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GBA Physiology > Renal and Acid/Base Physiology - Theoretical Questions > Flashcards

Renal and Acid/Base Physiology - Theoretical Questions Flashcards

1
Q

How is the Flow/Mass ratio of the Kidney in comparison with the Brain or Heart? Bigger/Smaller? Why?

A

Kidney: ~600 ml/min /200 g (one kidney)
Brain - ~700 ml/min /1500 g
Heart - ~200 ml/min / 400g
It’s about 5 times larger in the Kidney - For Filtration.

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2
Q

Pathway of the Renal Blood Flow:

A

Renal Artery-Segmental arteries-Interlobular Arteries-Arcuate arteries-Intralobular arteries-Afferent Arterioles-Glomerular Capillaries-Efferent Arterioles-Peritubular/Vasa Recta - Venules…

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3
Q

What is the most Effective Starling Force in the Renal Corpuscle?

A

Glomerular Capillary Hydrostatic Pressure.

Higher than in Systemic Capillaries.

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4
Q

What is the Starling Force in the Renal Corpuscle that changes the most while blood circulates there?

A

Glomerular Capillary Oncotic Pressure rises.

No protein filtration in Renal Corpuscle.

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5
Q

How does the regulation of renal circulation Protects glomerular capillaries?

A

Constriction of Afferent arterioles by Bayliss effect prevents them from receiving hydrostatic pressure which is too High

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6
Q

How does the regulation of renal circulation help balance out the flow between the different Renal Corpuscles capillaries?

A

Tubuloglomerular feedback:
Macula densa of DCT senses elevations in NaCl, releases Adenosine to Afferent Arterioles SMCs- constrict to limit filtration and allow flow to other Corpuscles.

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7
Q

How does the regulation of renal circulation help conserve Sodium and Water?

A

Glomerular Cell Cascade (JG Cells):
Macula densa of DCT senses decrease in NaCl,
releases Adenosine to JG cell which Releases Renin and Activate the Renin-Angiotensin-Aldosterone System.

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8
Q

How Angiotensin acts on the Afferent and Efferent Arterioles when in High / Low concentrations?

A

High Angiotensin-II: Constricts both Afferent and Efferent, GFR is Lower.
Low Angiotensin-II: Constricts Efferent, GFR is Higher.

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9
Q

What are the two main factors that support the High GFR and FF possible in the Renal Circulation?

A

1) Glomerular Capillary Pressure is Twice as High

2) Filtration Coefficient is 100 times higher - High Surface area and Permeability.

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10
Q

What are the Layers of the Renal Corpuscle Filtration Barrier?

A

1 - Fenestrated Endothelium (Negatively charged)
2 - Basement Membrane (Pouros + Negatively charged)
3 - Podocytes Layer (Negatively charged+Filtration Slits)

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11
Q

Defenition of Renal Clearance:

A

Renal Clearance: Volume of plasma per unit time from which all the given substance have been removed by the kidneys and Excreted in urine. Cx (ml/min)

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12
Q

How many Nephrons are in each kidney?

A

About a Million

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13
Q

What will happen with Albumin as it goes through the Renal Circulation?

A

Albumin is not filtered at all.

Large size and negative charge prevent it from passing the Filtration barrier.

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14
Q

What will happen with Glucose as it goes through the Renal Circulation? In DM?

A

Filtered but completely reabsorbed to Peritubular cap.

Glucosuria is common in DM - saturated transporters.

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15
Q

What will happen with PAH as it goes through the Renal Circulation?

A

Filtered and also Secreted by Peritubular capillaries.

We can say that 90% of PAH is excreted and doesnt get to the Renal veins (normally neglected).

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16
Q

What can we measure thanks to the unique excretion process done by PAH?

A

RPF will be equal to the clearance of PAH (Cpah).

Therefore RBF=Cpah/(1-Hematocrit)

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17
Q

What medicine goes in the same route as PAH? Why?

A

Antibiotics for Urinary tract infection.

To reach the urinary tract.

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18
Q

What will happen with Inulin as it goes through the Renal Circulation? What can we measure from that?

A

Inulin is Filtered and Not Secreted/Absorbed.

