Acid/Base/Potassium (ALL BRCU lectures done 7/19) Flashcards

7/19/2021 Lectures

1
Q

What are 3 things that enhance renal NH3 production and NH4+ excretion?
3 things that inhibit it?
#abk #brcu

A

Enhancers:
- Acidemia, hypokalemia, gluconeogenesis

Inhibitors:
- Alkalemia, hyperkalemia, angiotensin blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

abk #brcu

What are the three main processes for urinary H+ excretion?

A
  1. Proximal acidification
  2. Distal acidification
  3. Bicarb reabsorption/generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypokalemia stimulates acidemia/alkalemia?
Hyperkalemia?
#abk #brcu

A

Hypokalemia –> alkalemia (increased bicarb generation)
Hyperkalemia –> acidemia (decreased bicarb generation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

abk #brcu

NAGMA: gain of ____ and loss of ____
HAGMA: gain of ____ and loss of ____

(Like what kind of ions)

A

NAGMA: gain of chloride ion and loss of bicarb
HAGMA: gain of non-chloride anion and loss of bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DDx for HAGMA:
GOLD MARK
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the metabolites for the following:
Glycols: ethylene (?), propylene (?)
Oxoproline: (?)
L-lactate
D-lactate
Methanol: (?)
ASA: (?)
Renal failure
Ketoacidosis
#abk #brcu

A

Glycols: ethylene (oxalic acid), propylene (lactate)
Oxoproline: (pyroglutamic acid)
L-lactate
D-lactate
Methanol: (formic acid)
ASA: (lactate + ketones)
Renal failure
Ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DDx for HAGMA:
CUTE DIMPLES
#abk #brcu

A

Cyanide, citrate
Uremia
Toluene
Ethylene glycol
DKA
INH, iron
Methanol, metformin
Pyroglutamic acid, prolylene glycol, paraldehyde, propofol
Lactic acidosis, linezolid
Ethanol ketoacidosis
Salicyclates, starvation ketoacidosis, sodium thiosulfate (?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the metabolites for the following:
Cyanide, citrate: (?)
Uremia
Toluene: (?)
Ethylene glycol
DKA
INH, iron
Methanol, metformin: (?)
Pyroglutamic acid, prolylene glycol, paraldehyde, propofol: (?)
Lactic acidosis, linezolid: (?)
Ethanol ketoacidosis
Salicyclates, starvation ketoacidosis, sodium thiosulfate
#abk #brcu

A

Cyanide, citrate: (citric acid)
Uremia
Toluene: (hippuric acid)
Ethylene glycol
DKA
INH, iron
Methanol, metformin: (lactate)
Pyroglutamic acid, prolylene glycol, paraldehyde, propofol: (lactate)
Lactic acidosis, linezolid: (lactate)
Ethanol ketoacidosis
Salicyclates, starvation ketoacidosis, sodium thiosulfate

Toluene leads to an early HAGMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between diarrhea and RTA in NAGMA?
Which has a positive or negative urinary AG?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When should you determine the delta gap?
What are the steps you take to determine a mixed AB disorder?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Winter’s Formula?
When do you use it?
How do you interpret it?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the UCl for diuretics? Hyperaldo? Bartter? Gitelman?
#abk #brcu

A

UCl > 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyperaldo –> MetAc or MetAlk?
#abk #brcu

A

MetAlk

Direct stimulation of H-ATPase
Direct stimulation of Na/K exchange
More open ENaC channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When do you typically see pseudohypokalemia?
What is the WBC usually?
#abk #brcu

A

Seen in AML
Marked leukocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does increased B-adrenergic activity do to the K level?
What drugs can have this affect?
#abk #brcu

A

Cellular shift that causes hypokalemia (ex: stress induced epi)
Drugs: theophylline intoxication, rotodrine and terbutaline, albuterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does treatment of pernicious anemia do to K level? How?
#abk #brcu

A

Causes hypokalemia
Give back Vit B12, now the new cells take up the K

Also, rapidly growing leukemias and lymphomas
(think anabolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hypokalemia periodic paralysis:
Inheritance? Mutation?
Other clinical association?
#abk #brcu

A

AD
Mutation in a-1 subunit of DHP-sensitive Ca channel
Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

(Asian) male that has paralysis after large meal or extreme exercise: name the disorder? What other disorder is associated with this?
#abk #brcu

A

Acquired hypokalemic periodic paralysis (they usually have hyperthryoidism)

Diuretics can cause a hypoK, but you get both extra and intracellular depletion - so they aren’t as symptomatic as someone with paralysis. The paralysis guys have a such a large transgradient because the K is shifting intracellularly - you aren’t losing K like in diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In GI loss, what do you expect the UK to be?
#abk #bruc

