Potassium Acid-Base disorderreviews.berlinpharm.com/20190316/Potassium... · Hypokalemia Shift Loss...

Potassium Acid-Base disorder

Kanin Thammavaranucupt, M.D.Nephrology division, Maharat Nakhonratchasima Hospital

Potassiumtransport along

nephron

ENaC

ROMK Ald

Alkalosis

Hypokalemia

Shift Loss Poor intake(less likely)

Adrenergic surge

Nonadrenergicsurge

ShiftAdrenergic surge ?

Yes No

SepsisSympathetic

PheochromocytomaBeta-agonistTheophilline

Amphetamine, Caffeine, Cocaine

Thyrotoxicosis PP

Congenital[Hypokalemic PP, Andersen]

AlkalosisAnabolism

[Insulin/TPN/active leukemia]

HypothermiaDrugs: paracetamol,

chloroquine

Hypokalemia


DiarrheaSweat/Exercise

Cl--losing diarrheaLaxative abuse

Remote vomitingRemote diuretic

Spot urine K > 1524hr-urine K > 20

UK/UCr > 1.5FEK > 5TTKG > 2

Renal Non-renal

Adrenergic surge

Nonadrenergicsurge

GS/Thiazide

BS/Lasix

Alkalosis ?

Hypokalemia


Renal Urine K >20 ?

TTKG > 4 ?

Normal BP ?

Y

Y

Y

Urine Cl >20 ?

Y

diarrhea, sweating, laxative abuseremote vomiting/ diuretic

TTKG < 3: Polyuria

1°’/2° HyperaldosteronismCushing AME CAH Liddle Licorice

Acidosis : DKA, AKA, RTAVariable : Hippurate,Penicillin

Adrenergic surge

Nonadrenergic surge

Recent vomiting

UCa/UCr (mmol/mmol)(molar ratio)

< 0.15

> 0.20

N

N

N

N

NHypoMg

Y

35-year-old man with proximal muscle weakness for 6 hraccompanying palpitation and weight loss.

Na 138 mEq/L K 2.0 mEq/L

Cl 104 mEq/L CO2 24.0 mEq/L

Urine Na 30, K 6 mEq/L

Which of the following mechanism would explain this electrolyte abnormality?

A. Renal potassium loss

B. Non renal potassium loss

C. Intracellular shift

D. Low potassium intake

E. Abnormal sodium/potassium ATPase pump

Hypokalemic periodic paralysis

Thyrotoxicosis periodic paralysis

Grave’s dz or Subclinical

Increased UCa, HypoPO4/Mg

Prevent: Keep euthyroid state

✓ Propanolol 40-120 mg/day

✓ RAIU or Sx for prevent relapse

60% type ICa channel

20% Type 2Na channel

Others

Treatment KCl (1st line)Propanolol 1 mg IV q 10 min x 3

Treatment KClAcetazolamide

AD

Precipitated by high carbohydrate, vigorous exercise

MetabolicAlkalosis

GFR

ECF

UCl

UK

HCO3 gainMilk-alkali/Ca-alkali, CaCO3

Blood transfusion (Citrate)Ringer lactate (Lactate)Acetate solutionAnion exchange resinDialysis

Low

Low

< 20

High

> 20

Aldosteronism

MetabolicAlkalosis

GFR

ECF

UCl

UK

Low

< 20

High

> 20

Increase

Post hypercapniaContraction alkalosisRemote diureticCl-losing diarrheaVomiting/NG drainage

Urine Na > 20✓ Recent vomiting (UpH > 6.5)✓ Non-absorbable anion (UpH < 6.5)

Urine Na < 20✓ Remote vomiting (UpH < 5.5)

Villous adenomaCongen.chloridorrhea

MetabolicAlkalosis

GFR

ECF

UCl

UK

Low

< 20

High

> 20

< 20

BS/Furosemide (recent)GS/Thiazide (recent)

HypoMgTubulopathy (Alc, autoimmune)

MetabolicAlkalosis

GFR

ECF

UCl

UK

Low

< 20

High

> 20> 20

Chronic diarrhea, Laxative abuse, severe hypoK

MetabolicAlkalosis

GFR

ECF

UCl

UK

Low

< 20

High

> 20

Urine Na Urine K Urine Cl

Diarrhea/ Laxative abuse

Acetazolamide

Diuretic Recent

Remote

Bartter’s syndrome

Gitelman’s syndrome

Vomiting Recent

Remote

Non-absorbable anion

Posthypercapnic

Metabolic acidosis/alkalosis

A 16-year-old female presented with nausea, vomiting,

diarrhea.

