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Genitourinary > Acid Base > Flashcards

Acid Base Flashcards

1
Q

Primary buffer

A

Bicarb = extracellular

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2
Q

Secondary buffer

A

Intracellular

Hours

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3
Q

3rd step

A

*Lungs = minutes to hours

*Renal base-then-acid excretion
Hours to days
If too high a load, overwhelms kidney

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4
Q

Formula

A

H + HCO3- H2CO3 CO2 + H20

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5
Q

Mechanisms of acidosis

A
  • increased acid production/load
  • decreased acid excretion
  • loss of bicarb ions
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6
Q

Increased acid load

A

ORGANIC

  • lactic acid->lactic acidosis
  • Ketoacids (b-Hydr/ acetoacetate) = DM, ETOH, Starvation

INORGANIC
*HCL
*Ammonium cloride
RAPIDLY DEVELOPING ACIDOSIS

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7
Q

Decreased acid excretion

A
  • Acid = mostly from metabolism of sulfur-containing amino a
  • H secreted to lumen (NH3to NH4) (HPO to
  • Ammonium excretion UPs dramatically in respons to acid
  • renal failure
  • incre?
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8
Q

Renal failure

Decrease

A
  • up NH4
  • down HCO3
  • increase unmeasured anions
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9
Q

Type 1 distal renal tubular acidosis

A
  • gfr preserved, urine pH=>5.3
  • less H+ secreted in tubular to combine with NH4 -> less excretion = Impaired H-ATPase pump
  • less carbonic anhydrase
  • up luminal permeability to H+
  • DISTAL tubule = more severe
  • 1ary = congenital,
  • 2ndary = Meds, Sjorgen’s syndrome, RA, SLE
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10
Q

3rd mech acidosis

Loss of bicarb

A
  • Big tubule = Colon (diarrhea = rich in Bicarb + sodium. Na loss, Less HCO3, more Cl, unmeasured ions to not change)
  • small tubule = urethra (tube disfuction- proximal renal tubule acidosis type 2 renal tubular acidosis, Down Proximal Bicarb reabsorption, will have loss unless distal tubule makes up for it)
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11
Q

Clin manifestations

Metabolic acidosis

A

*UP ventilation
*DOWN myocardial contractility (less pH 7.2)
*Ventr arrythmia
*down vascular resistance
*GI = N/V , ab pain, DIarrhea (especially DM)
MSK
*muscle weakness, osteomalacia, hypercalcuria
CNS
*lethargy, coma
INFANTS
*impaired bone growth, listlessness

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12
Q

Serum Anion Gap

A

UA-UC = Na - Cl + bicarb

Anion gap = UA - UC =

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13
Q

Anion gap

A

=Na - (Cl + HCO3)

*correct AG = (4.4-ablumin) - 2.5

AG normal = 10-12
12+ abnormal AG acidosis

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14
Q

High anion gap metabolic acidosis

A

Citrate
*Uremia
Toulene
Ethanol

*DM/ETOH/Starve ketoacidosis
Iron
Methanol
Paraldehyde
*Lactate 
Ethelyne Glycol
Salicylate

*THESE ARE NOT INGESTED

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15
Q

AG acidosis

CKD

A

*Dietary =>sulfate ions (not reabsorbed is secreted)

STAGE 2-3 = normal AGmetabolic acidosis (defective secretion/reabsorption)

Stage 4-5 CKD = high AG M acidosi
*retention of H ions + sulfate ion, less nephron mass/GFR

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16
Q

AG acidosis

DM ketoacidosis

A

*Insulin deficiency = UP free fatty acid = acetone production

*Glucagon excess = altered hepatic metab
Free fatty acid to ketoacids

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17
Q

DKA

Renal consequences

A

*insulin deficiency
*more K coming out of cells
OSMOTIC DIURESIS
*Loss of hypotonic fluid
*Loss of ketoa acid ions

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18
Q

AG acidosis

Lactic acidosis

A
  • byproduct of pyruvate acidosis
  • if lactate up = pyruvate inbalance, or down lactate utilization
  • DX = lactate level, venous pH down *upCO2 cuz DOWN pulmonary blood flow (hypoperfusion)
  • Tx : underlying disorder
19
Q

DX Acid base

A 
1= acidemic/alkalemic?
2= primary disorder, respiratory/metabolic?
3=respiratory (acute/chronic?)
4=Metabolic (Anion gap?)
5= Mixed? Gap/nongap?
6= compensated? If not, why?
20
Q

