loop of henle dips into hypertonic medulla
- water osmotically "pulled" from tubule, enters peritubular capillaries
- urine left in tubule is then more concentrated (same solutes, less water)
- ascending loop of henle returns to isotonic cortex - urine becomes hypertonic (less solute, same water)
-
54
benefits of counter current flow
- establishes osmotic gradient in teh medulla = allows for collecting ducts to produce hypertonic (concentrated) urine
- allows production of hypotonic (dilute urine)
- body can excrete excess water (but not solutes)
- counter current osmotic gradient formation
55
how is an osmotic gradient happen in the kidneys
- established by:
- selective permeability in tubule (water coming out but salt remains trapped in)
- selective ion transport in tubule
56
proximal tubule (before L of H) osmotic gradient
- Na actively reabsorbed (non selective), water passively flows (non selective) - 65% of total
- remaining urine still isotonic (300 mosm/L)
57
descending loop of henle osmotic gradient
- more water then Na leaves the tubule, because surrounding ECF is hypertonic
- filtrate (urine) becomes more concentrated
58
ascending loop of henle
- Na actively pumped out of tubule (about 25% of total Na reabsorption)
- impermeable to water (stays in tubule)
- filtrate becomes hypotonic (100 mosm/L)
59
urine concentration in the distal nephron
- distal tubule and collecting ducts are not naturally perneable to water
- filtrate (urine) entering the distal nephron will be hypotonic (100 mOsm/L)
- 80% of original filtrate (180L/day) reabsorbed before reaching the distal nephron
- 65% in proximal tubule (120L/day)
- 15% descending loop of henle (25L/day)
- 20% still remains
60
how is the rest of the water reabsorbed in the distal nephron
- make the collecting duct permeable to water
- water pulled out of the distal tubule (through water channels) due to osmotic gradient in medulla
- remaining filtrate (urine) more concentrated
61
ADH
- vasopressin
- binds to V2 receptor on collecting duct principle cells
- stimulates vesticles to unload aquaporins (water channels) into the apical membrane
- this allows water to pass through the principle cell, entering the peritubular capillary
62
ADH/Vasopressin
- 2 names, same meanings
- Adh = antidiuretic hoemones (keeps water in)
- vasopressin - increases blood pressure
- hormone is released by posterior pituitary gland in the brain
63
ADH primary controlled/released by
- hypothalamic osmoreceptors (blood osmol)
- NOT protected by the blood brain barrier
- baroroeceptors (vasomotor centre)
- angiotensin II
64
when is ADH released
- increase in plasma osmolarity (blood too concentrated)
- decrease in blood pressure (not enough fluid in the body)
65
ADH released results in
- increased pressure in the kidneys
- lower plasma osmolarity and increase in blood pressure
66
release of ADH is inhibited by
- low plasma osmolarity (dilute blood- try to remove excess water from the body) = alcohol and caffeine
-
67
inhibition of ADH can be overcome
- fight/flight
- sleeping (theres a natural ADH circadium rythm
- exercise
68
hypertonic urine
- concentrated up to 1200 mOsm/L
- 4x the plasma/ECF concentration
- equivalent to urine specific gravity - 1.033
- maximum ADH reponse
- body dehydrated = must conserve water
69
symptoms and causes of diabetes insipitus
- large amounts of dilute urine (normal patient 1-3L/day goes to 19L/day)
- always thirsty
causes:
- central DI - pituitary tumor that inhibits ADH production
- nephronegic DI: kidneys dont respond to ADH
70
urine concentration in animals
- deeper medulla - longer loops of henle
- allows for greater concentration of urine
- deeper medulla - longer loops of henle - better ability to produce concentrated urine
71
marine animals in hyperosmotic environments
- no access to fresh water
challenge: to conserve fresh water
72
marine animals in hypo osmotic environements
- no access to salt
challenge: conserve electrolytes
73
marine animals that fast for extended periods of time
- no water or salt
challenge : must conserve both
74
do marine animals drink sea water
- marine animasl dont have salt secreting glands like marine birds
- they dont drink sea water
- they produce highly concentrated urine (more than seawater) through their long loop of henle