Na 135, K 2.0, Cl 97, HCO3 28 mEq/L, pH 7.44, PCO2 48,

glucose 140 mg/dL. Urine: Na 50, K 50, Cl 40 mEq/L.

Urinalysis showed trace ketone.

Which ONE of the following is the most likely cause of

hypokalemia?

A. Vomiting

B. Diarrhea

C. Diuretic abuse

D.Diabetic ketoacidosis

E. Hypokalemic periodic paralysis

Urine Cl > 20Bartter syndromeGitelman syndromeDiuretic (recent)HypoK < 2 mEq/LHypoMgLaxative abuse


A 17-year-old man came to ED with fatigue and weakness. PE: mild ECF contraction. He had no hx of current diuretic use.

Na 138, K 2.9, Cl 92, HCO3 30 mEq/L, pH 7.48, PCO2 44

Urine: Na 25, K 60, Cl 85 mEq/L. Ca 50 mg/day (normal:

100-300)

What is the most likely cause?

A. Poor intake

B. Furosemide

C. Malabsorption syndrome

D.Gitelman’s syndrome

E. Bartter’s syndrome

A 30-year-old man come to ER due to weakness after wake

up. He had heavy alcohol drinking before sleep.

PE: BP 130/80 mmHg, HR 80/min, Neuro: proximal muscle

weakness gr II all extremities.

Na 140, K 2.0, Cl 110, CO2 30 mEq/L, Urine Na 45, K 35, Cl

40 mEq/L, UA: pH 6.0, protein- negative.

What’s the most likely diagnosis?

A. Hypomagnesemia

B. Laxative abuse

C. Recent vomiting

D. Post-hypercapnic state

E. Thyrotoxicosis periodic paralysis


An 18-year-old actress presents with fatigue for 2 weeks. Physical examination shows a BP of 120/80mmHg, grade III of proximal muscle weakness of all extremities. Others are unremarkable.

Na 138, K 2.2, Cl 90, CO2 30 mEq/L

Urine Na 25, K 20, Cl 3 mEq/L

The most likely diagnosis is?

A. Bartter’s syndrome

B. Gitelman’s syndrome

C. Surreptitious (self-induced) vomiting

D. Recent diuretic abuse

E. Hypokalemic periodic paralysis

Urine Cl < 20Contraction alkalosisCl-losing diarrheaPost hypercapniaRemote diureticVomitingNon-absorbable anion

A 16-year-old female presented with fatigue. BP

90/60 mmHg, PR 110 bpm, dry lip, JVP 0-1 cm.

Na 135, K 3.0, Cl 90, HCO3 34 mEq/L, pH 7.44, PCO2

48, glucose 90 mg/dL. Urine Na 30, K 35, Cl 10 mEq/L.

UA: pH 7, Sp gr 1.020, No WBC/RBC

Which one of the following is the most likely cause

of hypokalemia?

A. Laxative abuse

B. Active vomiting

C. Bartter’s syndrome

D.Gitelman’s syndrome

E. Non-absorbable anion

Urine Cl < 20Contraction alkalosisCl-losing diarrheaPost hypercapniaRemote diureticVomitingNon-absorbable anionUpH < 6.5

UpH > 6.5

A 60-year-old man presented with unconsciousness

for 1 hour. Physical examination revealed an alcohol

smell breath odor upon breathing.

Na 135, K 4.1, Cl 102, CO2 12 mEq/L, negative serum

ketone, glucose 394 mg/dL, BUN/Cr 23/4 mg/dL, and

measured plasma osmolality 344 mOsm/L.

What is the most likely diagnosis?