Clearance of Inulin will be equal to GFR.

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19
Q

What will happen with Creatinine as it goes through the Renal Circulation? How is different from Inulin?

A

Creatinine is Filtered and Not Secreted/Absorbed.

Since Creatinine is an Endogenous molecule it will form at a specific metabolic rate that could damage GFR measurements.

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20
Q

GFR Regulation by Sympathetic nervous system:

A

Norepinephrine will bind to Alpha-1 receptors of Afferent arterioles (Mostly) and cause decrease in GFR.

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21
Q

GFR Regulation by Atrial natriuretic peptide :

A

ANP dilates Afferent arterioles (lightly constricts effernts), Causes an increase in GFR.

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22
Q

GFR Regulation by Prostaglandins:

A

Prostaglandins dilate Afferent arterioles causes an increase in GFR.

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23
Q

GFR Regulation by Dopamine:

A

Dopamine dilates Afferent arterioles causes an increase in GFR.

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24
Q

What are the main functions of the Early Proximal Convoluted Tubule?

A

Early Proximal Convoluted Tubule : Reabsorption of 20% of Na allows for cotransport with Glucose (SGLT2), AA, Pi, Lactate and Citrate. Cl goes Paracellularly. Aq1 and 2.
Bicarbonate formed by CA reaction goes with Na.

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25
Q

what is the cause for Cl to be Reabsorbed paracellularly in the Late Proximal Convoluted Tubule?
What will this cause in response?

A

After the absorption of Na in the Early convoluted tubule the Cl amount that stayed in the filtrate causes elevation of Negative charge that will drive it to follow Na.
Then, again Na, Ca and K will follow for the same reason.

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26
Q

Late Proximal Convoluted Tubule -Job in Acid/Base regulation:

A

has a Na/H Exchanger - lowers blood pH.

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27
Q

Late Proximal Convoluted Tubule - Examples for gets secreted?

A

PAH, NE, Epi and Oxaloacetate

and H with H/Na Exchanger

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28
Q

Action of Acetazolamide:

A

Inhibition of Carbonic Anhydrase (CA) therefore NaHCO3 will not be transported later to peritubular capillaries.

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29
Q

How much of Na is Reabsorbed in the Proximal Convoluted Tubule? Which transporters are carrying glucose in each surface and each part of it?

A

60-70%
Early - SGLT2, Late - SGLT1, both on Apical surfaces.
Glut1 and Glut2 on the Basal surfaces for both.

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30
Q

How much NaCl is absorbed in the Loop of Henle?

A

25%

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31
Q

Which are the Passive segments of the Loop of Henle? What happen there?

A

Thin Descending Limb - Aq1 allow for water reabsorption forming a Hyperosmotic filtrate. Concentration segment.
Thin Ascending Limb - NaCl and Urea uptake forming a Hyposmotic filtrate. Impermeable to water.

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32
Q

What is the purpose of the TAL segment?

A

Dilution segment - Impermeable to water and Actively reabsorbs osmolytes.

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33
Q

What is being Reabsorbed in the TAL? How?

Inhibitor?

A

NCCK - Na, 2Cl and K - Inhibited by Furosemide.

Na, K and Ca also go Paracellularly.

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34
Q

What is the job of the TAL in regard to Acid/Base regulation?

A

NCCK Transporter:

NH4 (Ammonium Ion) could replace K in the Reabsorption.

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35
Q

Distal Convoluted Tubule:

What is being reabsorbed? How? Regulation? Drug Inhibitor?

A

Distal Convoluted Tubule:
Na-Cl Cotransporters: Inhibited by Thiazide
Calcium Reabsorption Channels - Stimulated by PTH

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36
Q

Distal Convoluted Tubule:

How much water is being reabsorbed in the distal convoluted tubule?

A

Distal Convoluted Tubule:
No water reabsorption is happening in the DCT!
Impermeable to water.

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37
Q

What are the segments of the nephron which are Impermeable to Water?

