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Urinary 6 Flashcards

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1
Q

What happens to pCO2 in resp acidosis?

A

increases

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2
Q

What is the respiratory compensation for metabolic alkalosis?

A

hypoventilation -> raises pCO2 -> extra acid which nudges ratio back down toward normal -> lowers pH closer to 7.4

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3
Q

What happens to HCO3- in met acidosis?

How does the HCO3-:pCO2 ratio change in met acidosis?

A

it decreases because bicarbonate buffers the excess acid

the ratio decreases -> pH falls

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4
Q

What is the primary problem in respiratory acidosis?

Give two causes of respiratory acidosis.

A

hypoventilation -> CO2 retention (hypercapnia)

  • exacerbation of COPD
  • opioid/benzo overdose (resp depression)
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5
Q

What does the Henderson-Hasselbalch equation show?

A

shows that pH is a balance between metabolic factors (HCO3-) and respiratory factors (pCO2)

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6
Q

How does the HCO3-:pCO2 ratio change in respiratory acidosis?

A

ratio decreases -> pH falls = acidaemia

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7
Q

What is the main problem in met alkalosis?

Give two common causes of met alkalosis.

A

excess bicarbonate or loss of hydrogen ions

  • severe vomiting
  • excessive GI suctioning
  • diuretics
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8
Q

What is an acid?

What is a base?

What is pH?

A

acid = substance that forms hydrogen ions H+ when dissolved in water

base = substance that forms hydroxide ions OH- when dissolved in water

pH = quantitative measure of the acidity or basicity of aqueous or other liquid solutions

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9
Q

How does the HCO3-:pCO2 ratio change in resp alkalosis?

A

ratio increases -> pH rises (alkalaemia)

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10
Q

In regards to respiratory acidosis and respiratory alkalosis, list the cause and give an example as to what would cause it.

Mention the effect of effect on PCO2 and the ratio impact.

A

RESP ACIDOSIS - hypoventilation (e.g COPD, resp depression from drugs)
- increased CO2 (hypercapnia) due to inadequate exhalation of CO2
- ratio impact: decreased HCO3-:pCO2 ratio = decreased pH

RESP ALKALOSIS - hyperventilation (e.g anxiety, high altitude)
- decreased pCO2 (hypocapnia) due to excessive exhalation of CO2
- ratio impact: increased HCO3:pCO2 = increase in pH

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11
Q

What is the main difference between respiratory acidosis and respiratory alkalosis?

A

RESP ACIDOSIS
- hypoventilation e.g COPD, resp depression from drugs
- INCREASED pCO2 (HYPERCAPNIA) due to inadequate exhalation of CO2

RESP ALKALOSIS
- hyperventilation e.g anxiety, high altitude
- DECREASED pCO2 (hypocapnia) due to excessive exhalation of CO2

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12
Q

Fill in the gaps and explain why.

A
  1. RATIO INCREASING, can happen in two ways:
    - more HCO3 (more base) -> alkalosis
    - less CO2 -> less acid -> alkalosis
    = pH rises = ALKALOSIS
  2. RATIO DECREASING:
    - less HCO3 -> acidosis
    - more co2 -> acidosis
    = pH falls = ACIDOSIS
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13
Q

What determines pH according to the Henderson-Hasselbalch equation?

A

the ratio of [HCO₃⁻] (base) to pCO₂ (acid)

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14
Q

What happens when the HCO₃⁻:pCO₂ ratio increases?

A

means that pH INCREASES = ALKALOSIS

  • more HCO3 (base - metabolic)
    OR
  • less CO2 (acid - respiratory)
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15
Q

What happens when the HCO₃⁻:pCO₂ ratio decreases?

