control and regulation of pH Flashcards

1
Q

Which of the following conditions is likely to be associated with respiratory alkalosis (pH>7.4) ?
A Breathing air enriched with 8% CO2
B Chronic Obstructive Pulmonary Disorder (COPD)
C Prolonged stay at high altitude (from sea level)
D Prolonged episode of vomiting

A

OPTION C - high altitude
HYPOXIC envrionemnt so we will voluntarily hyperventilate which will induce resp. Alkalosis as we expel c02.

But there is an eventual overshoot as our renal system attempts to resolve this

B-Obstructive so build up of c02 so r. Acid
Option D - not respiration, that’s metabolic
Option A - that would be acidosis as c02 is acidic

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2
Q

Which of the following conditions is likely to give rise to metabolic alkalosis?
A Breathing air enriched with 8% CO2
B Emphysema
C Prolonged stay at altitude (from sea level)
D Prolonged episode of vomiting
E Voluntary hyperventilation

A

vomiting - as you are there is a Loss of acid so the base rises in comparison

right so anything to do with C02 is acid so it can’t be A, E, B.
and vomiting is metabolic whilst altitude is respiratory

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3
Q

Give the normal range of blood pH

A

7.4 is optimum pH should be between 7.35 and 7.45
If above = alkalosis
If below =acididosis

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4
Q

Do you know the carbon dissociation equation

A

C02 + H20 = Hc03- + h+ //carbonic acid intermediate

This is why C02 is acidic as the more C02 there is, the more the equilibrium shifts in favour of making the hydrogen
And Bicarbonate is alkali

Mediated by carbonic anhydrase enzyme

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5
Q

How doesnthe [H+] change in acidosis and alkalosis

A

Proton increases in acidosis

Proton decreases in alaklasos.

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6
Q

ROME

A
# helfyl for a davenport plot
Respiratory opposite
Acidosis: high C02, low pH
Alkalosis: low C02 high pH
Metabolic
Acidosis: low pH low bicarb
Alkalsosi high pH, high Bicarb
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7
Q

what makes something an acid or a base

A

acid - donates protons, accepts electrons - hydrogen ion

base - donates electrons, accepts protons - bicarbonate

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8
Q

what is the difference between acidosis and acidemia (same for alkalosis and aklaemia)

A

-aemia relatates to the blood e.g. hypoxeamia

so acidaemia is the low pH of blood// below 7.35 but the process that the pH lowers is acidosis

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9
Q

where in the body is pH controlled

A

the lungs (gas composition/respiratory side of -osis) and the kidneys (bicarbonate excretion/reabsorption/metabolic side of -osis) is main sites of pH control

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10
Q

our blood is naturally a weak acid. explain reasons as why this could be

A
  1. metabolic activity porduces lots of acids e.g. carbonic from OxP, lactic from glycolysis. keto from FA metabolism, sulphuric and phosphoric acids from protein metabolism
  2. we can also lose bases through excretion of Hc03- and the basic pancreatic digestive juices neutralizing with stomach acid
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11
Q

how does the body maintain a pH of 7.4 considering that our blood is naturally weakly acidic? # general machanisms

A

we can increase base production to replace the ones we have lost and lose acid instead
> increasing respiration/expelling more C02//hyperhypoventilate
> reabsorb or excrete more bicarbonate/ammonia in kidney -> urine

vomiting can also help to lose excess acid as HCl is lost from stomach

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12
Q

how can the body maintain pH # specific mechanisms

– outline how buffering works

A
  1. chemical buffering is one way to maintain pH. Quite a fast process and makesise of chemicals like histidine, phophates and lactic acids/organic acids which have pKa of 6.5-6.8 which are appropriate to maintain blood pH of 7.4
  2. volatile buffering makes use of C02+water and RBC express carbonic anhydrase which enables equilibrium
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13
Q

why is it called VOLITILE buffering?

A

because, C02 is not always in solution and can be expelled by the lungs in its gaseous form

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14
Q

how can the body maintain pH # specific mechanisms

– outline how organ responses works

A
  1. lungs// FAST compensatory mechansisms, one can hyper/hypo ventilate to alter levels of Co2
    minutes and seconds
  2. SLOWER renal compensatory mechanisms where nephrons can reabsorb HC03- or generate ammonium ions and excrete more protons = acidic urine // these both would raise the pH
    hours to days
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15
Q

what does a shoft to the right on a davenport plot mean?