A

Impermeable to Water:
Thin Ascending Limb
TAL -Thick Ascending Limb
“Early” Distal Convoluted Tubule (DCT)

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38
Q

Collecting Duct and “Late” DCT - Principal Cells:

What is being reabsorbed? How? Regulation? Drug Inhibitor?

A

Principal Cells: Na+H2O Reabsorption, K Secretion
ENaC - Stimulated by Aldosterone, Inhibited by ANP and Amiloride (K Sparing Diuretics) .
K channels on Apical Surface.
Vasopressin (ADH) - V2R(Gs) cause Aq2 stimulation .

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39
Q

Collecting Duct and “Late” DCT - Intercalated cells:

What is being reabsorbed? How?

A

Intercalated cells: H Secretion and K reabsorption.
H/K Exchanger - Reabsorption of K and H secretion.
H ATPase secrets.

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40
Q

Potassium in the Nephron:

Reabsorption and Secretion major elements.

A

Potassium in the Nephron: 67% Reabsorbed in the PCT.
TAL Reabsorbs with NCCK
Principal Cells K channels for Secretion
Intercalated cells Reabsorb with H/K Exchanger

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41
Q

Aldosterone - regulation of reabsorption/secretion of Potassium in the Nephron:

A

Regulation of Potassium in the Nephron:
Aldosterone - Stimulates Na/K ATPase on Basal side
allowing more secretion from Principal cells Apical side.
Hyperaldosteronism - Hypokalemia
Hypoaldosteronism - Hyperkalemia

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42
Q

Acid/Base - regulation of reabsorption/secretion of Potassium in the Nephron:

A

There is a general exchange of H and K in the nephron:
Acidosis leads to Hyperkalemia.
Alkalosis leads to Hypokalemia.

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43
Q

Thiazide and Loop Diuretics (Like Furosemide) - regulation of reabsorption/secretion of Potassium in the Nephron:

A

Thiazide and Loop Diuretics (Like Furosemide): Stop the Reabsorption (NCCK inhibition) and by Increasing the flow rate also increase the secretion of K. Could cause Hypokalemia.

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44
Q

K sparing Diuretics (Like Amiloride) - regulation of reabsorption/secretion of Potassium in the Nephron:

A

  Amiloride decreases K secretion (by itself, usually used with Thiazide)

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45
Q

Regulation of reabsorption/secretion of Calcium in the Nephron:

A

PCT and TAL reabsorb 90% back.

PTH is the only hormone able to regulate the rest 10% reabsorption by Ca channels stimulation in DCT.

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46
Q

Defenition of Countercurrent Multiplication:

A

Active process of the loop of Henle.
Creating the Corticopapillary osmotic gradient with the dilution segments (Ascending) and Concentration segment (Descending) allowing for transport of osmolytes and water at the correct positions.

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47
Q

What are the two major steps taking place one at the time in the Countercurrent Multiplication?
How are they working simultaneously to allow for the Corticopapillary concentration gradient?

A

Single effect and Fluid flow

Concentration of Interstitium around papillary end and Dilution of interstitium at the Cortical end.

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48
Q

What happens in the Single effect phase of Countercurrent Multiplication?

A

TAL :NCCK transporters in the allow for absorbs osmolytes. It is Impermeable to water causing hyperosmolarity in the TAL epithelium, the surrounding interstitium and the descending limb (Concentration) while the lumen gets Hyposmotic (Dilution segment).

49
Q

What happens in the Fluid Flow phase of Countercurrent Multiplication?

A

After Single effect more fluid (Filtrate) with higher osmolarity goes in the Thin Descending limb while water goes (Aq1) to the interstitial space (Osmosis). Basically shifting the all the hyperosmotic fluid towards the Papillary edge of the loop.

50
Q

What is the countercurrent exchange?

A

Passive process of the secretion and reabsorption of water of water and solutes from and to (respectively) the peritubular capillaries, maintains the concentration gradient set in the countercurrent multiplication - blood sets out with 325 mOsm (slightly hyperosmolar).

51
Q

Urea Recycling:

Where does the concentration of Urea in the filtrate becomes hypertonic relative to the interstitium?

A

Urea concentration becomes hypertonic in the proximal tubule where more water than urea gets reabsorbed.