A

UK < 20

Diarrhea is the most common cause

Vomiting has 5-10 meq in the gastric juice (so hypokalemia is more due to the kidney K loss due to hypovolemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

You have hypoK without an AB disorder: what are you thinking?
HyperK?
#abk #brcu

A

Clay ingestion (also low phos and Fe)
Red clay (hyperK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

HypoK with NAGMA: what are you thinking?
#abk #brcu

A

Small intestine disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

HypoK with MetAlk: what are you thinking? (3, one of them is a med)
#abk #brcu

A

Chronic laxative abuse

Congenital chloridorrhea (needs lifelong salt supplementation)
Villous adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do you expect the UK in kidney loss for hypoK? Why?
#abk #brcu

A

UK > 20
Coupling of increased distal Na delivery and increased MC activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

High renin and High aldo
DDx?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the renin and aldo in renal artery stenosis?
#abk #brcu

A

High renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the renin and aldo in renin secreting tumor?
#abk #brcu

A

High renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the renin and aldo in malignant HTN?
#abk #brcu

A

High renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Low renin and High aldo
DDx?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the renin and aldo in Conn’s syndrome?
#abk #brcu

A

Low renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the renin and aldo in BL adrenal cortical hyperplasia?
#abk #brcu

A

Low renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the renin and aldo in GC suppressible hyperaldo?
#abk #brcu

A

Low renin
High aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is GC suppresible hyperaldo?
What’s the big enzyme you need to know? How do you check?
Inheritance pattern?
What’s the treatment?
#abk #brcu

A
  • This is a crossover that results in a chimeric gene, where ACTH from the pituitary is driving the aldosterone production
  • Increased production of 18-oxocortisol and 18-hydroxycortisol (check in the urine)
  • AD (FMHx of HTN)
  • Treat with exogenous GC (decreases the ACTH release, which will decrease aldo production)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Low renin and low aldo
DDx?
#abk #brcu

A

Also Liddle
Activating mutation of the MC receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the renin and aldo in SAME?
#abk #brcu

A

Low renin
Low aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the renin and aldo in Cushings?
#abk #brcu

A

Low renin
Low aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the renin and aldo in congenital adrenal hyperplasia?
#abk #brcu

A

Low renin
Low aldo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some clincal ssx in 11 b-hydroxylase deficiency?
17 a-hydroxylase deficiency?
(in congenital adrenal hyperplasia)
#abk #brcu

A

11 beta = virilization
17 alpha = decreased sex hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pathophys for syndrome of apparent mineralocorticoid excess?
What is the enzyme issue?
How are you labs?
What are some acquired causes?
#abk #brcu

A

Cortisol isn’t being inactivated into cortisone
11 B-hydroxysteroid dehydrogenase deficiency leads to more cortisol which stimulates the MC receptor
Urinary cortisol levels&raquo_space; urinary cortisone
Glycyrrhetinic acid (licorice, chewing tobacco), grapefruit juice, bile acids (hyyperbili patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the renin and aldo in Liddle?
Treatment?
#abk #brcu

A

Low renin
Low aldo
Amiloride or triamterene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the renin and aldo in activating mutation of MC receptor?
Inheritance?
What’s the pathophys?
What med is CI in this?
#abk #brcu

A

Low renin
Low aldo
AD
Steroids usually antagonize, but here they activate the receptor
Spironolactone is CI (it’s now an MCR agonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are things that increase distal Na delivery?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name 4 things that decrease proximal reabsorption of Na.
#abk #brcu

A

Carbonic anhydrase inhibitors (acetazolimide)
Osmotic diuretics
Met Ac
Topirimate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Name 3 things that decreases TAL reabsorption of Na.
#abk #brcu

A

Loop diuretics
Mg deficiency
Bartter syndrome

remember that loops are secreted in the proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What other electrolyte abnormalities are associated with hypoMg?
#abk #brcu

A

Hypokalemic alkalosis
Hypocalcemia

Mg deficiency inhibits TAL Na absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Normal BP
Hypokalemia
MetAlk
Name the syndrome
#abk #brcu

A

Bartter syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Bartter syndrome:
HTN?
K level?
AB disorder?
Aldo?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the 5 different Bartter mutations?
Which ones are clinically associated with other medical conditions?
#abk #brcu

A

Know the deafness one and the AD hypocalcemia hypokalemic alkalosis, I can see this in a stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Bartter:
Renin? Aldo? Urinary Ca?
#abk #brcu

