1. Potassium Disorders
Alon Antebi MD
The Institution for Nephrology &
Hypertension
Carmel Medical Center
2. Distribution of potassium between
the cells and ECF
►The total body K+ stores: 3000-4000 meq
►98% ICF
►ICF: 140meqL
►ECF: 4-5meqL
►Kept by NaK ATPase
3. FUNCTIONS OF POTASSIUM
►participatingin the regulation of such
processes as protein and glycogen synthesis
►determinant of the resting membrane
potential (Em) across the cell membrane
5. ►Thus, both hypokalemia and hyperkalemia
can result in potentially fatal muscle
paralysis and cardiac arrhythmias
►the movement of as little as 1.5 to 2 percent
of the cell K+ into the ECF can result in a
potentially fatal increase in the plasma K+
concentration to as high as 8 meq/L or more
15. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+
16. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
17. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
18. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
19. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
► !!!!!!!
20. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
► !!!!!!!
► ????
21. Sodium-potassium-ATPase
►The activity of this pump is regulated by:
Catecholamines
Insulin
the state of K+ balance
thyroid hormone
PH
22.
23. Catecholamines
► alpha-receptors impairing and ß2-
receptors promoting the cellular entry of K
+
► ß-adrenergic blocker can aggravate
hyperkalemia
► stress response –
release of epinephrine
rise in insulin release
32. Rate of cell breakdown and
production
►Breakdown:
Severe trauma
Tumor lysis syndrome
Rhabdomyolysis
►Production:
Treated megaloblastic anemia with B12 or F.A.
34. ►Kidney handles about 90-95% of K+ daily
load
►normal range is 40 to 120 meq/day
►tubular cell in the distal nephron:
Principal cells
Intercalated cells
35. ►Almost all of the filtered K+ is reabsorbed in
the proximal tubule and the loop of Henle
►less than 10% of the filtered load is
delivered to the early distal tubule
67. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
68. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
►Monitor ECG
69. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
►Monitor ECG
►Shift Potassium
I.V. Insulin 10U + 50ml D50W [works in 15 minutes]
follow by I.V. D5W 100ml/h
Inh. 20mg Albuterol over 10 minutes [works in 30 minutes]
I.V. 0.5 mg Albuterol
70.
71.
72. ►Diuretics
type
renal function?
►Kaexalate (Na Polystyrene)
30 to 50 gram
each gram removes 1meq K+
retention enema (give with 50 ml sorbitol)
73. ►Diuretics
type
renal function?
►Kaexalate (Na Polystyrene)
30 to 50 gram
each gram removes 1meq K+
retention enema (give with 50 ml sorbitol)
►Dialysis
74. EXERCISE 1
►47 Years old woman is hospitelised because
of Acute Cholecystitis
►She is getting Abx & IV Saline 0.9%, Gastric
Tube
►You are called on the third day of treatment
because of:
►Na=139 K=2.8 Cl=85 (95-105)
►PH=7.59, PCO2=57 PO2=92, HCO3=46
75. EXERCISE 2
►19 Years old soldier arrives in the ER
because of weakness
►She weights 40Kg, BP= 110/70
►K=2
►Na=140
►Cr=0.9
►Glu= 90
►Ca=8.9
80. ►What is the DD?
►Does she take Laxatives?
►How can you convince the psychiatrist to
examine her?