52
Q

Urea Recycling:

What happens in the thin descending limb?

A

Urea is being secreted in the thin ascending limb as it osmolarity is higher in the interstitium.

53
Q

Urea Recycling:

What parts of the nephron are impermeable to Urea?

A

Ascending segments of the Loop of Henle

54
Q

Urea Recycling:

What happens in outer part of the Collecting duct?

A

ADH released from Neurohypophysis up regulates (if needed) the translocation of Aquaporins Aq2 allowing for more water reabsorption and therefore concentrating Urea in the Duct.

55
Q

Urea Recycling:

What happens in inner part of the Collecting duct?

A

ADH released from Neurohypophysis up regulates the UT1 for transport of Urea as well as Aq2 for water to follow it back to the Interstitium.

56
Q

What is the corticopapillary gradient :

Numbers? Composition?

A

300 mOsm in the Cortex Interstitium
1200 mOsm in the Medullary Papilla interstitium
Of the Papilla interstitium 600 mOsm comes from Na and the other 600 from Urea.

57
Q

What happen when ADH is secreted less ? What is the concentration in the Medullary Papilla interstitium?

A 
Dilution in the kidney.
600 mOsm (No Urea recycling) .
58
Q

What is Diabetes Insipidus? What are the cause? What kinds are there?

A

Defect in ADH Signaling causing higher Urine Production. Could be Nephrogenic - Kidney response is defect or Central Secretion of ADH by Hypothalamus is not sufficient.

59
Q

Actions of Aldosterone:

A 
↑ Na+ reabsorption (ENaC, distal
tubule principal cells)
↑ K+ secretion (distal tubule
principal cells)
↑ H+ secretion (distal tubule
α-intercalated cells)
60
Q

Actions of ANP:

A

↑ GFR
↓ Na+ reabsorption (PKG inhibits ENac)
-Renin inhibiting

61
Q

Actions of Angiotensin II:

A

↑ Na+–H+ exchange and HCO3 reabsorption (proximal tubule).
↑ Aldosterone Synthesis in Zona Glomerulosa
↑ Thirst centers and ADH Secretion
↑ Vasoconstriction of Afferent and Efferent Arterioles (only in High concentration)

62
Q

Actions of PTH:

A 
↓ Phosphate reabsorption
(proximal tubule)
↑ Ca2+ reabsorption (distal
tubule)
Stimulates 1α-hydroxylase for Calcitriol Production
(proximal tubule)
63
Q

What are the receptors for PTH, ANP, ADH and ATII?

A

PTH - Gs PTH receptor
ANP - Guanylate cyclase receptor
ADH - V1 is Gq (Blood side), Guanylate cyclase receptors and V2 is Gs (Lumen side).
ATII - AT1R is Gq

64
Q

Regulation of body fluid compartments - what is the main goal?

A

60-40-20 rule:
Keeping TBW on 60% and the ICF with 40% and ECF with 20% relative to the whole body volume - by maintaining the 290 mOsm/L concentration.

65
Q

Pathway of activation of Renin-Angiotensin-Aldosterone system:

A

Renin is the enzyme secreted by the Juxtaglomerular cells upon receiving Adenosine signal from Macula densa cells (low Na). It cleaves Angiotensinogen (from Liver) to Angiotensin-I which is converted by ACE in the lungs to Angiotensin-II (Which stimulates Aldosterone..).

66
Q

Osmoreceptor cells:

Where? How? What ?

A

Osmoreceptor cells:

  • Hypothalamus: Supraoptic Nuclei, Sampling Blood.
  • Blood Hyperosmolarity leads to their Shrinkage (while Hyposmolarity cause them to expand).
  • Activate Thirst centers and Signal to PVN to secrete ADH.
67
Q

Osmoreceptor cells: What happens when corrected the Hyperosmolarity with them?

A

Negative Feedback
Pressure stabilizes and Osmolarity rises - therefore less stimulation for Hypothalamus to produce ADH.
GI osmoreceptors (and less ATII) also give the same signal.