A

davenport plot line represents the ppCo2

so a shift to the right represents a lower ppCo2 which makes sense becuase as we move to the right, the h increases so it becomes less acidic because the ppCo2 is dropping!!

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16
Q

describe a standard davenport plot

A

x axis is pH, y axis is HC03- levels, the line is ppCo2

standard pH is 7.4, ppc02 = 40mmHg, conc of bicarb is 24mM

17
Q

describe what can cause respiratory acidosis and alkalosis and how we could compensate

A

r.acidosis - high c02,lowbicarb due to lung and heart diseases where there is insufficient C02 removal. also soe drugs and anaesthetic can increas ppc02
compensate by increasing HC03-

r. alkalosis - low C02, high bicarb due to issues with respiration like hypoxia, hyperventilation so compensate by reducing HC03-

18
Q

what is carbonic anhydrase? where is it expressed?

A

enzyme that is expressed in RBC, renal tubules and pancreatic cells that catalyses the hydration and dehydration of C02

19
Q

describe what can cause metabolic acidosis and alkalosis and how we could compensate

A

metabolic has no effect on the ppC02!!
m.alkalosis - high bicarb/high pH, due to excess base intake or lots of vomiting (loss of base)
treat by increasing the ppC02

m.acidosia - low bicarb due to diarohae, or gain of acids e.g diabetes hyperglycaemia or renal failure to filtrate/excrete appropiately
treat by decreasing the ppc02

20
Q

ph regulation : counterbalance

A

m. acidosis = low ph, ,low bicarb, or gain of acid, so we want to lower c02 to compensate

For example, if a person is experiencing a metabolic acidemia, their body will attempt to induce a respiratory alkalosis to compensate

21
Q

what condition would voluntary hyperventilation be associatec with?

A

acute, respiratory alkalosis as you are breathing in lots of oxgen and expelling lots of C02
so there is a loss of acid

22
Q

what would cns depression, neromuscular disorders or lung obstructions be a cause of?

A

respiratory acidosis
> can’t expel the c02 so it builds up in blood
> respiratory centre in medulla oblongata is not sending signals to enbale expiration
> nerve endings are damaged

23
Q

what would cns hyper activation (from anxiety, drugs, fever, in pain) , hypoxeamia

A

respiatroy alkalosis
> hypoxia you will breathe in more 02 to gain more oxygen but then expel more c02
> cns firing increases which can then raise heart rate

so c02 decreases in blood

24
Q

what would diabetic ketoacid, lactic acidosis, uremia(toxin build up), diarrohea

A

metabolic acid
> kindey failure in uremia so unable to filter
> diarrohea can lead to loss of bicarb, loss of base

25
Q

what is vominting, mineralcorticoid excesss (aldosterone), hypercapnia compensation, fluid volume loss from dehydration, hemorrhage

A

metabolic alkali - loss of acid
vomiting reducing the acid contents in stomach
> taking diuretics will reduce fluid volume -> electrolytes and H+ levels will fall
> aldosetone can reabsorb water and sodium but excrete conc.acidic unrine. cortisol (cushing) can mimic effect of aldosterone // loss of acid
> long term renal compensation for hypercapnia/COPD/resp.alk is to then remove the excess acid via urine

26
Q

why is acidosis an issue to the heart

A

can decrease the contractility of mycardial tissue
> low CO, low MAP
> low TPR, vasodilation so low blood pressure
> also lead to v.tachycardia

27
Q

why is hypercapnia a risk for both acidemia and alkalemia?

> spans both resp and metabolic!!!

A

so when i think of hypercapnia i think this is high c02 (could be from COPD, CNS depression) so that is classic resp.acid

now to compensate for this, body will increase bicarb production and excrete acidic urine but this takes TIIME

but in a hospital, we will put patient on a ventilator, this will offset the excess Co2 but we are still left with and elevated bicarb so now we get post hypercapnia metabolic alkalosis