A

High renin and aldo
Hypercalciuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name 2 things that decreases DCT reabsorption of Na
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What do nonreabsorbable anions in the filtrate do to distal Na delivery?
How does it affect K excretion?
What are some of these anions?
#abk #brcu

A

Also, toluene exposure (hippurate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Kidney K Handling algorithm
#abk #brcu

A

if you have MetAc and hypoK, treat the hypoK first (if you give BC, the K will go lower b/c it shifts into the cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are some causes of pseudohyperK?
#abk #brcu

A

Venipuncture
Increased WBC or Plt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are 2 factors that shift K into the cell?
4 factors that shift K out?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Name 3 drugs that shift K out of the cell?
#abk #brcu

A

Digoxin
Chan su (herbal)
Succinylcholine (causes depolarization and leads to K accumulation in the NM junction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are some meds/conditions that impair renin release?
Impair aldo metabolism?
(figure)
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are some other names for Gordon syndrome?
#abk #brcu

A

Familial hyperK HTN
Pseudohypoaldo type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

HTN, hyperK, NAGMA
Cl dependent
AD
Responds to thiazides
Name the syndrome
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

WNK4 inactivating mutation
Name the syndrome
What are some associated lab abnormalities?
#abk #brcu

A

Associated hyperCalciuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is pseudohypoaldo type 1? How is it different than type 2?
#abk #brcu

A

HyperK, MetAc, with hypoTN
AR pattern: inactivating ENaC; lots of pulm infections
AD pattern: inactivating MC receptor; mild and improves with age
Gordon’s (type 2) has HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are 3 causes of high sweat Cl?
#abk #brcu

A

CF
Congenital hyperchloridia
Pseudohypoaldo type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Name all the kidney syndromes
(figure)
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are some ways to determine the respiratory compensation for primary MetAc?
#abk #brcu

A

First: most accurate
Second: easiest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are some causes of low anion gap?
#abk #brcu

A

Low albumin
Severe NAGMA
Increased unmeasured cations (but with accompanied Cl or BC)
- Increased Ca or Mg, lithum, IgG paraproteinemia, polymyxin B
Spurius Cl elevation
- Bromide, iodide, salicyclate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are some causes of a high anion gap?
#abk #brcu

A

Severe volume depletion (increased albumin)
Resp and Met alkalosis
Increased IgA (anion)
Increased TG
Severe hyperphos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the only 2 things that lower you Cl level?
#abk #brcu

A

MetAlk
Chronic RespAc
Does what to you Cl level?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Na 150
Cl 100
BC 20
Name the AB disorder
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Na 130
Cl 100
BC 6
Name the AB disorder
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the only 2 things that increase you Cl level?
#abk #brcu

A

NAGMA
Chronic RespAlk
Does what to your Cl level?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the 3 different types of lactic acidosis?
#abk #brcu

A

Type A: tissue hypoxia
Type B: nothing to do with hypoxia or hypoperfusion
Type D: bacterial overgrowth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the causes of hyperK in DKA?
What is NOT a cause?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What kind of acidosis do you see in early vs. late DKA?
#abk #brcu

A

NAGMA in early DKA (ECF volume is near normal)
Once you have decreased EABV, you get in increased AG

NAGMA in the recovery phase of DKA due to indirect loss of NaBC in the urine with kidney retention of NaCl and admin of NaCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the metabolites and their effects of methanol? Ethylene glycol?
Treatment?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

In EtOH ketoacidosis, which comes first: thiamine or glucose and why?

A

Thiamine then glucose to minimize the risk of Wernicke or Korsakoff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Propylene glycol: what kind AB disorder?
#abk #brcu

A

HAGMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

RespAlk and HAGMA: whats the intoxication?
#abk #brcu

A

Salicylate poisoning

Sometimes as NAGMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What kind of AB disorder do you get with salicylate toxicity?
Uric acid level?
Glucose level?
#abk #brcu

A

RespAlk + HAGMA
Low dose salicylate -> increase uric acid
High dose salicylate -> decreases uric acid
Hypoglycemia

Sometimes a NAGMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Steps to do an AB disorder question
(figure)
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are your compensation ratios for bicarb and CO2?
(figure)
#abk #brcu

A

There are a lot of different ways to do it, but maybe just learn the box?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the correction factors of a VBG to ABG for pH and pCO2?
#abk #brcu

A

pH: add 0.05
pCO2: subtract 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the correction factor for albumin when you determining the anion gap?
#abk #brcu