A. Salicylate poisoning

B. Alcoholic ketoacidosis

C. Methanol poisoning

D. Diabetic ketoacidosis

E. Ethanol overdose

AG = 21Wide-gap MA

1. pH: 7.42. pH, PCO2 opposite direction?

pH PCO2 → Primary respiratory acidosis3. Resp: 1 ,2 ,4, 5 & Acute-Acute-Chronic-Chronic & a/b/a/b

(absolute primary at respiratory cause: PaCO2 < 15 or > 55 mmHg)

4. Metabolici. Expected PaCO2

MA : PaCO2 = (1.5 x HCO3) + 8 ± 2(absolute: HCO3 < 15) = 15 + HCO3 (if pH 7.2-7.5)

MB : ∆ PaCO2 = 0.6 x ∆ HCO3

(absolute: HCO3 > 45) = 15 + HCO3

ii. AG: Corrected AG = AG + 2.5 x (4.5 - Alb) >>> Normal 10 ± 2iii. ∆AG/∆HCO3 (= AG-10/25-HCO3)

< 1 : Wide + Normal gap MA1-2 : Pure wide gap MA> 2 : Wide MA + MB

Step approach to acid-base disturbance

Wide GapMetabolic acidosis

Ketoacidosis L-lactate

Lactic acidosis Normal

Osmolargap

GFR < 20Advance renal

failure

<10 >10




Osmolargap


failure

<10 >10

DKA

AKA

SKA

• Hx of chronic ethanol abuse, decreased food intake, and often Hx of nausea and vomiting

• Glucose levels usually low but may be slightly elevated

Pathogenesis

✓ Alcohol withdrawal + Vol depletion + Starvation →↑ Catecholamines, Cortisol, Glucagon, GH →↑ Fatty acid oxidation → Ketosis

✓ Ethanol metabolism →↑NADH:NAD→ Ketosis, lactic acidosis

Alcoholic ketoacidosis

Comprehensive Clinical Nephrology, 5thEd. 2015

Treatment✓ Thiamine supplement (first!!!)

(If give after IV glucose → induce WKS)

✓ IV Glucose for ↑ Insulin → Inhibit ketosis

✓ Correct HypoPO4, HypoK, HypoMg(from tubular loss and cellular shift)

✓ No insulin requirement

Alcoholic ketoacidosis

Brenner & Rector’s The Kidney, 10th Ed




Osmolargap


failure

<10 >10B|B1, B2, B3

A |Hypoxia

B1 Liver diseaseMalig, B1 def

B2MFM, NRTI, Salicylate,

Alc, Cyanide

B3 Inborn errormetabolism




Osmolargap


failure

<10 >10

Osmolar gap

<10 >10

D-lactate

Toluene

Pyroglutamic acid

Salicylates

Methanol, Ethanol

Ethylene glycol

Isopropanol

Propylene glycol

Paraldehyde, Formaldehyde

Osmolar gap

>10Methanol

Formic acid

Ethylene glycolGlycolic, Oxalic, Lactic

Isopropanol Acetone

Propylene glycolL-,D-lactate


OG > 25, Blindness Rx: Fomepizole, EtOH, Folic acid

Antifreeze สีทาบ้าน Ca oxalate crystal

Rx: Fomepizole, EtOH, B1, B6

Rubbing alcohol, No metabolic acidosis BUT ketonuria

IV lorazepam/phenytoin/bactrim

Ethanol Acetic, Lactic, Ketosis

OG > 25 but not severe acidosis

Osmolar gap

<10 >10

D-lactate

Toluene

Pyroglutamic acid

Salicylates

Methanol, Ethanol

Ethylene glycol

Isopropanol

Propylene glycol


Osmolar gap

<10

D-lactate

Toluene

Pyroglutamic acid

Salicylates

40 year-old man complained of sudden abdominal pain. CT: Bowel gangrene at jejunum. Small bowel resection with jejunocolonic anastomosis was done (residual small bowel 70 cm) for 2 months ago. He comes to ER with dyspneaNa 132, K 3.8, Cl 90, HCO3 12 mmol/L, serum L-lactate 1.5 mmol/L, BUN/Cr 25/0.9 mg/dL, serum ketone negativeWhat’s your definite treatment?A. HemodialysisB. Sodium bicarbonateC. NeomycinD. Saline solutionE. Search for other toxic agents