A

pH decreases = ACIDOSIS so its either:

  • less HCO3 (metabolic)
    OR
  • more CO2 (respiratory)
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16
Q
  1. What is the difference between respiratory acidosis and metabolic acidosis?
  2. What is the difference between respiratory alkalosis and metabolic alkalosis?
A
  1. RESP ACIDOSIS = increased pCO2 (hypercapnia) due to inadequate exhalation of CO2 e.g hypoventilation from COPD or resp depression from drugs

MET ACIDOSIS = loss of BICARB e.g diarrhoea or ACCUMULATION OF ACID e.g DKA - decreased HCO3 due to bicarb buffering excess acid

  1. RESP ALKALOSIS = decreased pCO2 (hypocapnia) due to excessive exhalation of CO2 from HYPERVENTILATING e.g anxiety

MET ALKALOSIS = excess bicarb e.g from vomiting or loss of hydrogen ions = INCREASED HCO3

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17
Q

Your blood pH depends on which two main factors? What is each controlled by?

A

CO2 -> acid -> controlled by lungs

HCO3- -> bicarb -> controlled by kidneys

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18
Q

What would you get with each:

a) CO2 too high

b) CO2 too low

c) HCO3- too low

d) HCO3 too high

A

a) high CO2 = acidosis

b) low CO2 = alkalosis

c) low HCO3 = acidosis

d) high HCO3 = alkalosis

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19
Q

What occurs in respiratory acidosis?

A
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20
Q

What occurs in metabolic acidosis?

A
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21
Q

What occurs in respiratory alkalosis?

A
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22
Q

What occurs in metabolic alkalosis?

A
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23
Q

What kind of blood imbalance does vomiting cause and why?

How do the kidneys attempt to compensate?

A

metabolic alkalosis

  • stomach secretes hydrochloric acid into the lumen to digest = for every H+ pumped into the stomach, a HCO3- IS GENERATED INSIDE YOUR BLOOD
  • when you vomit gastric acid you are losing H+ from the body because the acid never reaches your intestine to be neutralised =
    -> LESS H+ IN BLOOD = LESS ACID = MORE ALKALINE = MET ALKALOSIS
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24
Q

What is met acidosis?

What are the two main mechanisms causing met acidosis?

