Renal Control of Acid-Base Balance Flashcards
(43 cards)
1
Q
- Volatile reactions that occur in the body
A
- Aerobic glucose metabolism
- Fat metabolism
- Aerobic glucose metabolism
2
Q
- Fixed reactions that occur in the body
A
- Cysteine metabolism
- Phosphoprotein metabolism
3
Q
- An increase in 0.3 pH _ H+ concentration
A
- Halves (pH and concentration of H+ are inversely related)
4
Q
- Arterial blood H+ concentration
- Arterial blood H+
A
- 4.0 x 10-5
- 7.40
5
Q
- Venous blood H+ concentration
- Venous blood pH
A
- 4.5 x 10-5
- 7.35
6
Q
- Interstitial fluid H+ concentration
- Interstitial fluid pH
A
- 4.5 x 10-5
- 7.35
7
Q
- Intracellular fluid H+ Concentration
- Intracellular pH
A
- 1 x 10-3 to 4 x 10-5
- 6.0-7.4
8
Q
- Urine H+ Concentration
- Urine pH
A
- 3 x 10-2 to 1 x 10-5
- 4.5-8.0
9
Q
- What are the buffer systems of the body?
A
- Bicarbonate
- Hemoglobin
- Phosphate
- Plasma Proteins
10
Q
- What is the pK of the bicarbonate buffer system?
- What does this represent?
A
- 6.1
- Half of the solution is H+ and half is H2CO3
11
Q
- What organs play a role in the buffer system?
A
- Lungs
- Kidney
- Bone
12
Q
- H+ ions can be buffered by
A
- Plasma proteins
- Hemoglobin
13
Q
- If acidemia occurs, ICF does what to H+?
A
- Takes in H+
- Cell will take in H+ and kick K+ out of the cell
14
Q
- If alkalemia occurs, ICF does what to H+?
A
- ICF donates H+
- H+ raised in ECF
- Lower ECF K+ by bringing it into cells
15
Q
- How does an increase in alveolar ventilation change pH?
A
- An increase in alveolar ventilation increases pH
16
Q
- Of the bicarbonate filtered by the kidney, _ % is reabsorbed
- Where does reabsorption of HCO3- occur?
A
99.9%
- Reabsorption occurs in
- PCT (85%)
- Thick Ascending Limb of LOH (10%)
- Collecting Duct (>4.9%)
17
Q
- How is bicarb reabsorbed in the proximal tubule?
A
- Na+/H+ exchanger on the APICAL membrane pumps H+ into tubular fluid
- H+ will combine with the HCO3- that has been filtered into the glomerulus
- Via Carbonic acid, H2CO3 will be converted to H2O and CO2
- H2O and CO2 will diffuse into the cell
- Will combine AGAIN via carbonic anhydrase INTRACELLULARLY
- H+ will be recycled back into tubular fluid
- HCO3- will be reabsorbed via:
- Na+/3HCO3- cotransporter on basolateral membrane
- HCO3-/Cl- antiporter on basolateral membrane
18
Q
- How does phosphate buffering of secreted H+ ions work?
- What does this buffer system help regenerate?
A
- NaHPO4- in the tubular lumen combines with H+ that is secreted into the tubular lumen via that Na+/H+ exchanger on the basolateral membrane
- This buffers the H+ ion and then NaH2PO4 is eliminated in the urine
- Buffering of secreted H+ regenerates that plasma HCO3- that has been consumed elsewhere when the NaH2PO4 lost an H+ to a less acidid body compartment and now carries the H+ into the urine
19
Q
- What is the most abundant AA in the bloodstream?
A
- Glutamine
20
Q
- Production, Transport, and Excretion of Ammonia by the Nephron for Generation of New Bicarbonate
A
- Ammonium is transported by the NKCC in the TAL of the LOH on the APICAL membrane
- It replaces K+ and diffuses into the cell where it is “ion trapped”
21
Q
- Alpha intercalated cells are present in the _
- They are responsible for the _ of H+ and _ of HCO3-
A
- Collecting Ducts
- SECRETION
- REABSORPTION
22
Q
- Beta intercalated cells are present in the _
- They are responsible for the _ of H+ and the _ of HCO3-
A
- Collecting duct
- Reabsorb H+
- Secrete HCO3-
23
Q
- “New bicarbonate” is generated during the process of _ when secreted H+ is buffered by NH3, NH4+, phosphate, etc for excretion
A
- Urinary acidification
24
Q
- _ must equal nonvolatile adid production to maintain acid-base balance
A
- NAE (Net Acid Excretion)
25
\_ synthesis and secretion is responsible for ~2/3 of NAE
* Ammonium (NH4+)
26
* How do you calculate NAE?