Editor's Notes
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ascending loop of henle\n
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\nCD:\nprinciple cell \n\nsecrete k\n\n2 things control aldosterone in blood\n1) RAAS axis\n2) K levels\n- high aldosterone when: high levels of K/ low levels of blood flow\n\n\nactivate na/k atpase channel\nenac in luminal membrane- so na absorbed and k secreted\n- may control secretion of k in principle cell in cases of hyperkalemia\n\n\n\n
CD:\n\nintercalated cell\n-type a) secrete h cations and absorb K\n- secrete protons and reabsorb bicarb\n-type b)\n\nprinciple secrete k, intercalated reabsorb k--- can control k levles in CD\n1) aldosterone levels affect it\n2) k level itself: if k is hgher than in the lumen- then will cause excretion of k into the lumen\n\nmin ways: aldosterone\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
skip\n
eat a lot of k\n\naldosterone\nurine k increase\nbut after 20 days, aldost level goes down, and if contnue eating the k- you dont get hyperkalemia- k level elevated slightly and will still be in normal levels\n- how does this happen? high level of aldost in beginning but then normalizes, and still dont get hyperkalemia\n- bc after 20 days- in luminal membrane have a lot of enac, -upregulation- secrete a lot of k even though aldost is low again-- dont elevate bp anymore, --can control the k level\n\n-can control k level unrelated to blood level- otherwise, anytime eat uch k, will be hypervolemic and high bp due to aldost\n- so initially high aldost, but then level out\n
can cause hyperkalemia with these drugs\n- butdoesnt happen usually- why?\nbc although have low aldost activity- the bp high in beginning- high distal delivery- so dont cause hyperkalemia\n- when you do cause hyperkalemia- in case of low effective blood volume in addition to these drugs- acture kidney injury, dehydration\n---when low bp, or kidney injury or combo of diff drugs-- then can get hyperkalemic state\n
block na/k/cl: barter syndrome\n- hypokalemic (lose k in distal bc of block of the transporter)\n- like furosemide\n\ngittleman- inactivation of na/k cotrasporter (sim to thiazide)\n- hypokalemia bc o renal excretion bc of the transporter\n\nin either situation: always excrete cl in urine-- dont absorb the cl and no roblem with non-reabsorbed aniona\n- so dd of lose k through kideny is based onthe cl level in the urine\n\n\ngittleman, barter, diuretics:\nhigh cl in urine\n\n\n\nhypokalemic pt\n- is kidney responsible or intake or shift?\n- take k level in urine\n-if high when pt hypokalemic- tehn means kidney not reabsorb the k even though hypokalmeic- the kidney is the problem\nhow know where the prob is in the kidney?:\nneed to know= 1) met alk/acidosis 9acid base status) 2) cl level in the urine (cl level)\n\n
when normal bv-- aldosterone is not the problem- the problem is the distal delivery = high distal delivery\n\ndiarrhea: urinary k is low (bc kidney not responsible for this)\nplace where is responsible: renal tubular acidosis\n\nhigh urinary k level- kidney is the problem\nlow urinary k- the kidney is not the responsible one- diarrhea, low intake, or problem with shift (extracatechol, beta agonist...)\n\n\n\nurine cl low = non reabsorbed anions (vomit, or carbapenems- cant reabsorb the na proximally c of the anions- so absorbes distally withcl)\nurine cl is high = diuretics or barter or gittelman, or mg defficiency (hypokalemic pt with hypocalcemia- look for the mg levels- usually due to hypomagnesemia- need to correct the mg)\n\n\nHTN pt:\n- hypokalemia bc of kidney- main problem is hyperaldosterosism\n\nwhat can cause pathologically high aldost:\nA) high renin high aldost\n- renin secreting tumor\n- pt will have high renin and high aldost levels\n- renal artery stenosis- low effective blood to kidney\nB) low renin, high aldost- hyperaldosteronism, \nC) renin low, aldost low, but still high aldost activation of principlecell = \n- activation of enac\n- neg feedback of actiavtion of receptors for aldosterone- can be due to few path things\n- activation by cortisol- activate receptor of aldost\n- cortisol inactivated by enzyme- somtimes enzyme has genetic mutaiton or is inactivated by licorice-- not converted and can activate the receptor- high level cortisol- hypervolemic, high bp, aldost level suppressed- bc of high activation of receptor\n- hypokalemia- extra urinary excretion, high bp, low aldost: cushings syndrome, 11 beta defficiency or mutation or inactivation by licorice\n- hyper activation of receptor but renin and aldost are suppressed\n\nits either:\n1) renin or 2) aldosterone or 3) activation of receptor by something lese\n\n
hypokalemia cause tachy\nhyperkalemia cause brady \n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
intake not usually effect- but if have other problems will (like if dont have kidney, or low effective blood volume- no filtration, no distal deli ery- no excretion)\n\n\neither extreme situation- ate so much k ( rare)\ndont have kidney (kidney failure) - most common\nhave kidney but fail bc of low ebv - most common\nor hypoaldosteronism (rare)\nsome drugs that block raas axis and cause low aldost - most common\n\n\nhigh k in lab- not really higjh k in blood\n- lab problem (hemolysis)\n.......\n\nmetabolic acidosis- shift of k from inside cells to outside\n\n
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heparin suppress aldost secretion from adrenal gland\n
pts on dialysis shoulndt eat these\n
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not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
high pco2 \nhigh hco3\nhypokalemic\n\nhypokal\nalkylotic\nlow bp/normal bp\n\ngastric tube- doesnt absorb anything from the gastric outlet to the gut (similar to idea of vomitting)\n- metabolic alkalosis, kidney try to get rid of bicarb- non-absorb anion- high distal delivery- increased excretion of k\n\n- high urinary k\n- low urinary cl\n\n
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high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