A

a decrease in blood pH due to low bicarb from either losing base or gaining acid

  1. loss of bicarb e.g diarrhoea
  2. addition of acid e.g DKA
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25
What happens to CO2 during met acidosis?
body hyperventilates to blow off CO2 -> compensatory resp alkalosis
26
What is a common mnemonic for causes of high anion gap metabolic acidosis?
MUDPILES: Methanol, Uraemia, DKA, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates
27
What are the key lab findings in met acidosis?
low pH low bicarb low pCO2 (compensation)
28
What is met alkalosis? What are common causes of met alkalosis?
an increase in blood pH due to excess bicarb or loss of acid 1. loss of acid: vomiting, NG suction, diuretics 2. gain of base: antacid overdose
29
How do the lungs compensate for met alkalosis?
hypoventilation -> they want to try and retain CO2 to bring pH down toward normal
30
What electrolyte imbalance often accompanies met alkalosis and how?
hypokalaemia - too little H+ in the blood, body wants to fix that -> cells will try to help by moving H+ ions out of cells and into blood to lower pH HOWEVER when a positive charge moves out, another cation moves in to keep the electrical balance right = POTASSIUM - H+ moves out of cells into blood - K+ moves into cells = extracellular potassium levels drop
31
What are the key lab findings in met alkalosis?
high pH high bicarb high CO2 (compensation)
32
What is resp acidosis? What are common causes for respiratory acidosis?
decrease in blood pH due to increase in CO2 (hypercapnia) from hypoventilation COPD, asthma, CNS depression (opiates, head injury), airway obstruction
33
How do the kidneys compensate for respiratory acidosis?
they retain HCO3- and secrete H+ to raise pH
34
What are the key lab findings in resp acidosis?
low pH high CO2 high bicarb (if compensating)
35
What is respiratory alkalosis? List common causes.
an increase in blood pH due to a decrease in CO2 (hypocapnia) from hyperventilation anxiety/panic attacks, pain, fever, high altitude
36
How do the kidneys compensate for resp alkalosis?
they excrete bicarb and retain H+ to lower pH
37
List 4 causes of metabolic acidosis with an increased anion gap. List 2 causes with a normal anion gap.
INCREASED ANION GAP - ketoacidosis - lactic acidosis - kidney failure - aspirin overdose - methanol poisoning NORMAL ANION GAP - diarrhoea - renal tubular acidosis
38
How is "anion gap" calculated? What does it help you figure out and what is its significance?
AG = Na+ - (Cl- + HCO3-) helps you figure out why metabolic acidosis is happening, when acid builds up in blood - bicarb goes down BUT whether the anion gap changes tells you WHAT KIND of acid caused it (if extra acids are being added or if you're acidotic because you're losing base/bicarb) INCREASED AG = happens when EXTRA ACIDS are added to body that are not balanced by chloride, they have "unmeasured anions" e.g lactate which raise the gap NORMAL AG = acidosis isn't from adding acids, its from losing bicarb and chloride goes up to balance the charge = gap stays normal
39
What are clinical effects of Metabolic Acidosis? List 3 causes.
- headache - decreased BP - hyperkalaemia - muscle twitching - nausea, vomiting, diarrhoea - kussmaul breathing - changes in LOC e.g confusion, increased drowsiness CAUSE - DKA - severe diarrhoea - renal failure - shock
40
What are clinical effects of respiratory alkalosis? List 3 causes.
- seizures - hyperventilation - tachycardia - hypokalaemia - numbness and tingling - light headedness - nausea and vomiting CAUSES: - hyperventilation i.e anxiety, PE, fear - mechanical ventilation
41
What are some clinical effects of respiratory acidosis? List 3 causes.
- hypoventilation -> hypoxia - dyspnea - headache - hyperkalaemia - dysrhytmias - drowsyness/disorientation CAUSES - respiratory distress - opiates, drug overdose - COPD - asthma - atelectasis
42
What are the clinical effects of metabolic alkalosis? List 3 causes.
- restlessness followed by lethargy - tachycardia - confusion - nausea, vomiting - tremor, muscle cramps, tingling of fingers and toes CAUSE: - severe vomiting - excessive GI suctioning - diuretics
43
How much bicarbonate is reabsorbed in the nephron? And where specifically?