68
Q

Actions of ADH:

A 
↑ H2O permeability (late distal
tubule and collecting duct
principal cells)
↑UT1 for urea absorption in DCT
↑Vasoconstriction Gq V1 on Afferent Arterioles - Lower GFR
69
Q

What detects blood volume?

A

Low pressure Baroreceptors (Cardiopulmonary)
High Pressure Baroreceptors
Macula Densa cells of JG apparatus (Indirectly by NaCl concentration).

70
Q

What is the name of the state of the body fluids after high water Intake?

A

Hyposmotic Hypervolemia

71
Q

Hyposmotic Hypervolemia, What is the response to it?

A

Renal Response - GFR (High BP) and Water Secretion are Higher (PCT and DCT less reabsorption ).
Hypothalamic Response - Osmoreceptors Swell - Less ADH.

72
Q

What is the name of the state of the body fluids after high water Loss?

A

Hyperosmotic Hypovolemia

73
Q

Hyperosmotic Hypovolemia, What is the response to it?

A

Renal Response -GFR is Lower (Low BP) Water Absorption is Higher
Hypothalamic Response - Osmoreceptors Shrink- more ADH and Thirst center stimulation.

74
Q

Hyperosmotic Isovolemia: Cause and Response?

A

High salt Intake (salty popcorn)

Just as in Hyperosmotic hypovolemia

75
Q

Isosmotic Hypervolemia: Cause and Response?

A

High water uptake as a response to Hyperosmotic Isovolemia causing the correction of Osmolarity but volume to by too High (Drinking after salty popcorn).
Atria secrets ANP - ENaC Blocked - Na secretion.

76
Q

What are the basic Important muscular components of the Urinary Bladder? (or more generally Urine storage system)

A
  • Detrusor Muscle: Able to Empty the Urinary Bladder
  • Internal Urethral Sphincter : Gate of urinary bladder
  • External Urethral Sphincter Gate of urine out of body
77
Q

What is the state of each muscular component of the urinary system in the Filling of the urinary bladder? ANS contribution?

A

Sympathetic stimulation of Beta-2 receptors on Detrusor muscle cause it to relax and Alpha-1 receptors on Internal Sphincter cause contraction to prevent leakage.
External sphincter is voluntary and contracted .

78
Q

What is the state of each muscular component of the urinary system in the Emptying of the urinary bladder? ANS contribution?

A

Parasympathetic stimulation of M1/3/5 (Gq) on Detrusor muscle cause its contraction propelling urine outwards and stimulation of M2/4 (Gi) allow relaxing of Internal sphincter for passage. External Sphincter is voluntary and relaxed.

79
Q

How many times does the kidney filter the entire blood plasma in one day?
(Just for fun)

A

RPF is 600 ml/min or 180 L/Day .
Plasma Volume is 3.5L~
Therefore the Kidney filter almost 60 times the entire Plasma in one day!

80
Q

What is a buffer?

What is its importance to blood?

A

Mixture of Weak acid and its conjugate base (or the other way around) that resists pH change.
The blood plasma buffers keep its pH on 7.38-7.42 scale.

81
Q

Which are the blood buffers (plasma)?

A 
Bicarbonate Buffer
Protein Buffer (Albumin and Hemoglobin)
82
Q

Which are the buffers in the ICF?

A

Bicarbonate Buffer
Protein Buffer (Albumin and Hemoglobin)
Phosphate buffer

83
Q

Which are the buffers in the interstitium and CSF?

A

Bicarbonate Buffer mostly

84
Q

Which are the buffers in the Urinary tract?

A

Phosphate Buffer
Creatinine Buffer
Uric Acid Buffer
Ammonium Buffer

85
Q

What are the Volatile acids?

A

Acids that can turn into Gas products in the body this is mainly Carbonic Acid - which can reversibly turn to CO2
(Respiratory Product)

86
Q

What is the name of the enzyme catalyzing the formation of Carbonic Acid? What Ion is integrated into it for its activity?

A

Carbonic Anhydrase - Uses Zn Ion

Turns H2O + CO2 to H2CO3 which can dissociate freely to H+ and HCO3-

87
Q

Examples for Fixed acids?

A

Metabolic products:

Lactate, Ketone Bodies, Sulfuric Acid, Phosphoric Acids.