AG = 30ΔG/ΔHCO3 = 1.7

D-lactate is not metabolized by L-LDH

Cause

1. By product of metabolism of bacteria (Lactobacillus) which overgrow in GI tract ➢ Jejunoileal bypass

➢ Short bowel syndrome

➢ Small bowel obstruction

2. Propylene glycol metabolite

3. DKA

D-lactic acidosis

Clinical✓ Episodic metabolic acidosis (typically after high carbohydrate

meals) with neurological S&S (confusion, slurred speech, ataxia, loss of memory)

LAB✓ Serum D-lactate level > 3 mmol/L

✓ Both high or normal gap MA

✓ Normal osmolal gap

Treatment✓ ATB (Metronidazole, Neomycin, Vancomycin)

✓ Low carbohydrate diet

✓ Sodium bicarbonate

D-lactic acidosis

Brenner & Rector’s The Kidney, 9th Ed 2012Halperin ML. Kidney Int 1996;49:1

From amine and other compound of bacterial product (Not D-Lactic)

Source: Aspirin, Oil of wintergreen (Methyl salicylate)

Salicylates

Treatment✓NG lavage for onset < 1 hour

✓Multiple – dose activated

charcoal for onset 1-2 hr

✓IV glucose (due to ↓ cerebral

glucose conc)

✓Alkalinize urine (urine pH 7.5-8.0)

• Less accumulation in CNS and

increase urinary excretion

Pyroglutamic acidosis

Congenital (glutathione synthetase def)

Acquired: glutathione reduced by oxidative stress (critical illness) and overdose acetaminophen

Risk factor in therapeutic dose user • woman, vigabatrin, glycine def

(sepsis, malig, preg, DMII, malnutrition, liver/renal disease), Heterozygote of glutathione synthetase(1/10,000)

Comprehensive Clinical Nephrology, 5thEd. 2015

LAB: Urine 5-Oxoproline level

Treatment: NAC → Increase glutathione

Osmolar gap

<10

D-lactate

Toluene

Pyroglutamic acid

Salicylates

Short bowel with bact overgrowth, DKA, Propylene glycol

Glue sniffing Hippuric acidEarly: wide gap, Late: NAGMA

Low glutathione level + paracetamol

Resp alkalosis with ketosis with lactic acidosis

Rx: MDAC, glucose, alkalinized urine

Toxin & High anion gap acidosis

AG OG Ingestion Manifestation

↑ normal Acetaminophen Hepatitis

↑ normal Salicylates (Lactate, Ketone) Fever, tinnitus, Met acid + respiratory alkalosis

↑ ↑ Ethanol (Acetic acid) Alcoholic fetor, hepatitis, ∆MS, met alkalosis from vomiting

↑ ↑ Methanol (Formic acid) ∆MS, blurred vision

↑ ↑ Ethylene glycol (Glycolic

acid, Oxalic acid, Lactate)

∆MS, hypoCa, Ca oxalate, renal failure, cardiopulmonary failure

↑ ↑ Propylene glycol (Lactate) High OG, unexplained lactic acidosis, D-lactic acidosis, AKI

normal ↑ Isopropyl alcohol (Acetone) ∆MS, fruity breath, ketonuria

High OG alone but No MA

L Li

A ASA (Salicylate)

V Valproate

A Alcohol (Methanol, EtOH, Ethylene glycol, Isopropanol)

T Theophylline

Hemodialysis

A 60-year-old man presented with unconsciousness for

1 hour. Physical examination revealed an alcohol smell

breath odor with blurred vision.

Na 135, K 4.1, Cl 102, CO2 12 mEq/L, negative serum

ketone, glucose 394 mg/dL, BUN/Cr 23/4 mg/dL, and

measured plasma osmolality 344 mOsm/L.


A. Salicylate poisoning

B. Alcoholic ketoacidosis

C. Methanol poisoning

D. Diabetic ketoacidosis

E. Ethanol overdose

AG = 21Cal Posm = 300Serum OG = 44

A 19-year-old man come to ER due to alteration of consciousness. He was asymptomatic 8 hours ago. PE: BP 90/60 mmHg, PR 110 bpm, RR 32 tpm. Heart/lungs: WNL. No neurological deficit.

Na 142, K 3.6, Cl 108, CO2 14 mEq/L, BUN/Cr 14/1.5 mg/dL, BS 114, serum osm 290 mOsm/kg ABG: pH 7.42, PCO2 20 mmHg.