about 80% of filtered bicarb (HCO3-) is reabsorbed in the PCT
44
Explain the step by step process as to how bicarbonate is handled in the nephron.
1. H+ IS SECRETED INTO THE LUMEN (in PCT cell) 2. SECRETED H+ meets filtered HCO3- -> forms H2CO3 (carbonic acid) 3. H2CO3 broken down into Co2 + H2O via CARBONIC ANHYDRASE IV (CA-IV) 4. CO2 and H2O can easily diffuse into tubular cell (they're small and uncharged) 5. INSIDE CELL: CA-II reforms H2CO3 from CO2 and H2O -> H2CO3 then splits again into H+ and HCO3- - H+ goes back into lumen to keep cycle going - HCO3- goes into blood through NBCe1 cotransporter (Na+-HCO3- symporter)
45
Where in the nephron is most bicarbonate reabsorbed?
in the proximal convoluted tubule (PCT) — about 80% of filtered HCO₃⁻ is reabsorbed there
46
Does filtered bicarbonate cross directly into PCT cells?
no - It’s chemically converted to CO₂ and H₂O in the lumen, then reformed as HCO₃⁻ inside the cell
47
Which transporters secrete H⁺ into the tubular lumen?
Na⁺/H⁺ exchanger (NHE3) H⁺-ATPase (proton pump)
48
What happens when secreted H⁺ meets filtered HCO₃⁻ in the lumen?
they combine to form H₂CO₃ (carbonic acid).
49
Which enzyme breaks down H₂CO₃ in the lumen, and into what?
carbonic anhydrase IV (CA-IV) splits H₂CO₃ into CO₂ + H₂O
50
What happens to CO₂ inside the tubular cell? (when it has freely diffused in there with H2O after H2CO3 was broken down in the lumen)
Carbonic anhydrase II (CA-II) converts CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. The H⁺ is recycled into the lumen, and HCO₃⁻ goes to the blood
51
Which transporter moves HCO₃⁻ from the tubular cell into the blood?
the Na⁺–HCO₃⁻ cotransporter (NBCe1) on the basolateral membrane
52
Which two carbonic anhydrase isoforms are involved in reclaiming bicarb and where are they found?
CA-IV → on the luminal (brush border) side CA-II → inside the PCT cell
53
What is the function of a-intercalated cells? What is the function of b-intercalated cells? Where are these located?
a-cells (acid secreting) - reabsorb HCO3- into the blood and secrete H+ into the tubular lumen - active during acidosis b-cells (base-secreting) - secrete HCO3- and reabsorb H+ - active during alkalosis late distal convoluted tubule and collecting duct
54
Which intercalated cells are active during acidosis? What do they do?
a-intercalated cells - reabsorb HCO3- into the blood and secrete H+ into the lumen
55
Which intercalated cells are active during alkalosis?
b-intercalated cells - secrete HCO3- and reabsorb H+ into the lumen
56
In what condition are a-intercalated cells particularly important and why?
in acidosis = body needs to excrete H+ and restore bicarb function of these cells: - excrete H+ in lumen - reabsorb HCO3-
57
What is the renal compensation for respiratory acidosis?
kidneys retain HCO3- to buffer the excess acid
58
What is the primary problem in respiratory alkalosis? Give 2 causes.
- high pH - low CO2 = breathing out too much CO2 (excessive CO2 exhalation) causes: - hyperventilation e.g panic attack, fear, PE, high altitude
59
What is the normal range of plasma pH? What is acidemia and what does it reflect? What is alkalemia and what does it reflect?
7.35-7.45 pH <7.35 -> reflects too much acid (H+) in the blood or too little base (HCO3-) pH >7.45 -> reflects too much base or not enough acid
60
What is the main problem in metabolic acidosis?
- low pH - increased acid or decrease bicarb buffer
61
What happens to pCO2 in respiratory alkalosis?
decreased
62
What is the function of b-intercalated cells? Which transporter do they use in alkalosis and which side of the cell is it on?
- excrete HCO3- and reabsorb H+ Pendrin - Cl-/HCO3- exchanger - bicarb is moved out of cell into urine - chloride moves into cell at the same time on the apical (lumen-facing) side
63
What is the function of a-intercalated cells? Which transporter do they use in acidosis and which side of the cell is it on?
excrete H+ and reabsorb HCO3- AE1 - Cl-/HCO3- exchanger - HCO3 into blood - Cl- into lumen
64
What is meant by the 'limiting pH' in urine? What is the lowest pH it can reach? How do the kidneys keep excreting acid beyond that?