88
Q

How can we know if someone has Metabolic/Respiratory and Acidosis/Alkalosis based on their CO2, Bicarbonate and pH values?

A

ROME mnemonic: (pH signifies Acidosis/Alkalosis)
Respiratory - Opposite : pH ↑ and PCO2 ↓ (Alkalosis)
Respiratory - Opposite : pH ↓ and PaCO2 ↑ (Acidosis)
Metabolic - Equal : pH ↑ and HCO3 ↑ (Alkalosis)
Metabolic - Equal : pH ↓ and HCO3 ↓ (Acidosis)

89
Q

Where is Bicarbonate Reabsorbed in the Kidney?

Which transporters on each side?

A

Bicarbonate is Reabsorbed in Proximal Tubule.
On the Basal Surface Na/K ATPase, NaHCO3 cotransporter and Cl/HCO3 Exchanger.
On the Apical Surface Na/H exchanger for H secretion.

90
Q

Factors in upregulating Bicarbonate Reabsorption:

A

1) Acidosis - CO2↑ - Carbonic Anhydrase↑ - Bicarbonate↑.
2) Filtered Load - Almost all Bicarbonate Filtered is reabsorbed back.
3) Low ECF Volume - Causes ATII to activate H/Na Exchanger and cause more free Bicarbonate for absorption (“Contraction Alkalosis”)

91
Q

What is NAE? Must be equal to what? Why?

A

Net Acid Excreted, must be equal to Acid production.

This is crucial for stabilizing pH in the Body.

92
Q

How can we calculate NAE?

A

NAE = [Ammonium] + [Titratable Acids] - [Bicarbonate Excreted]

93
Q

Where is the Proton Secretion of the kidney happens mostly?

A 
Collecting Ducts (+Late DCT): α-intercalated cells
(In PCT it is reabsorbed back in the form of water)
94
Q

What is the Henderson hasselbalch equation?

A 
pH = pK + [A-]/[HA] 
pH = −log10 [H+] (pH units)
pK = −log10 equilibrium constant (pH units)
[A-] = concentration of base form of buffer (mM)
[HA] = concentration of acid form of buffer (mM)
95
Q

What incorporates the Secreted H+ in the lumen so that it won’t be able to get back in the Interstitium or tubular cells?

A

Hydrogen Phosphate (HPO4-2) and the Secreted Proton form in the lumen Dihydrogen Phosphate (H2PO4-1), which is a Titratable acid that is mostly excreted and not back to the tubular cells. (Phosphate Buffer).

96
Q

How does the Protons form in the α-intercalated cells? Where are the other products go?

A

Just as in the PCT cells with Carbonic Anhydrase forming Carbonic Acid which readily dissociates to Bicarbonate and a Proton. Here we also have a Bicarbonate/Chloride exchanger on the Basal side.

97
Q

What is the effect of the Amount of Urinary buffers on the Secretion of Protons in the α-intercalated cells?

A

Urinary Buffers↑ - H+ Secretion↑
The higher the amount of buffers the more it can counteract pH drop in the lumen, pH drop below 4.4 in the filtrate shuts down the H+ Pumps on the Apical surface.

98
Q

What is the effect Aldosterone on the Secretion of Protons in the α-intercalated cells?

A

Aldosterone Stimulates the formation of H+ Pumps on the Apical surface of the Intercalated cells (Also indirectly by promoting Bicarbonate reabsorption in the PCT)

99
Q

What is the effect of pK of Urinary Buffers on the Secretion of Protons in the α-intercalated cells?

A

pK↑ - H+ Secretion↑

Effectively preventing the pH drop to 4.4 and the H+ ATPases to stop. Phosphate Buffer has a strong pK of 6.8.

100
Q

What are the steps of Secretion of Protons incorporated into ammonium Ions?

A

1) Ammonia produced from Gln in PCT cells diffuses down to Tubular lumen and binds secreted H (Na/H ex.).
2) Some Ammonium is picked back for Countercurrent multiplication by NCCK of TAL.
3) Ammonia from the interstitium Ammonium (step2) diffuses to Lumen of Collecting ducts and binds protons secreted by α-intercalated cells

101
Q

What is the transporter on the Basolateral side that is responsible for the coupling of Plasma Potassium levels with Acidosis/Alkalosis?

