acid-base balance Flashcards by Monica Palumbo

proton regulation

must be tightly regulated because very reactive
ECF levels kept al low levels, 4nEq/L
should be 3-5nEq/L

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pH of ECF

7.4

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acidosis

process

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acidaemia

state

<7.35

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alkalosis

process

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alkalaemia

state

>7.45

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venous blood compared to arterial blood

more acidic

higher partial pressure of carbon dioxide

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interstitial fluid

usually same an venous blood pH

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pH effects of metabolism

practically every step of every metabolic process is pH dependant
deviate from optimal pH causes decrease in reaction efficiency, especially due to compromised enzyme activity

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acidosis affect on neuromuscular system

inhibitory

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alkalosis affect of neuromuscular system

excitatory

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why does pH affect neuromuscular system

plasma Ca2+ binding to albumin is pH dependant
acidosis increases free Ca2_
bathmotropy - calcium blocks Na channels, raises AP threshold

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bathmotropy

when free calcium interacts with Na channels and switches them off, which raises the AP threshold

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potassium balance in pH

acidosis - more serum [K]

alkalosis - less serum K

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consequences of acidosis

headaches, confusion, lethargy, tremors, sleepiness, cerebral dysfunction,
come
hyperventilation

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consequences of alkalosis

muscular weakness, pain, cramps, spasms, (smooth and skeletal muscle), tetany
hypoventilation

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most acid comes from

CHO/fat metabolism (CO2)

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acids produced in the body

metabolic activities continuously add H to the body
glycolytic metabolism - lactic acid
oxidative metabolism - CO2/carbonic acid
FA/AA metabolism - ketoacids
inorganic acids produced from intermediary metabolism
stomach acid production loads HCO3 - blood
pancreatic HCO3 production loads H+ - blood

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vomiting causes

alkalosis

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buffers

HCO3- in ECF
proteins, haemoglobin, phosphates in cells
phosphates, ammonia in urine

chemical buffering

solutions preventing change in pH
intracellular and extracellular buffers provide an immediate response to acid-base disturbances
bonde also buffers acid loads
immediate but exhaustible

pulmonary regulation

PCO2 is regulated by changes in tidal volume and respiratory rate
CO2 is exhaled - blood pH increases
can only removed acid

renal regulation

kidneys control adjust the amount of HCO3- and/or H+ that is excreted
excreting HCO3- causes decrease in blood pH
excreting H + causes increase in blood pH

buffer power

determined by the pH appropriateness of the system

- pKa should patch pH

capacity of buffer determined by

total [buffer] | relative [HB] and [B]

chemical buffer systems

HCO3- (ECF buffer) NH3 (renal tubular fluid) PO42- (ICF) proteins (ICF, Hb n RBCs)

ventilation

ventilation rates control pH balance | - increased ventilation removes CO2

hyperventilation causes

increase pH | decrease [H]

hypoventilation causes

increase [H] | decrease pH

renal control

kidneys constantly remove HCO3- from blood to maintain balance, we must re absorb HCO3- back into the blood kidneys can't do that first it has to be converted

conversion of HCO3- for reabsorption

HCO3- + H+ > H2CO3 > H2O + CO2 to do this, kidney must secrete H+ at a 1:1 ration with HCO3-

if H secretion = HCO3- filtration

no change in pH

if H secretion > HCO3- filtration

acid loss

if H secretion < HCO3- filtration

base loss

how is HCO3- reabsorbed

2nd degree active transport - CO2 diffuses into cells - carbonic anhydrase inside the cell forms CO2 into H2CO3 which becomes HCO3- and H+ - the H+ then leaves the cell again 1st degree active transport - H+ pumped directly put into the lumen

acid being secreted as ammonium

ammonium is produced by removing amine group from amino acids amine group is actively transported out of the cells as ammonium via counter transportation for Na

2 direct mechanisms

1. Na/K ATPase - alkalosis causes a shift of K+ from the plasma > ICF 2. electronuetrality - K+ will be passively secreted as an obligate cation partner to HCO3-

why do states of alkalosis cause hypokalaemia

because K+ ions are being secreted with the HCO3- ions to maintain electronuetrality

arterial blood gas analysis

PCO2 - reflect respiratory component | HCO3- - reflects the metabolic component

AB disorders

- may be metabolic or respiratory - metabolic - due to production, ingestion or loss of acids/bases - respiratory - due to hyper/hypoventilation

riased HCO3-

alkalosis

raised pCO2

acidosis

respiratory disorder leads to

metabolic compensation

metabolic disorder

respiratory compensation

subtypes of metabolic acidosis

[Na+] is greater than [HCO3-] + [Cl-] difference between the two issues the anion gap usually 12 mEq/L major increase in anion gap implies existence of an organic acidosis (poisoning)

plasma anion gap exists because

- gap exists because there must be elctronuetrality

increased anion gap

organic acidosis diabetic/sstarvation ketoacidosis, lactic acidosis, poisoning sulphates, methanol, ethylene glycol, os salicylates (aspirin)

normal anion gap acidosis

diarrhoea (HCO3- loss) | carbonic anhydrase-inhibitors