A

Correction for albumin:
(4-albumin) x 2.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the equation for a urine anion gap?
What’s the etiology of a positive UAG? Negative UAG?
#abk #brcu

A

Na+K-Cl
Positive - renal cause (low NH4 excretion)
Negative - nonrenal cause (appropriate NH4 excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Toluene is associated with what metabolite?
#abk #brcu

A

Hippuric acid
is a metabolite of what?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the equation for a urine osmolal gap?
#abk #brcu

A

Measured UOsm - [2x(Na+K)+(UUN/2.8)+(Glucose/18)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Which of the RTAs cause hypoK?
#abk #brcu

A

Proximal RTA (type 2)
Classic distal RTA (type 1)
Mixed (type 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Which of the RTAs cause hyperK?
#abk #brcu

A

Aldo deficiency/resistance (type 4)
Non-MC voltage defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the K level and the type of MetAc:
progressive CKD?
Uremic acidosis?
#abk #brcu

A

Progressive CKD: normal K and NAGMA
Uremic acidosis: normal K and HAGMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the K level in the following?
Proximal RTA?
Distal RTA?
Mixed RTA?
Aldo deficient/resistance?
#abk #brcu

A

Top three - hypoK
Bottom - hyperK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the updated names (locations) of the 4 RTAs?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Urinary bicarb loss - what kind of RTA?
#abk #brcu

A

Type 2 proximal RTA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the overall pathophys for a Type 2 RTA?
#abk #brcu

A

Urinary bicarb loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

NaPi-2 mutation, cystinosis (MC), glycogen storage diease, wilson’s - what kind of RTA?
#abk #brcu

A

Type 2 proximal RTA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are some other etiology for generalized proximal RTA dysfunction?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is type 2 RTA also known as?
What are reasons for an acquired form of Type 2 RTA?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

MM, amyloidosis, heavy metal toxins (Pb, Cd, Hg) - what kind of RTA?
#abk #brcu

A

Type 2 proximal RTA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Carbonic anhydrase (acetazolimide), ifosfamide, cisplatin, tenofovir - what kind of RTA?
#abk #brcu

A

Type 2 proximal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are some meds that can cause Type 2 RTA?
#abk #brcu

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

UpH < 5.5
Normal UAG
Fanconi syndrome
Name the RTA
#abk #brcu

A

Proximal RTA
UpH?
UAG?
What other syndrome?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Proximal RTA
UpH?
UAG?
What other syndrome?
#abk #brcu

A

UpH < 5.5
Normal UAG
Fanconi syndrome

99
Q

What medication can give you an isolated proximal RTA? Mixed RTA?
#abk #brcu

A

Carbonic anhydrase (isolated prox RTA)
Topirimate (mixed RTA)

100
Q

Carbonic anhydrase inhibitors give you what type of RTA?
#abk #brcu

A

Isolated proximal RTA
(topirimate - mixed RTA)

101
Q

Poor H+ excretion - what kind of RTA?
#abk #brcu

A

Type 1 distal (classic)

102
Q

What is the overall pathophy for Type 1 RTA (classical)?
#abk #brcu

A

Poor H+ excretion

103
Q

Sjogrens, RA, sickle cell, hypercalciuria (medullary sponge, hyperpara, excessive VitD), obstructive uropathy - there are all acquired forms of what kind of RTA?
#abk #brcu

A

Type 1 Distal

104
Q

What are some acquired forms of distal RTA?
#abk #brcu

A
105
Q

Ampho B, lithium, isofofamide, topirimate, toluene - what type of RTA?
#abk #brcu

A

Type 1 distal

106
Q

What are some meds that cause a distal RTA?
#abk #brcu

A
107
Q

UpH >= 5.5
UAG +
Hypocitraturia
Hypercalciuria
Name the RTA?
#abk #brcu

A

Distal RTA
Urine pH?
UAG?
Findings in urine?

108
Q

Distal RTA
Urine pH?
UAG?
Findings in urine?
#abk #brcu

A

UpH >= 5.5
UAG +
Hypocitraturia
Hypercalciuria

109
Q

Type 4 RTA will have what renin and aldo levels?
#abk #brcu

A

For aldo deficiency: high renin and low aldo
But there is hyporenin and hypoaldo type 4 RTA too

110
Q

Congenital AI, heparin, ACE/ARB - what kind of RTA?
#abk #brcu

A

Type 4 distal
low aldo

111
Q

What are some reasons for hyporenin hypoaldo Type RTA?
#abk #brcu

A

DM nephropathy
NSAIDs (decreased PGs)
CNIs
Obstructive uropathy

112
Q

DM nephropathy
NSAIDs (decreased PGs)
CNIs
Obstructive uropathy
What kind of RTA? Renin and aldo levels?
#abk #brcu