A

H/K Exchanger (Secondary Active Transport)
In Acidosis - Potassium to Plasma↑ - Hyperkalemia.
In Alkalosis - Potassium to Plasma↓ - Hypokalemia.

102
Q

What is the effect of Urinary pH on Ammonium Excretion?

A

pH↓ - Ammonium formation↑

103
Q

What is the effect of Ammonia production on Ammonium Excretion? What is the mechanism?

A

Ammonia Produced↑ - Ammonium formation↑

Acidosis causes Glutamine breakdown to increase as an adaption which ultimately gives more Ammonium the urine.

104
Q

What is the adaption to Henderson-hasselbalch equation which is used for Acid-Base disorders?

A

pH = pK + [Bicarbonate]/ (α x Pco2)

α - the solubility coefficient for CO2 (~0.03)

105
Q

Metabolic Acidosis:

What are the parameters disturbed?

A

Metabolic Acidosis: (ROME mnemonic)

pH↓ + Bicarbonate↓

106
Q

Metabolic Acidosis:

What could be the causes?

A

Metabolic Acidosis: Causes

Renal failure, Lactic acidosis, Diarrhea, Diabetes

107
Q

Metabolic Acidosis:

What could be the compensation mechanisms?

A

Metabolic Acidosis: Compensations

Respiratory -Central Chemoreceptors will cause DRG and VRG to promote Hyperventilation (RR↑ and breath volume)

108
Q

Metabolic Alkalosis:

What are the parameters disturbed?

A

Metabolic Alkalosis: (ROME mnemonic)

pH↑ + Bicarbonate↑

109
Q

Metabolic Alkalosis:

What could be the causes?

A

Metabolic Alkalosis: Causes

Vomiting (Acid loss), Primary Hyperaldosteronism

110
Q

Metabolic Alkalosis:

What could be the compensation mechanisms?

A

Metabolic Alkalosis: Compensations

Respiratory -Central Chemoreceptors will cause DRG and VRG to promote Hypoventilation (RR↓ and breath volume↓)

111
Q

Respiratory Acidosis:

What are the parameters disturbed?

A

Respiratory Acidosis: (ROME mnemonic)

pH↓ + PCO2↑

112
Q

Respiratory Acidosis:

What could be the causes?

A

Respiratory Acidosis: Causes

Emphysema, CO2 reach air, Opioids

113
Q

Respiratory Acidosis:

What could be the compensation mechanisms?

A

Respiratory Acidosis: Compensations

Renal - Excretion of Protons in Ammonium or Dihydrogen Phosphate form (Slow)

114
Q

Respiratory Alkalosis:

What are the parameters disturbed?

A

Respiratory Alkalosis: (ROME mnemonic)

pH↑ + PCO2↓

115
Q

Respiratory Alkalosis:

What could be the causes?

A

Respiratory Alkalosis: Causes

Voluntary Hyperventilation, High Altitude, Aspirin

116
Q

Respiratory Alkalosis:

What could be the compensation mechanisms?

A

Respiratory Alkalosis: Compensations

Renal - Decreased Reabsorption of Bicarbonate in PCT.

117
Q

What is a Mixed Acidosis?

Give examples/Causes

A

Mixed Acidosis: PCO2↑+ Bicarbonate↓
When pH drops below 7.1.
Diabetes+COPD or Renal Failure+Drug Overdose

118
Q

What is the Anion Gap? Value? “Filled” by?

A

Blood being electroneutral while more Na is present than the opposing Cl and Bicarbonate.
It is Normally 8-16 mEq/L. It is “filled” by Proteins, Phosphates, Citrates and Sulfates.

119
Q

What does it mean if the Anion gap grows?

A

Metabolic Acidosis is presented in Growth of Anion gap.

Loss of Bicarbonate, Could be replaced by Cl (Hyperchloremic) or other anions. (Bicarbonate/Cl Exchanger on RBCs).

GBA Physiology (12 decks)

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