What is the most likely cause of this acid-base disorder?A. Alcoholic ketoacidosis

B. Ethylene glycol toxicity

C. Methanol toxicity

D. Salicylate toxicity

E. Pyroglutamic acidosisAG = 20

ΔG/ΔHCO3 = 1OG = 5

Expected HCO3 = 20 ± 2

A 43-year-old hospital janitor with a history of

chronic alcohol consumption was brought to ER

because of having a stuporous consciousness.

Na 140, K 4.0, Cl 106, HCO3 24 mEq/L, Cr 1 mg/dL,

serum osmolal gap = 22, and urine acetone 4+

Which one of the followings is the most likely cause

of his illness?

A. Alcohol ketoacidosis

B. Starvation ketoacidosis

C. Ethylene glycol intoxication

D. Isopropyl alcohol intoxication

E. D-lactic acidosis

No MAUrine ketone

Fruity smell (acetone)

No incresed AGHigh OG

A 35-year-old man with severe abdominal pain for 6 hr. He

took paracetamol 4 g/day for relieve pain. He got 10-cm

small bowel resection with pathology of no ischemic bowel.

After surgery: Na 135, K 4.7, Cl 95, HCO3 15 mEq/L

ABG: pH 7.32, PCO2 28, PO2 86 mmHg

serum osmolal gap = 10, serum lactate 2.2 mmol/L

What is the most likely cause of acidosis in this patient?A. D-lactic acidosis

B. Salicylate poisoning

C. Pyroglutamic acid

D. Glue sniffing

E. Sepsis Expected PaCO2

= 30 ± 2

AG = 25ΔG/ΔHCO3 = 1.5

OG = 10

Compensated resp alkalosis

A patient with a history of Sjogren’s syndrome. Na 139, K 3, Cl 114, HCO3 15 mEq/L. Urine Na 15, K 10, Cl 12 mEq/LWhat is the most likely diagnosis?A. Type I renal tubular acidosis (RTA)B. Type II RTAC. Type III RTAD. Type IV RTAE. Chronic diarrhea

AG = 10Normal gap MA

Normal gapMetabolic acidosis

U pH

Test for renal acid secretion

UAG or UNC

UOG

U NH4

Non-renal HCO3

loss

DiarrheaUreteral diversionsBiliary or pancreatic fistulasDrugs: CaCl2, MgSO4

Cholestyramine

Acid load

HClNH4ClTPN

Dilutional acidosisSaline infusion

Pitfall of urine net charge (false positive)1. Non-HCl (Ketosis, Salicylate, D-lactate, Hippurate) 2. Unusual salt of antibiotic

Urine net charge (UNC) = Urine anion gap = Urine Na + K – Cl

Acidosis: ไตขับกรดได้ (NH4Cl) → UNC -veไตขับกรดไม่ได้ (NH4Cl)→ UNC +ve

Urine osmolal gap = measured – calculated osmolarityไตขับกรดได้ → Urine osmolal gap > 100

2(UNa + UK) + Uglu/18 + UUrea/2.8

Normal gapMetabolic acidosis

U pH > 5.5

Defect of renal acid secretion

UAG +

UOG < 100

U NH4 < 50 mmol/L

Non-renal HCO3

loss

DiarrheaUreteral diversionsBiliary or pancreatic fistulasDrugs: CaCl2, MgSO4

Cholestyramine

Acid load

HyperalimentationHClNH4Cl

YES NO

Dilutional acidosisSaline infusion

Yes No

Bicarbonate loading test

pRTA

7.5% NaHCO3 2-3 mmol/kg IV rate 1-2 mEq/kg/hr

until plasma HCO3 > 20 mEq/L

FE-HCO3 > 15%

Serum K

Low K High K

U pH< 5.5

U pH> 5.5

RTA4

Voltage dependent dRTA

Bicarbonanteloading test


Acid loading test

Low K

Bicarbonate loading test8.4% NaHCO3 ( 1mmol/L ) 2 ml/kg IV stat then 2 ml/min

OrNaHCO3 PO ➔ plasma HCO3

- > 30 meq/L

Until U pH > 7.8 x3 times (30-60 mins)