A

Type 4 RTA
hyporenin hypoaldo

113
Q

Spiro, amiloride, triamterene, TMP, pentamidine, CNI - what kind of RTA?
#abk #brcu

A

Type 4 RTA

114
Q

What are some meds that can cause Type 4 RTA?
(figure)
#abk #brcu

A
115
Q

Obstructive uropathy - what kind of RTA?
#abk #brcu

A

Non-MC voltage defect
Type 4 RTA

116
Q

Interstial nephritis (sickle cell) - what kind of RTA?
#abk #brcu

A

Non-MC voltage defect
Type 4 RTA

117
Q

Lupus nephritis - what kind of RTA?
#abk #brcu

A

Non-MC voltage defect
Type 4 RTA

118
Q

What are some non-MC voltage defect reasons for Type 4 RTA?
(figure)
#abk #brcu

A
119
Q

Pseudohypoaldo type 2
Other names for this? Inheritance? Aldo? BP? K? AB disorder?
#abk #brcu

A

Pseudohypoaldo type 2
Familial hyperK HTN
Gordon syndrome
AD
HTN (volume expansion)
Low aldo
HyperK
MetAc

120
Q

AD
HTN (volume expansion)
Low aldo
HyperK
MetAc
Name the syndrome
#abk #brcu

A

Pseudohypoaldo type 2
Familial hyperK HTN
Gordon syndrome

121
Q

Different types of Type 4 RTA
Pathophys? Disease? Renin? Aldo?
(figure)
#abk #brcu

A
122
Q

Different RTAs: K? UAG? UpH? Bicarb?
(figure)
#abk #brcu

A
123
Q

Treatments for hypokalemic RTA?
#abk #brcu

A
124
Q

Treatment for hyperkalemic RTA?
#abk #brcu

A
125
Q

Treatment for Gordon syndrome?
#abk #brcu

A
126
Q

Definition of MetAlk
What are values in the compensation table?
(figure)
#abk #brcu

A
127
Q

In MetAlk, what is your cut off for Cl sensitive and Cl resistant for UCl levels? Which one is volume “depleted”? “Expanded”?
#abk #brcu

A

UCl < 20 = sensitive (depleted)
UCl > 20 = resitant (expanded)

128
Q

What are some Cl sensitive states for MetAlk? What is the UCl?
#abk #brcu

A

GI: vomiting/NG suction; hereditary Cl losing Drh; laxative use disorder
Urinary: diuretics (exception UCl is high in recent med use)
UCl < 20

129
Q

What are some Cl expanded states for MetAlk? What is the UCl?
#abk #brcu

A

Exogenous alkali
MC/GC excess
Tubular disorders (exception: Bartter and Gitelman are volume depleted)
Severe hypoK
UCl > 20

130
Q

Milk alkali syndrome:
AB disorder?
Urine pH?
Chloride resistent or sensitive (UCl)?
#abk #brcu

A

Met Alk
Urine pH high
Cl resistant (UCl>20)
Name the disorder.

131
Q

Met Alk
Urine pH high
Cl resistant (UCl>20)
Name the disorder.
#abk #brcu

A

Milk alkali syndrome

132
Q

Which MetAlk etiolgies have a high aldo level?
#abk #brcu

A
133
Q

Which MetAlk etiology have a high cortisol level?
#abk #brcu

A
134
Q

Liddle syndrome
Inheritance? Pathophys? K level? Renin/Aldo levels? Treatment options?
#abk #brcu

A
135
Q

Name the disorder
#abk #bcru

A

Liddle

136
Q

Bartter
Inheritance? Acquired etiologies? Renin/aldo? UCl? UCa? Treatment?
#abk #brcu

A
137
Q

Name types 1-4 of bartter - which channels are affected?
#abk #brcu

A
138
Q

Name the syndrome
#abk #brcu

A

Bartter

139
Q

Gitelman
Inhertance? Channel defect? Mag level? Renin/aldo? UCl? UCa? Treatment?
#abk #brcu

A
140
Q

Name the syndrome
#abk #brcu

A

Gitelman

141
Q

Gitelman vs. Bartter
Which one has high UCa vs low UCa?
#abk #brcu

A

Gitelman: low UCa
“giteLman = Low”
Bartter: high (high-normal) UCa

142
Q

Bartter, gitelman, liddle: high or low renin?
#abk #brcu

A

Bartter and Gitelman: high renin
(therefore high aldo)
(normal is 1-6)
Liddle: low renin
(Liddle = Low)

143
Q

Severe hypoK: high or low renin?
#abk #brcu

A

Low renin with hypoK

144
Q

MetAlk summary
#abk #brcu

A
145
Q
A

Or, delta AG + BC (7+6) = 13
13 < 24 = NAGMA

146
Q

What are the steps to do a delta gap? What are the cutoffs for a concurrent NAGMA or MetAlk?
#abk #brcu

A
147
Q

What kind of AB disorders (or clinical scenarios) do you see for the following?
Salicylate ingestion?
Metformin overdose?
Toluene ingestion?
Diethylene glycol ingestion (brake fluid?)
D-lactic acidosis?

