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Sita GenitoUrinary System > Lecture 16: Acid-Base Balance and Disorders 1 > Flashcards

Lecture 16: Acid-Base Balance and Disorders 1 Flashcards

1
Q

Definition of pH

A 
Concentration of H+ ions in solution (pH = -log(10) x [H+])
ECF pH (extracellular plasma) --> tightly regulated --> maintained in narrow range --> Enzymes, structures, proteins etc able to continue PHYSIOLOGICAL PROCESSES (maintain correct Structure and Function)
Normal pH = 7.4 (7.35 - 7.45)
- when outside narrow range = disease state
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2
Q

pH related calculations

A

pH = -log10 [H+]
Note: [H+] hydrogen concentration units molL-1
Note 2: [H+] = 10^-pH molL-1
Normal pH –> [H+] = 10^-7 = 40nmolL-1

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3
Q

Intracellular vs Extracellular/Plasma Fluid pH

A

Acidity: Extracellular/Plasma pH higher/less acidic > intracellular pH
Note: Plasma = Liquid component of blood = 20% of ECF
Measurability:
1) Intracellular is largest body of fluid (2/3) –> measure directly
2) Measure plasma pH –> Indirect measure of ECF

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4
Q

Acidosis and Alkalosis pH total range

A

< 6.9 7.2 7.35 7.45 7.6 7.9 <

incompatible w. life severe acidosis acidosis normal alkalosis severe alkalosis incompatible w. life

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5
Q

Accuracy of acidosis and alkalosis

A

AcidOSIS and AlkalOSIS = Pathological processes –> cause a change in pH
AcidEMIA and alkalEMIA = acidic or alkaline blood plasma pH
Note: blood plasma pH is used as an indirect measure for ECF pH

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6
Q

Causes of Acidosis and alkalosis

A

Normally has a Primary acid/base disorder

- but can be mixed –> even 3x acid/base disorders possible

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7
Q

Buffer equations

A

(H+) Weak acid/base + Base (A-) Acid (HA)
Note: pK as Base and Acid concentrations are equal
Want to decrease pH/Increase acidity:
Added Weak Acid (H+) + Reduced Base [A-] Increased Acid [HA]

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8
Q

Concept of a buffer

A

Buffers:
Adds or Removes H+ –> Decreases range of pH changes
H+ are only temporarily removed –> Not eliminated from body
pK of a buffer –> pH when [A-] = [HA]
pH = pK + log ([A-] / [HA])

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9
Q

Bicarbonate as a buffer in blood

A

H+ + HCO3- H2O + CO2
(40nmol/L) + (24mmol/L) Ommol/L + (1.2mmol/L = 5.3 kPa)
CO2 tension pressure = 5.3 kPa = 1.2 mmolL-1

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10
Q

Proteins as a buffer in blood

A
  1. albumin
  2. Hb haemaglobin
    H+ + A- HA
    ** draw molecules
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11
Q

Henderson-Hasselback equation

A

pH = 6.74 + log ([HCO3-] / pCO2)
- this ratio determines pH
if pH = Concentration of [H+] nmolL-1 –>
[H+] = 182 x (CO2 partial pressure (kPa) / [Bicarbonate])
–> [H+] = 182 x ( 5.3 kPa / 24 mmolL-1) = 40 nmolL-1 = [H+] nmolL-1

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12
Q

kPa conversion into pressure

A

1 kPa = 7.5 mmHg
–>
CO2 = 5.3 kPa = 1.2 mmolL-1

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13
Q

Respiratory control of pCO2

A

metabolism –> CO2 (15,000 mmol/day (acidic)) –>
1. Henderson-Hasselbach equation = allows bicarbonate to buffer natural system –> snatches up H+ created by dissociated HH equation –> No significant changes in bodily pH
2. Ventilation rate –> CO2 expired –> controls pCO2
Note: 3: insurance policy utilising ventilation: High [H+] –> acidosis/increased bodily acidity–> Low bodily pH –> stimulates increased ventilation –> increased CO2 expiration rate –> removal of [H+] /acidic CO2 –> Return to equilibrium

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14
Q

Clinical reelvance of HH equation

A

ICU

Operating theatre with anaethesised patients

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15
Q

Changes in pCO2 on pH

A

Increased pCO2 –> acidosis

Decreased pCO2 –> alkalosis

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16
Q

Methods of Blood gas measurement

A
  1. Venous or Arterial blood collection
  2. Anaerobic blood sample (no air)
  3. Blood gas analyses
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17
Q