Urine pH < 5.5 Urine pH > 5.5

U PCO2 < 50 mmHgU-B PCO2 < 20 mmHg

U PCO2 > 70 mmHgU-B PCO2 >20 mmHg

U PCO2 < 50 mmHgU-B PCO2 < 20 mmHg

U PCO2 > 70 mmHgU-B PCO2 > 20 mmHg

Rate dependent RTA

NH3 defect Classical dRTA(H-ATPase, H/K ATPase)

Back leak dRTA(Ampho B)

Yes No

Bicarbonate loading test

pRTA

7.5% NaHCO3 2-3 mmol/kg IV rate 1-2 mEq/kg/hr

until plasma HCO3 > 20 mEq/L

FE-HCO3 > 15%

Serum K

Low K High K

U pH< 5.5

U pH> 5.5

RTA 4

Voltage dependent dRTA



Acid loading test

RTA 4

Renin AGN, BB, COXi/CNI, DM, PHA II (Gordon’s syndrome), TID (A-B-C-D-P-T)

High K, Urine pH < 5.5

Ang I ACE-I

Ang II ARB

Adrenal gland

Heparin, Ketoconazole, Etomidate, 1°adrenal insuff, 21-OH def.

MR

ACE

Ald

Voltage-dependent dRTA

Pseudohypoaldosteronism (PHA) type I, II

A Amiloride, Triamterene, Pentamidine

TID

High K, Urine pH > 5.5

B Bactrim (Trimethoprim)

C CNI (CycloA, Tacrolimus)

D alDactone

E Eplerenone, Drospirenone (Yasmin)

UTO

KT

from Angiotensinogen (liver)

JGA

Voltage dRTA

Palmer BF. Am J Kidney Dis 2010;56(2):387-93

PHA type I PHA type II

Clinical Renal salt wasting, HypoNa, HyperK, MA

Salt-sensitive HT, HyperK, MA

Mechanism Decrease Na reabsorb in CCD Impaired removal of NCC in DCT, ENaC, ROMK,

TRPV5

PAC, PRA level

High PAC, High PRA Low PAC, Low PRA

Urine Ca Normal Increased Urine CaOsteoporosis

Treatment Salt supplement,Fludrocortisone?

Thiazide

Mirrorimage

Liddle’s syndrome Gitelman’s syndrome

A 28-year-old woman presented with weight loss for 4

kg and episodic fatigue with fainting during the past 1

month. PE: BP 100/70 mmHg, P 84/min, JVP 0-1 cm.

Na 120, K 5.7, Cl 100, HCO3 15 mEq/L

ABG: pH 7.33, PCO2 30 mmHg

Urine Na 60, K 15, Cl 50 mEq/L.


A. Hyperkalemic distal RTA

B. Liddle’s syndrome

C. Adrenal insufficiency

D. Diabetic nephropathy

E. Pseudohypoaldosteronism type 2 (Gordon’s syndrome)

A 38-year-old woman come to OPD due to headache 2

months. He received Lisinopril for 1 month ago. Her

brother and father were dead from intracerebral

hemorrhage. She took oral contraception for 10 years.

V/S: BP 152/98 mmHg, BT 37c, PR 90 bpm.

Na 132 K 5.7 Cl 108, HCO3 18 mEq/L

What is the most likely diagnosis?A. Liddle’s syndrome

B. Pseudohypoaldosterone type II

C. Mineralocorticoid defect from oral contraceptive pill

D. Angiotensin I defect from ACEI

E. Glucocorticoid-remediable aldosteronism

GRA AME CAH Liddle Gordon

Mode of inheritance

AD AR AR AD AD

Genetic cause CYP11B1 gene fused with CYP11B2 gene on chr 8q

Inactivatingmutation in HSD11B2 gene

Type IV: CYP11B1 geneType V: CYP17A1gene

Mutation in SCNN1B/SCNN1G gene on chr 16p

WNK1 and 4 mutation (2 different loci on chr 12, 17)

Elyteabnormality

HypoKMK

HypoKMK

HypoKMK

HypoKMK

HyperKMA

Onset HT Early Early in severe Early Early Late

PAC/PRA High PACLow PRA

Low PACLow PRA

Low PACLow PRA

Low PACLow PRA

Vary PACLow PRA

Mechansimof HT

Increasedabsorb Na, water

Stimulate MC receptor by Cortisol

Excess cortisol precursors act MC receptor

Increasedabsorb Na, water (ENaC)