it is the lowest pH the kidneys can acidify urine to - about 4.5 kidneys can secrete a ton of H+ into the urine but there is a point where the gradient is just too steep - at a pH of 4.5, the H+ conc is already about 1,000 times higher than in the blood and that's the limit of active proton secretion uses the two main buffering systems: 1. phosphate buffer 2. ammonium buffer
65
In order to maintain a normal pH of 7.4 in the blood, a __1__ ratio of bicarbonate to carbonic acid must be constantly maintained.
20:1
66
Note the significance of the H+/K+ antiporter (K+/H+-ATPase) in metabolic acidosis and hyperkalaemia. Why do you think that this could be clinically important? What would you need to keep in mind whilst treating this?
the H+/K+ ATPase pump swaps H+ and K+ ions between cells and the blood: - H+ goes into cells, K+ comes out - K+ leaves cell, H+ goes in in met acidosis = too much H+ in blood -> H+ moves into cells via this pump and K+ moves out = HYPERKALAEMIA -> acidosis can cause hyperkalaemia in hyperkalaemia, the high K+ outside cells drives K+ into cells which pushes H+ out = HYPERKALAEMIA CAN WORSEN ACIDOSIS high potassium: arrhythmias and cardiac arrest
67
When the kidneys reach the limiting pH, what two main buffering systems do they use? What is their purpose?
1. phosphate buffer 2. ammonium buffer to excrete H+ safely in the urine without dropping urine pH so low that it damages the tubules - they let the kidneys get rid of acid in a buffered, non-destructive way while regenerating bicarb for the blood
68
What is the meaning of 'non-volatile acid excretion'? What proportion of non-volatile acid excretion is via the ammonium buffer? What proportion of non-volatile acid excretion is via the phosphate buffer?
non-volatile acid excretion = acid that cannot be breathed off as CO2 so the kidneys have to excrete it in the urine instead ammonia buffer = 60% phosphate buffer = 40%
69
How and where does the phosphate buffer system work?
in the distal convoluted tubule and collecting duct 1. tubular cells secrete H+ into lumen 2. that H+ binds to MONOHYDROGEN PHOSPHATE (HPO₄²⁻) -> FORMS DIHYDROGEN PHOSPHATE (H₂PO₄⁻) which is excreted into the urine for every H+ secreted and excreted with phosphate, one new HCO3- enters the bloodstream via the A-INTERCALATED CELLS via the HCO3/CL- exchanger (AE1)
70
How and where does the ammonium buffer system work?
in the PCT and collecting duct 1. in proximal tubule cells, GLUTAMINE is broken down -> produces NH3 (ammonia) and HCO3- 2. NH3 diffuses into the tubular lumen 3. secreted H+ combines with NH3 -> NH4+ (ammonium) 4. NH4+ trapped and excreted in urine for every H+ excreted as NH4+, a new HCO3- enters the blood
71
Which form of phosphate acts as the urinary buffer? Where does the "new" HCO3- in the phosphate buffer system come from?
monohydrogen phosphate (HPO₄²⁻) - binds to H+ and forms dihydrogen phosphate (H₂PO₄⁻) which is excreted it is produced inside the tubular a-intercalated cells from CO2 + H2O via carbonic anhydrase
72
Which cell type is responsible for secreting H+ in the phosphate buffer system?
the a-intercalated cell in the distal nephron and collecting duct
73
How is ammonia (NH3) produced in the kidney? What happens to NH3 in the tubular lumen?
from the metabolism of glutamine in proximal tubular cells it combines with secreted H+ to form NH4+ (ammonium) which is excreted
74
What is "titratable acid"?
the H₂PO₄⁻ excreted in urine after monohydrogen phosphate has mopped up H+ (phosphate-buffered acid measured in urine)
75
Why can't the kidneys keep secreting H+ once urine pH reaches 4.5?
gradient becomes too steep - further H+ secretion is blocked unless H+ is buffered
76
What is the primary mechanism for HCO3- ion reabsorption in the PCT?
Na+/H+ antiporter (Na+/H+ exchanged 3 - NHE3)
77
What is the role of urinary buffers?
to "mop up" secreted H+, preventing urine from reaching limiting pH and allowed continued acid excretion
78
In short, how do the two buffer systems work?
ammonia buffer - secreted H⁺ binds to NH₃ → forms NH₄⁺ (ammonium), which is trapped and excreted in urine phosphate buffer - secreted H⁺ binds to HPO₄²⁻ (monohydrogen phosphate) → forms H₂PO₄⁻ (dihydrogen phosphate), which is excreted
79