- strong hormonal adaptation for water retention
75
how do marine animals get freshwater
- consumed through food
- metabolic water: from metabolizing blubber
- decrease water loss via decreased respiration and increase condensation of watter in upper respiratory tracts
76
how do desert animals get water
- break up fat, releasing water to excrete waste
77
urea recycling
- protein breakdown produces highly toxic ammonia (NH3)
- NH3 is converted to a less toxic form urea (CO(NH2)2) in the liver
- urea is primary waste product excreted in urine
- on 50% of the filtered urea is excreted
78
why is only 50% recycled from collecting duct
- urea in tubule is osmotic (keeps water in tubule)
- decreased ability to reabsorb water
however:
- passive reabsorbtion of urea occurs in inner medulla
- urea enters ECF, then loop of henle
- urea makes medulla more hypertonic, allowing for increase H2O reabsorbtion
79
what is happening to the blood during kidney filtration
- peritubular capillaries supply the kidney with oxygen
- vasa recta: special peritubular cappilaries that provide the medulla with oxygen, and in particular, run parallel to the L of H of juxtamedullary nephrons
- blood flows down into medulla, then flows back up towards cortex
80
vasa recta blood flow
- plasma equilibrates with hypertonic ECF in medulla (solute gain and water loss)
- plasma becomes almost isotonic again in cortex (solute loss and water gain)
- leaving nephron: plasma has regained almost all solutes and water that were filtered without disturbing medullary ECF gradient
81
unidirectional flow = medullary washout
- blood woulf equilibrate with ECF in medulla
- would remove extra solutes from the EFC when blood leaves medulla
- would remove osmotic gradient required to concentrated urine
82
urine composition
- variable with species and animal condition
- yellow colour due to urobilin ( biliruben metabolite (heme portion of hemoglobin))
-
83
why would urine be night red
- RBCs in urine
- cloudy but will settle out
- bladder infection or inflammation - that is causing damage
- post renal issue ( after collecting duct)
84
why would urine be red/brown
- hemoglobin/myoglobin
- RBC pre filtration are not strong enough and they burst, letting heme free and its a small enough protein to fit through filtration
- pre renal condition
= anemia
85
odor due to urine and components
- very small proteins sometimes present through in urine (pass through glomerulus) = miscoalbuminuria = especially after exercise
- mucus, RBC, WBC
86
why does bladder have mucus
- created to protect against urine pH
87
should urine be steril?
- depends on collection site
- if it was collected straight from the bladder yes
- but urine sample manually will collect bacteria as its leaving the body
88
what causes mineral crystals
- phosphate or oxalate crystals
- crystals are normally soluble in urine and excreted easily but may precipitate out if
- mineral concentration in urine is too high:
- mineral conc. in urine is too high (drink lots if prone to stones)
- urine pH changes (diet)
-
89
acidic pH for cats
- change in diet, lower meat content - higher pH - hgiher precipitation of minerals - higher instances of kidneys stones
-
90
carnavores + omnivores
more acidic ph
91
herbivores
more alkaline pH
92
renal diseases
- renal dysfunction can cause many different clinical signs, depending on:
- severity of kidney disease
- time course of kidney disease (acute vs chronic)
- specific location of kidney damage
- animals environemnt
93
step 1 in kidney disease
- decrease inability to concentrate urine
- solute transport dysfunction/ loss of osmotic gradient
- decreased number of functional nephrons = increased volume of siltrate produced
- increases overall volume
94
step 2 in kidney disease
- decreased waste removal from the plasma
- decreased GFR = less filtration of urea and creatinine
- decreased clearance of urea and critinine
- increased urea and creatinine
- increased osmolarity = casuing swelling, and accumulation of water
- azotemia ( increased waste products in the blood) and uremia ( increased urea in blood)
- causes ulcers, vomiting and depression
95
other consequences of kidney dysfunction
- metabolic acidosis (exces H retention)