Increased NCC in distal tubule

Other features

Cerebral hemorCeltic ancestry

Same as Licorice

Type IV: ambiguous in girl, precocious in boy, 1° amenorrhea

Hypercalciuria

Treatment Steroid,amiloride, triamterene

Spironolactone, eplerenone, amiloride

Steroid, spironolactone,eplerenone

Low Na diet, amiloride,triamterene

Low dose HCTZ

Familial HT

A 38-year-old woman come to OPD due to headache 2

months. He received Lisinopril for 1 month ago. Her

brother and father were dead from intracerebral

hemorrhage. She took oral contraception for 10 years.

V/S: BP 152/98 mmHg, BT 37c, PR 90 bpm.

Na 132 K 5.7 Cl 108, HCO3 18 mEq/L

What is the most likely diagnosis?A. Liddle’s syndrome

B. Pseudohypoaldosterone type II

C. Mineralocorticoid defect from oral contraceptive pill

D. Angiotensin I defect from ACEI

E. Glucocorticoid-remediable aldosteronism

AD HypoK with MK

low PAC, low PRA

AD HypoK with MK

low PAC, high PRA

Etiology of distal RTA

✓ Familial: AD, AR✓ Endemic: NE in Thailand✓ Ehlers-Danlos syndrome✓Hereditary elliptocytosis✓ Sickle cell anemia✓Medullary cystic disease✓Marfan’s syndrome

Inherited

✓Autoimmune disease✓ Sjogren, SLE, Thyroiditis✓ Cryoglobulinemia✓ PAN, PBC

✓Hypercalciuria with nephrocalcinosis✓ 1oHyperPTH, Vit D intox✓ Medullary sponge kidney ✓ Fabry’s disease, Wilson

✓Drug & toxins: Ampho B, Toluene, Ifosfamide, Hg, Li, analgesic, foscarnet

✓ TID: UTO, KT

Acquired

Etiology of proximal RTA

ถา้ Ifosfamideมนั MM, Medullary cystic diseaseจะ Wilson, Sjogren’s syndromeพา 2o HPTH with chronic hypocalcemiaครอบครวั Familialสา Cystinosisวติ Vitamine D deficiencyตรี KTออก Outdated tetracyclineไป Paroxysmal nocturnal hematuria (PNH)ท า Tenofovir/Topiramate/Toluene/TKIอะ Amyloidosis/Acetazolamide/Aminoglycosideไร Lead/Mercury poisoning

CA inhibitor (No Fanconi syn)- Acetazolamide- Topiramate

RTA 1 (distal) RTA 2 (proximal) RTA 4

HypoK

Urine AG +Urine osmolal gap < 100

Renal stone (CaP)Nephrocalcinosis

- K-citrate- NaHCO3 1-2 mEq/kg/day

HypoK HyperK

Urine AG +/-Urine osmolal gap > 100

Urine AG +Urine osmolalgap < 100

Fanconi syndrome- glucosuria, hypouricemia, hypophosphatemia

- K-citrate- NaHCO3 5-15 mEq/kg/day

- Prednisolone- Fludrocortisone

U-H-U-G-A-P

A patient with a history of Sjogren’s syndrome. Na 139, K3, Cl 114, HCO3 15 mEq/L. Urine Na 15, K 10, Cl 12 mEq/LWhat is the most likely diagnosis?A. Type I renal tubular acidosis (RTA)B. Type II RTAC. Type III RTAD. Type IV RTAE. Chronic diarrhea

AG = 10UAG = 13

Patient with the following laboratory test results

Na 128, K 1.2, Cl 110, HCO3 10 mEq/L

ABG: pH 7.28, pCO2 25 mmHg

Urine: pH 6.2, Na 74, K 20, Cl 81 mEq/L

Which condition is the most likely cause of the acid-base abnormalities?

A. Laxative abuse

B. Salicylate poisoning

C. Vomiting

D. Glue sniffer

E. Antifreeze ingestion

AG = 8UAG = + 13

Thank you for your attentionQuestions are always welcome…

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