A
148
Q

Patient has an instestinal surgery - what kind of AB disorder are you thinking?

A

D-lactic acidosis

149
Q

Osmolal gap and cranial nerve palsies - what kind of ingestion?

A

Diethylene glycol (brake fluid)

150
Q

What kind of ingestion gives you a respiratory alkalosis?

A

Salicylate ingestion

151
Q

HAGMA and NAGMA with no lactic acidosis - what kind of ingestion?

A

Toluene ingestion

152
Q

What kind of poisoning give you visual disturbances?

A

Methanol poisoning

153
Q

What kind of poisoning gives you calcium oxalate crystals with AKI?

A

Ethylene glycol

154
Q

What are the big differences in toxic alcohol poisonings?
(figure)

A
155
Q

Does RRT remove metformin?

A

HD removes metformin and treats the acidosis, so you should RRT early and RRT long
There will be rebound because the VoD is large (>3L/kg)

156
Q

Hypokalemia NAGMA DDx
(figure)

A
157
Q

If you have chronic diarrhea, what do you expect the UpH to be?

A

Urine pH > 5.5
(< 5.3 is normal)
(> 5.5 +/- acidification defect)

158
Q

Intestinal bypass surgery - what kinda of urinary metabolite findings?

A

Hyperoxaluria (from fat malabsorption)

159
Q

How do you calculate the urine osmolal gap?
What is the cutoff number and what does it mean?

A
160
Q

What are the cutoffs for an acidification defect for D-RTA?
Urine pH?
UAG?
UOG?

A

Urine pH > 5.3
UAG < (-20) (aka more positive)
UOG < 150

161
Q

Urine pH > 5.3
UAG < (-20) (aka more positive)
UOG < 150
What kind of ABDO?

A

D-RTA

162
Q

What kind of disorder also comes with D-RTA? Why?

A
163
Q

Common causes of D-RTA?
Syndromes? Meds?

A
164
Q

What’s the AB D/O?

A

HAGMA, NAGMA, RespAc

165
Q

What are the only 2 things that allow for a high Cl without a high Na?

A

Chronic RespAlk
NAGMA
(usually they both move together)

166
Q

Toluene breaks down into hippurate and causes what kind of disorder?

A

Overproduction of aciduria (you pee out hippuric acid)
Can get a NAGMA (late) or HAGMA (acute when coupled with volume depletion)

Toluene can cause an extra-renal acidosis

Urinary AG is normally negative; but if you have extra anions, you can get a positive UAG (looks like an RTA); so you use the UOG (normal is 10-100); if there is a huge UOG there is some type of extra Osm getting voided (aka the kidney is actually normal function - not abnormal like an RTA); UAG can be misleading in the setting of unmeasured anions (B-OH-butyrate and acetoacetate in ketoacidosis, hippurate in toluene exposure)

167
Q

80kg pt; assuming no additional acid production, how much BC is required to raise the BC from 12 to 20?

A

(20-12) x (80 x 0.5) = 320mEq

168
Q

What are complications of bicarbonate therapy?
(figure)

A
169
Q

What are AE of acidemia?
(figure)

A
170
Q

IV lorazepam - what’s the medication toxicity?

A

Propylene glycol

171
Q

Propylene glycol toxicity - what medication do you suspect?
What kind of gap do you get?

A

IV lorazepam (ativan)
HAGMA (lactic acid) and OG as well

172
Q

Malnourished patient with tylenol intoxication - what is the etiology?

A

Pyroglutamic acid (oxoproline)
(HAGMA without a lactate)

173
Q

Sepsis-like patient with high lactate and HAGMA, but no source of bacterial sepsis?

A

Propylene glycol induced lactic acidosis (HAGMA + lactate)
Usually seen in IV lorazepam (but also other meds)

174
Q

Antifreeze ingestion - what do you suspect and do you find?

A

Ethylene glycol
AKI
Calcium oxalate crystals

175
Q

AKI
Calcium oxalate crystals
What kind of ingestion?