- hyperkalemia ( excess plamsa K)
- other electrolyte imbalances (Na and Ca2)
- hypoproteinemia (due to proteinuria)
- anemia - EPO production
96
dialysis
- artificial filtering of the blood - for acute kidney injury or kidney failure
- hemodialysis : blood pumped out of patient, then equilibrates with isotonic solution
- excess urea, creatinine H from plasma diffuses into dialysis solution
- cleaned blood is then pumped back in
- helps to regulate blood pressure
97
peritoneal dialysis
- isotonic solution pumped into abdomen
- equilibrates with plasma across peritoneal membrane , then removed
98
urinary tract infections
- urine is normally sterile
- bacterial infections occur throughout urniary tract but mostly in bladder
- clinical signs:
- red ad white blood cells in urine (dark red or brown urine) - pain urinating
- causes: leptospirosis, e coli and other bacteria
- remedies: lots of water to try and flush the bacteria
antibiotics
99
urinary tract blockage
- uroliths (crystals that form stones)
- tumours
- mucous
- plus up the urinary tract (usually in the urethra) so urine cannot be excreted)
- lead to hyperkalemia (cant excrete K)
- blocked cats are usually males
100
autoimmune kidney disease
- immune mediated glomerulonephritis
- antibodies attack glomerulus
- inflammation ans scarring of glomerulus
- if glomerulus is destroyed, rest of the nephron is non functonal
- arterial blood shunted to other nephrons = increased glomerulus pressure
101
toxins affecting the kidney
- lead or murcury poisoning in cattle
- certain antibiotics (gentamicin)
- certain anti-inflammatory drugs (ibuprofen)
102
ethylene glycol (antifreeze ) posioning
- not directly toxic but alcohol dehydrogenase (AD) produced oxilic acid, which binds to calcium and creates calcium oxalate crystals in proximal renal tubules leading to perminante and acute renal failure - immediate crystalization
- time to treat is important
- will cause perminante kidney stones
- treatment: 4-MP deactivate AD and ethonol - outcompete EG for AD
103
bladder rupture
- cats or dogs hit by vihicles
- feedlot steers (water bellies)
- urine leaks from bladder into abdomen
- urea and K higher in urine than plasma , so reabsorbed across peritoneum into the blood
- hyperkalemia, acidosis
104
acid-base balance
- acid = something that donates H ( like Hal, H2CO3)
- base = compound that accepts H (like NH3, NaOH)
- pH of the blood venous = 7.35 and arterial 7.45
- other body compartments may have different pH ( stomach, urine and rumen)
- other pH values for comparison:
- distilled water 7, coffee 5 and salt water 8
105
acidosis
- when the pH of blood falls below 7.35
- bloo pH <7.2 is bad news
- <7 is critical = dead
106
alkalosis
- when blood pH is greater than 7.45
- blood pH >7.6 is serious
- >7.8 is critical
107
why does acid-base status mattter
- pH changes can alter protein structure = conformational changes = all functions are lost
- changes in pH can alter enzyme structure (altered or loss of binding site )
- results in drastic changes in enzymatic activity
- required for all cellular functions
- structure of protein channels in membranes
108
acidosis causes
- will cause depression of the central nervous system
- because of decreasing Ca influx into excitable cells = it is more difficult to get an action potential
- hyperpolarization
- can lead to a coma
-
109
diabetic coma
- actually due to acidosis - high level of glucose stops responding and wont enter into cells will metabolize fat = increase acid, decrease pH
- not enough glucose in cells - start breaking down fat - ketones are released and are acidic - acidosis
110
alkalosis causes
- alkalosis increase pH will cause over excitability of the nervous system
- afferent (sensory) nervous system - leads to a pins and needles feeling
- efferent (motor) nervous system - muscle twitches
111
potassium homeostasis
- H/K exchange in the kidney
- is H concentration increases = acidosis
- kidney will secrete extra H into urine through the H/K exchanger
- more K is retained - hyperkalemia
- is H concentration decreases (alkalosis
- kidney will save H by excreting K instead
- more K is excreted - hypokalemia
112
carbonic acid formation
write oh formula
catalyzed by carbonic anhydrase (red blood cells kidney tubule cells, parietal cells)