Importance of specificity of Anaerobic blood sample

A

Important not to contain air in Anaerobic blood sample

- as wont be anaerobic –> will effect pCO2 and pO2 concentrations

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18
Q

Blood-gas measured and calculated quantities

A 
Measured quantities:
1) pH
2) pCO2
3) pO2
Calculated quantities:
1) bicarbonate HCO3-
2) base excess
19
Q

3x Respiratory CO2 distrubances

A

HH equation = pH = 6.74 + log (HCO3- / pCO2)

  1. Normal:
    a) HCO3- = 24mmolL1 b) CO2= 5.3 kPa –> pH 7.4
  2. CO2 retention –> increased [H+] –> Respiratory acidosis
    a) HCO3- same b) CO2 increased = 9 kPa –> pH lower 7.15
  3. Hyperventilation –> decreased [H+] –> excessive CO2 loss
    a) HCO3- same b) CO2 decreased = 3kPa –> pH increased 7.6
20
Q

Acute asthma clinical example

A

Decreased pH –> acidEMIA
Increased pCO2 –> Hypercarbic (–> verge of respiratory failure)
decreased pO2 (not relevant)
Same HCO3- (metabolism not affected)
1. Normal Asthma: High breathing rate –> increased expiration of CO2 –> decreased [H+] –> Respiratory Alkalosis
2. ACUTE asthma –> Acute Bronchiolar Constriction –> UNABLE to Ventilate properly –> Increased levels of CO2 –> Increased [H+] –> Respiratory acidosis
Note: Hypercarbia –> verge of Respiratory failure –> require ICU

21
Q

Hypercarbia

A

Caused due to excessively high levels of CO2 (extremely acidic/low pH)
Due to e.g. Acute Bronchiolar constriction/acute asthma
Once Hypercarbic –> are on verge of respiratory failure –> require ICU

22
Q

Hyperventilation clinical example

A 
Increased pH --> alkalEMIA
Decreased pCO2 --> Hypocarbia
pO2 (relatively higher)
Same HCO3- (metabolism not affected)
1. Respiratory Alkalosis
Treatment: breathe into a plastic bag
23
Q

Hyperventilation Treatment via breathing into a plastic bag

A

Hyperventilation –> decreased plasma CO2 levels and hence acidity –> respiratory alkalosis
Plastic bag –> Closed space –> High Ventilation into it increases concentration of expired CO2 within bag –> consumption of bag’s CO2 –> Increased plasma CO2 concentration and increased acidity –> return to Normal pH range –> Normal breathing rate

24
Q

3x Metabolic HCO3- distrubances

A

HH equation: pH = 6.74 + log (HCO3- / pCO2)

  1. Normal: HCO3= 24 mmolL-1 pCO2= 5.3 kPa
  2. Metabolic acidosis:
    a) Decreased HCO3- = 10mmolL-1 Same pCO2 Decreased pH
  3. Metabolic Alkalosis
    b) Increased HCO3- = 40mmolL-1 Same pCO2 Increased pH
25
Q

Diabetic Ketoacidosis

A

Diabetes Type 1 –> complete lack of insulin –> glucose remain in plasma as unable to enter cells –> hyperglycaemic –> glucose undergoes anaerobic metabolism –> generate ketone bodies e.g. Betahydroxy-butyric acid –> increased metabolic acid production –> Metabolic acidosis
Increased metabolic acidity –> decreased pH –> Increased H+ –> Totally up HCO3- as a buffer
Acutely: Bicarbonate used up –> plasma [H+] > exceeds Renal H+ excretion –> Low pH + Low Bicarbonate
Cannot manipulate H2O –> so changes CO2 concentration

26
Q

Role of Kidney in acid-base balance

A

Metabolism (proteins and dietary intake) –> Metabolic acid 100mmol/day –> HH equation –> Renal H+ excretion –> Urinary buffers
a) H+ + (phosphate) PO4(3-) H3PO4 (phosphoric acid)
b) H+ + (ammonia) NH3 NH4 (ammonium ions)
Urine pH = b/w 5 and 8
- diffusion trapping
- can vary depending on need

27
Q

Causes of Metabolic Acidosis

A
  1. Increased acid production
  2. Decreased renal acid excretion
  3. Bicarbonate loss
28
Q