A

Ethylene glycol (antifreeze)

176
Q

Malnoutrition and chronic tylenol exposure?
What’s the cause?
Whats the ABDO?
Gaps?

A

Oxoproline (pyroglutamic acid)
HAGMA + high OG
Lack of lactate or ketones (other reasons for HAGMA)

177
Q

Oxoproline toxicity: what kind of ABDO?

A

HAGMA and high OG
(lactate will be low)

178
Q

What are causes of Type B, L-lactic acidosis?
(figure)

A

Malignancies, DKA, Mangosteen (fruit), HIV meds, metformin, toxic alcohols, acute liver fulminant failure, severe thiamine deficiency

179
Q

What are causes of Type B, D-lactic acidosis?
(figure)

A

Gut bacteria overgrowth in short gut (looks “drunk”), DKA, propylene glycol

180
Q

What’s a normal OG? Whats the formula?

A

Normal OG < 10

181
Q

Alcohol intoxications: metabolite? complications? treatment? dialyze?

A
182
Q

Which of the alcohols is not like the other and why? Methanol, ethylene glycol, isopropyl alcohol (aka isopropranol or rubbing alcohol)?

A

Isopropyl alcohol does not cause a metabolic acidosis; it gets metabolized into acetone which is not an acid

183
Q

NAGMA, postive UAG, UOG < 100: name the condition?
(figure)

A

D-RTA

184
Q

What are the UAGs?
Extrarenal? P-RTA? D-RTA? Toluene?

A

Extrarenal - Negative
P-RTA - Positive
D-RTA - > 0
Toluene - > 0 (but otherwise doesn’t look like RTA)

185
Q

BC > 15
urine pH < 5.5
Met Ac
Hypokalemia
Name the condition

A

P-RTA

Can’t reabsorb BC in the prox tubule

186
Q

P-RTA
BC level?
urine pH?
AB d/o?
K level?

A

BC > 15
urine pH < 5.5
Met Ac
Hypokalemia

187
Q

Etologies of P-RTA
(figure)

A

know the acquired defects: MM, heavy metals, amyloidosis, PNH, cisplatin, ifosfamide, aminoglycosides, imatinib, tenofovir, valproic acid, CA inhibitors (acetazolimide, topirimate, zonisamide (SZ med)) CA inhibitors are known for increased stone risk

188
Q

How do you dx P-RTA?

A

Fe of BC

189
Q

How do you manage P-RTA?

A

BC replacement
K replacement
Thiazides

190
Q

D-RTA
BC level?
urine pH?
Clinical associations?
Urine findings?

A

BC < 15
urine pH > 5.5 (but not always)
Growth impairment and polyuria
Hypercalciuria, nephrocalcinosis, stones
(type 4 D-RTA doesnt have increased risk of nephrocalcinosis because it has a low urine pH)

191
Q

BC < 15
urine pH > 5.5 (but not always)
Growth impairment and polyuria
Hypercalciuria, nephrocalcinosis, stones
What kind of disorder?

A

D-RTA

Can’t secrete H+

192
Q

Etiologies of D-RTA
(figure)

A

Know the hypoK and hyperK (Type 4) etiolgoies
HypoK: SS, RA, SLE, PBC, Li, ifosfamide (more prox than distal), ampho, bisphosphonates
HyperK: aldo deficiency or resistance, DM, tubulointerstitial nephropathy, sickle cell, obstructive uropathy, CNIs, K-sparing diuretics, NSAIDs, RAAS blockers, hepatin

193
Q

How do you test for D-RTA?

A
194
Q

How do you manage D-RTA?

A
195
Q

Name a genetic condition that will give you a mixed RTA?
Inheritance? Other clinical findings? Genetic mutation?

A
196
Q

AR with mixed RTA with osteoporosis (young kids)
Name the disease and the mutation

A
197
Q

What is the UOG with toluene intoxication?
What kind of an ABDO?

A

Usually > 100-150
NAGMA

198
Q

Diarrhea causes what kind of ABDO? UAG? UpH? Any other labs values you should think of?

A

NAGMA
UAG < 0
UpH may be high (>5.5)
HypoK

199
Q

What are 3 GI causes of NAGMA?

A

Diarrhea, ileal conduit, D-lactic acidosis

200
Q

When should you be really cautious with alkalinzation?

A
201
Q

Common causes of Cl sensitive MetAlk?
Whats the UCl?

A
202
Q

Describe the phases of vomiting
(figure)

A
203
Q

Severe MetAlk with BC > 45 - whats the cause?

