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A&P II (Spring 2024) > Lecture 20: Acid/Base Physiology (Final Exam) > Flashcards

Lecture 20: Acid/Base Physiology (Final Exam) Flashcards

1
Q

For the purposes of A&P, what is normal pH?

A

7.4

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2
Q

What occurs to serum proteins when excess hydrogen ions are present?

A

Conformational change of the protein occurs.

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3
Q

What are volatile compounds?
Give examples.

A

Compounds that can escape to a gaseous phase easily.

Ex. CO₂ , VAA’s

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4
Q

Whats an example of a bodily acid that is non-volatile?
How is this compound removed from the body?

A
  • Lactic acid
  • Renal excretion
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5
Q

The majority of acid in the body is found in the form of ____.

A

CO₂

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6
Q

Where do the components of CO₂ come from?

A
  • O₂ from respiration
  • C from food diet
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7
Q

What is the central acid/base formula?

A
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8
Q

What enzyme converts H₂CO₃ to CO₂ and H₂O ?

A

Carbonic Anhydrase.

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9
Q

Excess CO₂ would push the acid/base formula to the _____.

A

right

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10
Q

What cell membrane pump is adversely affected by acidosis?

A

Na⁺ K⁺ ATPase Pump

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11
Q

What is the result of a dysfunctional Na⁺K⁺ATPase pump due to acidosis?
Why does this occur?

A
  • Hyperkalemia
  • Occurs due to excessive ICF H⁺ causing efflux of H⁺ and K⁺ to the ECF.
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12
Q

What organ deals with acidosis in the short term?
What organ deals with acidosis in the long term?

A
  • Short term = Lungs
  • Long term = Kidneys
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13
Q

pH is a _______ scale. This means that small changes in pH equate to ______ changes in [H⁺].

A

logarithmic ; large

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14
Q

Strong acids dissociate into ______ conjugate bases.

A

weak

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15
Q

Weak acids dissociate into _____ conjugate bases.

A

strong

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16
Q

What does H₂CO₃ dissociate into?

A

H⁺ : acid
HCO₃⁻ : conjugate base

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17
Q

How is pH calculated?

A

pH = -log[H⁺]

or

pH = pK + log (A⁻ ÷ HA)

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18
Q

What is a product of abnormal metabolism?

A

Lactate

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19
Q

Ketones are _______ and therefore have to be ______ excreted.

A

non-volatile ; renally

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20
Q

How are H⁺ excreted in the urine?

A

NH3 + H⁺ → NH₄⁺

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21
Q

What is a normal serum HCO₃⁻ level?

A

24 mOsm/L

22
Q

What occurs to hemoglobin when around excess hydrogen ions?

A

O₂ will dissociate off the Hb molecule

23
Q

What is the primary protein buffer necessary for normal HCO₃⁻ activity?

A

Hemoglobin

24
Q

If the PCO₂ is excessively high, then a commensurate increase in what is needed to prevent acidosis?

A

HCO₃⁻

25
Q

What is the most important blood buffer?
What is necessary for this buffer to be effective?

A

HCO₃⁻ is most important buffer but requires normal serum protein concentrations.

26
Q

What is the lowest possible pH on the 20mmHg PCO₂ isobar?

What about the highest?

A

Lowest ≈ 7.36 w/ a HCO₃⁻ of almost 10 mmol/L
Highest ≈ 7.75 w/ a HCO₃⁻ of around 24 mmol/L

27
Q

Given the graph below, how would a stronger buffer change the graph?

A

The buffer line would be more steep.

28
Q

Polycythemia would result in a __________ buffering capacity.

Why?

A

Increased buffering capacity

This is due to excess Hb capacity to “capture” excess H⁺.

29
Q

Anemia would result in a ________ to buffering capacity.

A

decrease

30
Q

Name the other buffering compounds aside from plasma proteins and bicarbonate.

A
  • Sulfur compounds
  • Phosphate compounds
  • Ammonia compounds
31
Q

What buffer compounds are found primarily intracellularly?

A
  • Sulfur
  • Phosphate
32
Q

What two phosphate buffer compounds were mentioned in lecture?

A
  • ATP
  • H₂PO₄ → H⁺ + HPO₄⁻
33
Q

What is the general pK of phosphate compounds?

A

pK ≈ 6.8

34
Q

What is the normal pH of urine?

A

≈ 5

35
Q

How many ATP molecules are produced via glycolysis?

A

2 ATPs

36
Q

How many ATP molecules are produced via the Krebs cycle (citric acid cycle)?

A

34 ATPs

37
Q

How many ATP molecules are produced via combined glycolysis and citric acid cycle?

A

36 ATPs

38
Q

What occurs with “uncoupled metabolism” ?

A

Excess H⁺ (or something else) inhibits proteins in the glycolysis/Krebs cycle → increase glucose usage w/ decreased ATP formation.

Possible anaerobic metabolism and excess lactate formation.

39
Q

Why is acute respiratory acidosis more acidotic than chronic respiratory acidosis?

A

Kidneys haven’t had time to increase HCO₃⁻ production to accommodate excess CO₂.

40
Q

When is metabolic acidosis seen?

A

When the kidneys don’t produced enough HCO₃⁻ to compensate for acidosis.

41
Q

Which of the following conditions is a result of hyperventilation?

A

Acute Respiratory alkalosis

↓PCO₂ → ↓CBF

42
Q

Differentiate the clinical presentations of early and late COPD patients.

A

Early: pink puffer, ↑PCO₂
Late: Blue bloater, ↑PCO₂ & ↓PO₂

43
Q

What famous textbook writer developed polio?
What did this prevent him from becoming?

A

Guyton developed Polio and was unable to become a cardiac surgeon.

44
Q

How was polio contracted?
What charity group was originally created to combat polio?

A
  • Swimming pools
  • March for Dimes
45
Q

What drug class, mentioned in class, when combined with alcohol will lead to severe consequences and possible death?

A

Barbiturates

46
Q

Which two commonly used anesthetics won’t cause depression of the central nervous system?

A

Ketamine and Dexmedetomidine

47
Q

What is the common pathophysiology of someone with an impact injury who had “the wind knocked out of them” ?

A

Phrenic nerve spasm

48
Q

Is the respiratory system affected with a C6 injury?

A

Yes; diaphragm is innervated by C3-C5 but accessory muscles can still be affected.

49
Q

Phrenic nerve injury, Eton-Lambert syndrome, sarcoidosis, extreme obesity, and pulmonary parenchymal disease are all examples of conditions that can cause _______ ________.

A

Respiratory acidosis

50
Q

What effects will high altitude have on PO₂ and respiratory drive?

A

High altitude = ↓PO₂ and ↑Respiratory drive

51
Q

What drug class can cause respiratory alkalosis?

A

Salicylates (ex. aspirin; stimulate the breathing centers of the CNS)

52
Q

Progesterone, encephalitis/meningitis, anxiety, salicylates, and asthma are examples of conditions that can cause _______ ________.

A

Respiratory Alkalosis

A&P II (Spring 2024) (24 decks)

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