Metabolic causes of Increased acid production

A

a) Lactic acidosis:
i) hypoxia
ii) poor tissue perfusion: drugs, airway metabolism, hypotension (blood loss, heart failure), ischaemia/MI/ruptured aortic anuerysm
iii) CO (carbonmonoxide) and Cyanide poisoning (pink but unable to utilise oxygen) (Hb cannot function)
b) Diabetic Ketoacidosis (DKA)
i) betahydroxbutyric acid + acetoacetic acids

29
Q

Metabolic causes of Decreased acid secretion

A

a) renal failure (end stage kidney diseases)

b) renal tubular acidosis (specific defects in renal tubular acid secretion)

30
Q

Metabolic causes of Bicarbonate loss

A

a) Severe diarrohea or vomiting –> as gut contents are rich in bicarbonate

31
Q

Rare causes of metabolic acidosis

A
  1. Methanol and ethylene glycol poisoning
    - methanol metabolises –> formic acid (glycolic and oxalic acids)
  2. Glue and paint sniffing
    - toluene metabolised –> hippuric acid
  3. Alcoholic Ketoacidosis
    - increased ketone. complex mechanism
  4. Genetic Metabolic disorders (organic acidemias) + Anatomical causes
    - propionic acidemia
    - metabolemia aciduria
32
Q

Causes of metabolic alkalosis:

A
  1. Ingestion of Sodium Bicarbonate –> high pH + high bicarbonate
  2. Loss of acid due to vomiting (stomach juice HCl) –> high pH
33
Q

Where does bicarbonate come from

A

Especially in regards to metabolic alkalemia

Bicarbonate comes from the conversion of CO2 –> there is a limitless supply of CO2

34
Q

Text examples

A
35
Q

Respiratory compensation in metabolic acidosis

A

Metabolic acidosis uncompensated: Low HCO3 + Low pH Normal H+
Partially compensated metabolic acidosis: –> ACIDOTIC BREATHING
Occurs as Low pH –> stimulates ventilation –> increased CO2 expiration –> Lowers pCO2 –> Majorly compensated (but not fully compensated) pH

36
Q

Methods of compensation for metabolic acidosis

A

Response to pH changes:

  1. Metabolic buffers (proteins + bicarb) : within sec-mins
  2. Ventilation: mins-hours
  3. Kidney renal: longer
37
Q

Return of pH after respiratory compensation of metabolic acidosis

A

Returns CLOSE to original pH (7.4), but NOT ENTIRELY compensated
- Fully compensated = suggests 2 Secondary/Mixed acid-base disorder

38
Q

Role of Kidney in Acid-base balance

A

Overall: finding ways to decrease acidity of acidic urine

  1. Reabsorption of Bicarbonate ( PT proximal tubule)
  2. Generation of new Bicarbonate ( PT proximal tubule)
  3. H+ secretion (DT distal tubule) (via Diffusion trapping of K+ and H+ , due to Na+ transmembrane difference)
39
Q

Bicarbonate Reabsorption

A

PT Proximal Tubule
Filtered bicarbonate is reabsorbed
HCO3- + Na+/other cation –> reabsorbed from urinary tubule into vasorecta

40
Q

Bicarbonate Generation

A

PT Proximal Tubule
Carbonic Anhydrase: Allows CO2 to enter PT –> HH equation inside PT –> increased HCO3- reabsoption and H+ secretion into lumen

41
Q

PT Bicarbonate generation counteracted

A

Acetazolamide –> Carbonic Anhydrase inhibitor –> Decreased HCO3- production –> Decreased buffering/secretion of H+ by kidney –> Artificial Metabolic acidosis
Mountaineers –> hypoxic/low O2 enviro –> increased minute ventilation to get sufficient O2 supply –> increased CO2 expiration –> hyperventilation –> respiratory alkalosis
- Acute mountain sickness/significant respiratory alkalosis: effects Brain vasculature/lungs

42
Q

H+ Secretion by Kidney

A

DT Distal Tubule
Diffusion Trapping: w. freely dispersed ammonia and phosphoric acid into cells from lumen
1. Epithelial Na Channel (ENaC) –> activated w. presence of aldosterone –> Na+ leaves DT into lumen via ENaC
2. Na membrane difference –> Increased positive charge in lumen –> Transepithelial difference in Electroneutrality (disturbed)
3. K+ and H+ pumped into DT (due to Na+ transmembrane difference) –> electroneutrality disturbed –> H+ now trapped in DT –> H+ (hence acid) excreted in urine –> Decreased acidity

43
Q

Method of Diffusion trapping

A

**

Sita GenitoUrinary System (28 decks)

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