A

Almost always due to a gastric cause

204
Q

Met Alk with BC > 45
UCl < 10
Hypokalemia
Whats the disorder?

A

Surreptitious vomiting

205
Q

What lab findings do you see in surreptitious diuretic use?

A

Varying MetAlk
UNa AND UCl (both very low or very high)

206
Q

Common causes of Cl-resistant MetAlk
(figure)

A
207
Q

Goiter, sensorineural deafness, metabolic acidosis: name the condition. Where is the channel mutation? What medication should you be cautious of and why?

A

Pendred syndrome - rare
Cl-Bicarb exchanger mutation in the collecting duct
Hypovolemia, MetAlk, HypoK if you use thiazides (because you are inhibiting the NCC channel and the pendrin channel already doesn’t work)

208
Q

What is pendred syndrome?
(figure)

A
209
Q

How to correct a severe MetAc?
(figure)

A
210
Q

Common causes of RespAlk and Resp Ac?
(figure)

A
211
Q

Low serum pH shifts the K how?
High pH?

A

Acidemia: shifts K out
Alkalemia: shifts K in

212
Q

What kind of indices do you use to evaluate K disorders?
(figure)

A
213
Q

What are some common causes of pseudohyperkalemia?
(figure)

A
214
Q

CLL - what kind of K disorder?

A

“reverse” pseudohyperkalemia

215
Q

Episodic weakness with rest after exercise - condition? K level?
(figure)

A
216
Q

Sofosbuvir can cause what kind of lab abnormality?

A
217
Q

HyperK with MetAc and salt wasting - name the syndrome. Treatment?
(figure)

A
218
Q

HTN in early adulthood, NAGMA, hyperK, hypercalciuria, osteoporosis, and stones - name the condition. Pathophys/mutation? Treatment?
(figure)

A
219
Q

Hypokalemic nephropathy: histology? pathogenesis? clinical findings?
(figure)

A
220
Q

AML or CML - whats the K level?

A

pseudohypokalemia (may also see hypophosphatemia and pseudohypoglycemia)

221
Q

Clay ingestion - K level?

A

Hypokalemia

222
Q

HypoK, hypoMag, hypoCal with secretory diarrhea - whats the syndrome?
(figure)

A
223
Q

Paralysis after strenuous exercise - condition?
(figure)

A
224
Q

Paralysis after strenuous exercise - condition?
(figure)

A
225
Q

Thyroid issue with period paralysis - hyperK or hypoK?
What other lab is noteworthy?

A
226
Q

Treatment for hypoK periodic paralysis?
Food?

A

BBL, K supplementation, low card diet, k sparing diuretics, CA inhibitors

227
Q

Which of the periodic paralysis conditions is treated with high carb vs low carb diet?

A

HyperK - treat with high carb diet
HypoK - treat with low carb diet

228
Q

Barbituate coma therapy (with thiopentone) causes what K value?

A

Initial hypoK then rebound hyperK
Replace slowly during the first 12-24 hours to reduce the rapid and severe rebound

229
Q

HypoK with Met Alk with gain of function ENaC - name the syndrome

A

Liddle

230
Q

DDx/algorithm for HTN, hypoK, MetAlk
(figure)

A
231
Q

Syndrome of apparent MC excess - what’s the ingestion/molecule that mimics this?
What ratio do you see?

A
232
Q

Abiraterone - what medication is this and what can it cause?
(figure)

A
233
Q

What is Geller sydnrome?
(figure)

A
234
Q

Ampho leads to high or low serum K?

A

MetAc and eletrolyte wasting
Low K in serum

235
Q

Hypercalcemia causes high or low serum K? what kind of AB DO?

A

HypoK with MetAlk (like a loop)

236
Q

Normotension, hypoK, MetAlk
High renin and High aldo
Bartter or gitelman?

A

Both

237
Q

Bartter
BP? K? ABO DO? Renin? Aldo?

A

Normotension, hypoK, MetAlk
High renin and High aldo

238
Q

Gitelman
BP? K? ABO DO? Renin? Aldo?

A

Normotension, hypoK, MetAlk
High renin and High aldo

239
Q

What are the differences between Bartter and Gitelmans?
(figure)

A
240
Q

Inheritance pattern for Bartter; channel mutations?
(figure)

A
241
Q

Which has more common and more severe hypoMag? Bartter or Gitelmans?

A

Gitelmans has really bad hypoMag

242
Q

What urine study is needed to determine Gitelman vs bartter?

A
243
Q

Metabolic disturbances for urinary diversions
(figure)

A
244
Q

List of etiologies for Type B lactic acidosis
(figure)

A