*
27
* What is an Acid-Base Nomogram
* Superimposed on Davenport DIagram Depicting HCO3, pH and PCO2
28
* How do you calculate ANION GAP?
* What is a normal range?
* ANION GAP=[Na+]-[Cl-]-[HCO3-]
* Can be anywhere from 3-11 or 8-16 (use lab values provided on exam)
29
* **Causes of metabolic acidosis (high anion gap)**
* **MUDPILERS**
* **M=Methanol**
* **U=Uremia**
* **D=DKA/Alcoholic KA**
* **P=Paraldehyde**
* **I=Isoniazid (**tb tx)
* **L=Lactic Acidosis**
* **E=EtOH/Ethylene Glycol**
* **R=Rhabdo/Renal Failure**
* **S=Salicylates**
30
* **Causes of non-anion gap metabolic acidosis**
* **HARDUPS**
* **H=Hypealimentation**
* **A=Acetazolamide**
* **R=Renal Tubular Acidosis**
* **D=Diarrhea**
* **U=Uretero-Pelvic Shunt**
* **P=Post-Hypocapnia**
* **S=Spironolactone**
31
* Renal tubular acidosis
* Accumulation of acid in the body d/t a failure of the kidneys to properly acidify the urine
32
* Type I RTA
* Distal tubules
* Acidosis
* Hypokalemia
* **Failure of alphaH+ secretion by the intercalated cells**
33
* Type 2 RTA
* **Occurs in the proximal tubule as a failure of the HCO3- channel on the basolateral surface to function, impairing HCO3- reabsorption**
* **Now there is no bicarb buffer**
* **Acidosis**
* **Hypokalemia**
34
* Type 4 RTA
* **Adrenal gland is not synthesizing aldosterone**
* **HIGH K+**
* **Decreases NH3 synthesis by the PT**
35
* Sx associated with Metabolic Acidosis
* Mild-asymptomatic
* With pH \<7.10:
* Nausea
* Vomiting
* Malaise
* **See long breaths at a normal rate with respiratory compensation**
36
* **Causes of metabolic alkalosis**
* **CLEVER PD**
* **C-Volume Contraction**
* **L-Licorice**
* **E-Endo (Conn, Cushing, [Bartter])**
* **V-Vomiting**
* **E-Excess Alkali**
* **R-Refeeding Alkalosis**
* **P-Post-hypercapnia**
* **D-Diuretics**
37
* Physiologic/Biochemical Causes of Metabolic Alkalosis
* Loss of H+
* EX: Vomiting, Hyperaldosteronism
* Gain of HCO3-
* EX: Ingestion of NaHCO3, Milk-alkali syndrome
* Volume contraction alkalosis
* EX: Loop or thiazide diuretics
38
* Metabolic alkalosis symptoms
* Mild-shows signs and symptoms of underlying cause
* **More severe-increased binding of Ca2+ and hypocalcemia**
* **Headache, Lethargy, Neuromuscular excitability, Delirium, Tetany, Seizures**
* **Lower threshold for angina sx, arrythmias**
* **Possible weakness if hypokalemia is also present**
39
* **Causes of respiratory acidosis**
* **CANS**
* **C-CNS depression**
* **A-Airway Obstruction**
* **N=Neuromuscular Disorders**
* **S=Severe pneumonia,embolism, edema**
## Footnote
**Chronic**
**COPD**
**Any disease leading to imparied ventilation**
40
* Respiratory acidosis sx?
* Acute
* Headache
* Confusion
* Anxiety
* Drowsiness
* Stupor
* Tremors
* Convulsions
* Possible Coma (CO2 Narcosis)
* Slowly Developing, Stable
* May be well tolerated
* Memory loss
* Sleep disturbances
* Excessive daytime sleepiness
* Personality changes
* Gait disturbance
* Tremor
* Blunted DTRs
* Myoclonic Jerks
* Asterixis (Flapping Wrist)
* Papilledema
41
* **Causes of respiratory alkalosis**
* **CHAMPS**
* **C=CNS Disease**
* **H=Hypoxia**
* **A=Anxiety**
* **M=Mechanical Ventilators**
* **P=Progesterone**
* **S=Salicylates, Sepsis**
42
* Respiratory alkalosis sx?
* Acute
* Light headedness
* Syncope
* Confusion
* Peripheral and circumoral paresthesias
* Cramps
* **All of these are thought to be d/t changes in cerebral blood flow and pH**
* **Tachypnea or hyperpnea is often the only sign**
* **Severe-carpopedal spasm d/t decreased levels of Ca2+ (since it is driven inside of the cell in exchange for H+ coming out of the cell and bringing the blood pH back towards normal)**
* Chronic-asymptomatic
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