Delta gap

A

Change in AG/Change in HCO3= 1 = change in bicarb CONSISTENT with change in AG

NO NON-ION GAP PROCESS

21
Q

Alkalosis

A

High extracelluar PH
Primary elvation of bicarb
Respiratory compensation

22
Q

Proton loss =

A

Increase in bicarb concentration

  • GI = n/v, adenoma, ..
  • renal = DIURETICS, …
23
Q

Loop diuretic

A

Up Na delivery to Principal cell, Tubular lumen more negative, H-+ pumped

24
Q

Contraction alkalosis

A

Lose fluid

*higher concentration bicarb = alkalosis

25
Q

Alkalosis

Add Bicarb

A

*Nabicarb
*milk-alkali syndrome
*hypercalcemia
*renal Bicarb reabsorption
*massive blood transfusion (citrate load)
CHECK HISTORY

26
Q

Bicarb reabsorption in nephron

A

Most PCT

Can malfunction in other places

*Na reabsorption = Bicarb reabsorption

27
Q

Alkalosis

Intracellular H movmenet

A

Hypokalemia = K moves out cell, H in

Refeeding syndrome = up increase, H + K movement into cells

28
Q

Maintanence of Met Alkalosis

A

*kidney can’t excrete HCO3

  • hypovolemia/chloremia/kalemia
  • mineralocorticoid excess
29
Q

Volume depletion

Alkalosis

A

Nephron main job = reabsorb Na (bicarb comes with)

  • ang 2 increases Na-H exchanger
  • low pH in PCT ups bicarb reabsoprtion

Free bicarb can’t bind with H to be excreted in cell to lumen, so goes into blood

30
Q

Volume depletion

Alkalosi

A

*2ndary hyperaldosteronism???

31
Q

Alkalosis

Cl- depletion

A
  • decrease Cl to macula densa = 2ndary hyperaldosteronism
  • UP Hatpase to mained electroneurtrality
  • DOWN Clbicarb exchange in intercalated cells, bicarb reabsoprted into blod

Giving chloride to volume depleted tx without tx volume

Cl

32
Q

Hypokalemia

Alkalosis

A
  • Up KHatpase = increase H secretion
  • UP KH transcellur exchagne = up H secretion
  • Up renal NH4 generation, Up Bicarb generation
33
Q

Alkalosis

A

*Down ventilation
*ventr arrythmia
*ortho HypoTN
*GI = N/V
*MSK = cramping, tetany
CNS = confusion, seizures

34
Q

Alkalosis

Cl responsive

A
  • w/ Extracellular fluid volume contraction (conserve Cl)
  • urine CL <20
  • Tx = NaCl (mabye K repletion)
35
Q

Alkalosis

Cl Resistant

A
  • w/ extracellular fluid volume expansion , HTN
  • depletion NaCL NOT RESPONSIBLE
  • urine cl high/normal >40
  • NaCl doesn’thelp
  • treat Dz
36
Q

Metabolic Acidosis - Normal AG

Causes

A 
H yperalimentation
A cetazolamide
R enal Tubular Acidosis
D iarrhea
U tereral diversion (neobladder)
P ancreatic fistula (bicarb loss)/ Post-hypocapnea
S pironolactone
37
Q

RTA type 2

A
  • PROXIMAL - less severe
  • HCO3 wasting
  • urine pH = variable
  • 1ary = congenitall
  • 2ary = CA inhibitor, autoimmune dz, meds
38
Q

RTA type 4

A
  • Urine pH <5.3
  • HYPER K
  • Aldosterone deficiency (congenital/meds), Tubular resistance to aldosterone (meds, tubulointerstitial dz)
39
Q

Metabolic Acidosis = High AG

Causes (ingestion + non-ingestion)

A 
C itrate
U remia
T oluene
E toh
R enal failure/Rhabodomyelosis
D iabetic ketoacidosis
I ron / Infxn / isoniazide
M ethanol
P araldehyde
L actate
E thylene glycol
S alicylate
40
Q

Metabolic Acidosis - High AG

Non-ingestion causes

A
  • Uremia
  • Ketoacidosis
  • Lactic Acidosis (sceptic)
41
Q

Metabolic Alkalosis often w/

A
  • Hypo Cl
  • Hypo K
  • hypovolemia
  • high aldosterone (?)
42
Q

Kidney H/HCO3 exchange

A
  • excrete H to bring in HCO3 = PCT

* UP in high pCO2, hypovolemia, hypokalemia

43
Q

Metabolic Acidosis = High AG

Mech

A
  • Acid in blood (H + anion) dissociates

* H to bicarb, then ion accumulates in serum

44
Q

Metabolic acidosis = Normal AG

A
  • lost Bicarb replaced by Cl-
  • AG normal, Cl serum high
  • diarrhea ,RTA II = loss of Na Bicarb (?)

Genitourinary (9 decks)

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