Fill in the blanks. Explain why glutamine is metabolised by the kidney and not the liver in acidosis.
when blood is too acidic, kidneys use glutamine from bloodstream KIDNEYS glutamine → 2 NH₄⁺ + 2 HCO₃⁻ - each glutamine yields 2 ammonium ions which are excreted into urine and 2 bicarb ions which are returned to blood for base LIVER liver converts NH₄⁺ → urea BUT IT PRODUCES H+, so urea production generates acid in acidosis you want to get rid of acid so glutamine is metabolised by the kidneys not the liver
80
Explain why glutamine is metabolised by the kidneys instead of the liver in acidosis. Explain why glutamine is metabolised by the liver instead of the kidneys in alkalosis.
because when liver converts ammonium (NH₄⁺) → urea, it produces H⁺ = UREA PRODUCTION GENERATES ACID
81
Which urinary buffer system can be upregulated in chronic acidosis?
the ammonia buffer
82
List 4 clinical effects of acidaemia on the CVS. List 4 clinical effects of alkalaemia on the CVS.
acidaemia - decreased threshold for arrhythmias - impaired cardiac contractility - arteriolar dilation - decreased CO alkalaemia - decreased threshold for arrhythmias - arteriolar constriction - reduced coronary flow - reduced anginal threshold
83
A patient with prolonged vomiting presents with muscle cramps, carpopedal spasm, and a pH of 7.55. Which electrolyte abnormality is most likely?
hypocalcaemia = alkalosis increases Ca²⁺ binding to albumin → ↓ free ionized calcium → tetany
84
Which metabolic abnormality is common in acidaemia but not alkalemia?
hyperkalaemia
85
List 3 electrolyte abnormalities associated with alkalosis.
hypokalaemia hypomagnesia hypocalcaemia hypophosphataemia
86
Consider a patient with underlying renal insufficiency. How would this impact the body’s ability to compensate for the acidosis caused by diarrhoea?
in patients with renal insufficiency or CKD, kidneys ability to produce and excrete NH4+ and titratable acids is impaired this means that the kidneys cannot effectively increase H+ excretion or regenerate bicarb = leads to reduced capacity to compensate for met acidosis as a result, ACIDOSIS can become more SEVERE, blood pH may continue to fall without adequate compensation
87
What respiratory change is seen in met acidosis?
compensatory hyperventilation - kussmaul breathing but prolonged effort may cause respiratory muscle fatigue
88
How does ECF K+ move into cells? What is this stimulated by?
Na+/K+ ATPase pump - stimulated by adrenaline, insulin, aldosterone H+/K+ exchangers - K+ enters cell when H+ leaves
89
How does K+ leave cells?
1. leaky K+ channels 2. cell lysis, exercise, acidosis cell lysis e.g rhabo - dumps intracellular K+ into plasma exercise - temporary rise in extracellular K+ from muscle acidosis - H+ enters cell in exchange for K+ leaving
90
Which organ is most sensitive to potassium imbalance and why?
heart cardiac cells rely on tight control of K+ gradients across the membrane for normal depolarisation and repolarisation small shifts in plasma K+ = alters resting membrane potential = messes with conduction and excitability
91
Why are cells initially more excitable in hyperkalaemia?
more K+ outside cell -> less K+ leaks out inside gets less negative = depolarised e.g 70mV (but threshold remains the same) distance between RMP and threshold is smaller = EASIER TO TRIGGER ACTION POTENTIAL
92
What is the normal RMP and what is the normal threshold for action potential? How does hypokalaemia affect this?
RMP: -90mV threshold: -60mV less K+ outside -> more K+ leaves cell inside gets even more negative = hyperpolarised (e.g -100mV) but threshold stays at -60mV = distance is now bigger harder to trigger action potential = CELLS ARE LESS EXCITABLE = MUSCLE WEAKNESS, ARRHYTHMIAS
93
What does elevated plasma K+ do to aldosterone?
94
List 3 causes of hyperkalaemia and hypokalaemia.
95
What are signs and symptoms of hypokalaemia?
96
What are signs and symptoms of hyperkalaemia?
97
What is the role of insulin in hyperkalaemia? What else can induce cellular uptake of K+?
insulin stimulates uptake of K+ by cells - stimulates Na+/K+ ATPase activity = ingested K+ moves rapidly into cells thyroxine stimulation beta-adrenergic stimulation
Med Term 3
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