- reversible reaction: if CO2 builds up, the concentration of H increases too
- henderson - hasselbalch
113
nutrient breakdown
- acids: protein of meat origin contains a lot of phosphorus and sulphur
- converted to sulphuric and phosphoric acid (increased H)
- bases: fruits, vegitables and plant material can produce excess HCO3
- reduces the amount of H in the body
114
metabolism: organic acids
- fat metabolism: triglycerides converted to long chain fatty acids
- fermentation : short chain fatty produced by bacteria in the rumen or hindgut, absorbed into the bloodstream
- anaerobic metabolism: lactic acid production
115
control of acid-base status
- chemical buffers: compounds that minimize changes in pH by accepting or donating H as needed when other compounds are added to a solution
- first line of defence against body pH change, respond immediately accepting protons to not drop/raise pH but to keep it the same
- respiration compensation: respiration/ventilation to get rid of CO2 and bring in O2
- metabolic (renal) compensation
116
chemical buffers
- most important buffer in the ECF (including blood)
- connot buffer excess CO2 production
- a buffer cannot buffer itself
117
protein buffer system
- amino acids in proteins can accept or donate H dont have to deal with extra H
- most important buffer in the ICF (because so much intracellular protein)
118
hemoglobin buffer system
- de oxygenated hemoglobin (after O2 is dropped off at the tissues ) has a greater affinity for H than does oxygenated hemoglobin (haldane effect
- 60% of CO2 in blood carried as HCO3 and H
- Hb buffer is why extra H doesnt change the pH of venous blood very much
119
phosphate buffer system
- good intracellular and urinary buffer
120
respiratory compensation
- H monitored in body by specialized receptors ( peripheral chemoreceptors. detect [H] in arterial blood) (central chemoreceptors detect [H] in the brain )
- when H increases (acidosis) chemoreceptors signial respiratory center to increase ventilation
- increased ventilation (rate and depth ) removes CO2, thus reducing H in the blood (correcting acidosis
- when H decreases (alkalosis ), the receptors will cause decreased ventilation so CO2 can build up
121
2nd line of acid/base defence against pH changes
- kicks in when chemical buffers are not sufficient
- a proton excreted = AA gets it chemoreceptors dont notice, if the buffers are full they are then alltering 2nd line of defence
- limitations of repsiratory compensation
- cannot totally correct acid-base disturbances, just minimize them
- cannot compensate for respiratory induced acid base problems
122
3rd line of defence against acid-base disturbances, after chemical buffers and respiratory compensation
- slowest to make changes (pH correction), but most potent mechanisms - the one that actually fixes the imbalances
- can completely correct acid - base distrubances
- pH of blood stays constant
- pH urine will vary to help maintain pH homeostasis
123
metabolic compensation
- H can be secreted from peritubular capillaries into tubule (proximal, distal and collecting duct)
- kidneys can increase secretion of H into urine through H/K exchanger (to correct acidosis) - lactic, sulphuric and phosphoric acid
- during alkalosis, kidney does not reabsorb H - slower H doesnt stops just slows
-
124
group in 4 categories
pH (acidosis and alkalosis
underlying cause (repiratory or metabolic
125
respiratory acidosis
- hypoventilation Pzco2 will increase over 40 mm hg and lead to increase in H in the body (acidosis)
- bodys response (once buffer is used up ) : compensate with metabolic alkalosis
- reabsorb more bicarbonate and excrete H in kidneys
126
respiratory alkalosis
- cause by hyperventilation
- pCO2 less then 40 leads to decreased H production
- bodys response : compensate with metabolic acidosis
- secretes less H into urine, thus excreting more bicarbonate
127
metabolic acidosis
- <24 HCO3 is used up, buffering excess H - to many H are used for buffers
- >24 not enough H available to join with HCO3 so bicarbonate concentration increases
- to many protons = to much HCO3
128
diarrhea
- intestinal secretions include large amounts of HCO3
- usually reabsorbed later in the intestines, but not when aniamls have diarrhea
