Clinical Correlations

Front 1

Diabetes insipidus

Back 1

hypernatremia

Front 2

chronic asymptomatic
hyponatremia. tx

Back 2

fluid restriction

Front 3

Hypotonic Hyponatremia: Treatment

Back 3

fluid restriction

Front 4

Usually worsens hyponatremia in SIADH

Back 4

0.9% saline (normal saline)

Front 5

SIADH

Back 5

40

Front 6

Loss of salt and water equally

Back 6

unchanged

Front 7

The diagnosis of addisons is made

Back 7

by an ACTH stimulation test

treatment is hydrocortisone therapy

Front 8

Loop diuretic

Back 8

200-300

Front 9

This patient has severe
hyponatremia with neurologic sequelae.
This would be classified as chronic, symptomatic hyponatremia. She should receive

Back 9

hypertonic saline (3%) and
correction should not exceed an increase in Na of > 8 mEq/L in the first 24 hours.

Front 10

Water deficit =

Back 10

TBW x (Na/140 - 1)

Front 12

Calculate water excess:

Back 12

TBW – (TBW x Na/desired Na)

desired sodium is 120

Front 13

Disorders
of
External Balalance of K

Back 13

Excessive Intake
Oliguric renal failure
Hypoaldosteronism
Potassium secretory defect
Pseudohypoaldosteronism

Front 14

Disorders
of
Internal Balance of K

Back 14

Insulin deficiency
Cell lysis
Metabolic acidosis
β-adrenergic antagonists
Periodic paralysis

Front 15

Digoxin causes hyperkalemia by what mechanism?

Back 15

inhibits Na/K ATPase

Front 16

Enalapril causes hyperkalemia by what mechanism?

Back 16

inhibits conversion of AI to AII

Front 17

Type IV RTA (most common cause is

Back 17

DM

Front 18

Which potential cause/causes would give you
a low transtubular K gradient (TTKG)?

Back 18

3 and 4

Front 19

Normal renal response to hyperkalemia:

Back 19

greater than 40 greater than 40 greater than 40

Front 20

His ECG is normal with no signs of
hyperkalemia. Therefore, treatment would
involve more conservative measure

Front 21

Decreased magnitude of RMP – more excitable the K is where

Back 21

HIGH up the AIR

Front 22

Shortened QT interval (reflect rapid
repolarization)

Back 22

High in the AIR k

Front 23

Cardiovascular manifestations of more
advanced hyperkalemia;

Back 23

Reflect delayed depolarization (slower rise in
Na influx)

Front 25

How does calcium gluconate treat hyperkalemia?

Back 25

antagonizes the cardiac conduction abnormalities

Front 26

How does insulin and glucose treat hyperkalemia?

Back 26

shifts K into the cell

Front 27

4. ion-exchange resin which binds K

Back 27

How does sodium polystyrene sulfonate treat hyperkalemia?

Front 28

How does sodium polystyrene sulfonate treat hyperkalemia?

Back 28

ion-exchange resin which binds K

Front 29

Removal of K – takes several hours to work but what agents do it

Front 30

common finding in DKA

Back 30

common finding in DKA

Back 31

acute tubular necrosis

Front 33

Pseudohyperkalemia

Back 33

Due to in vitro release of K from blood cells

Front 34

All of the following are ECG manifestations
of hypokalemia except:

Back 34

peaked T waves

Front 35

cell is less responsive

Back 35

Hypokalemia

Front 36

Purkinje fiber repolarization)

Back 36

Hypokalemia

Front 37

Hypertension present – 3 main causes

Front 38

Urine K. The normal renal response in
hypokalemia is to lower urinary K to less than

Back 38

< 20mEq/L

Front 39

Primary hyperaldosteronism has renin levels that are what?

Back 39

low the aldosterone suppresses them

Front 40

Aldosterone to renin ratio > 30

Back 40

primary hyperaldosteronism

Back 41

have high renin levels

Front 42

in apparent mineralocorticoid excess what are the aldosterone levels like

Back 42

low renin and low aldos when it apparent

Front 43

Indomethacin acts to raise K by which mechanism:

Back 43

inhibits renin release