Potassium Regulation Part I And Now Ii

Front 1

how do aldosterone and alkalosis effect potassium

Back 1

Decrease in plasma K (hypokalemia)

Front 2

αadrenergic antagonists effect plasma K by

Back 2

decreasing it just like Aldosterone and Alkolisis as well as beta agonists and insulin

Front 3

αadrenergic agonists does what to plasma K

Back 3

increases it

Front 4

the principle cell does what with potassium

Back 4

secretes it

Front 5

secretes potassium

Back 5

the principle cell

Front 6

reabsorbs potassium

Back 6

Intercalated cell

Front 7

Factors that stimulate K secretion (the principle cell does this by actively reabsorbing on the basolateral side and passively excreting on the luminal side)

Back 7

*Increased extracellular K

*Increased aldosterone

*Increased luminal flow rate and distal Na
delivery

Front 8

n Volume expansion
n High Na intake
n Diuretics

Back 8

All stimulate K secretion

Front 9

how does the intercalated cell actively reabsorb K

Back 9

it has and apical H-K (antiporter) atpase

Front 10

Enables urinary K to be < 15 mEq/day

Back 10

Intercalated Cell

Front 11

what is the most common cause of Hypokalemia worldwide?

Back 11

Diarrhea

Front 12

what is the most common cause of hypokalemia due to renal loss?

Back 12

diuretics

Front 13

*Prominent U wave

Back 13

hypokalemia

Front 14

o Delayed repolarization
o Reentrant arrhythmias

Back 14

hypokalemia

Front 15

EKG changes mainly due to delayed ventricular repolarization

Back 15

hypokalemia

Front 16

hyperpolarizes muscle cells

Back 16

Hypokalemia

Front 17

*Weakness, fatigue
*Flaccid paralysis

Back 17

Hypokalemia

Front 18

what are the renal manifestations of hypokalemia derived from

Back 18

the fact that with hypokalemia there is a decrease in medullary flow and an increase in vascular retention

Front 19

the fact that hypokalemia causes a decrease in medullary flow and an increase in HTN leads to what

Back 19

o Hypertension
o Tubulointerstitial disease
o Cystic disease
o Metabolic alkalosis
o Polyuria (CD resistance to ADH)

Front 20

Leukocyte “larceny”

Back 20

Pseudohypokalemia (AML)
n Leukocyte “larceny”
n (WBC > 100,000/cm 3

Front 21

Redistribution hypokalemia can be caused by what

Back 21

n Transcellular shift – regulation
n Hypokalemic periodic paralysis
o Familial
o Thyrotoxic hypokalemic paralysis (Asians)
n Barium or cesium

Front 22

n Transcellular shift – regulation
n Hypokalemic periodic paralysis
o Familial
o Thyrotoxic hypokalemic paralysis (Asians)
n Barium or cesium

these cause what

Back 22

Redistribution hypokalemia

Front 23

Barium or cesium

Back 23

Redistribution hypokalemia

Front 24

5

Back 24

amount of K in sweat

Front 25

Renal losses of K can be broken dow to what

Back 25

n Medications
n Hypokalemia with hypertension
n Hypokalemia with a normal blood pressure

Front 26

n *Thiazide diuretics
n *Loop diuretics

Back 26

meds that cause renal loss of K

Front 27

renal loss hypokalemia caused by endogenous hormone production can be caused by what?

Back 27

Primary hyperaldosteronism

Apparent mineralcorticoid excess

Glucocorticoid remediable aldosteronism

Front 28

Intrinsic Renal Defects that cause low potassium are what?

Back 28

Bartter’s syndrome

Gitelman’s syndrome

Liddle’s syndrome

Renal tubular acidosis (Types I and II)

Front 29

Conn’s syndrome is what?

Back 29

Adrenal adenoma that secretes aldosteron and causes a hypertensive hypokalemia

Front 30

Adrenal adenoma that secretes aldosteron and causes a hypertensive hypokalemia

Back 30

Conn’s syndrome is what?

Front 31

Secondary hyperaldosteronism can cause hypokalemia and this can be due to what?

Back 31

Renin secreting tumor

Malignant hypertension

Front 32

Hypertension present hypokalemia

Back 32

Conn’s syndrome
Malignant hypertension
Renin secreting tumor
Renal artery stenosis

11βhydroxysteroid
dehydrogenase deficiency

Glycyrrhizic acid
Liddle’s syndrome
Cushing’s syndrome

Front 33

Liddle’s syndrome and cushings syndrome have what in common

Back 33

they cause a Hypokalemic state in the prescence of HTN

Front 34

what converts cortisol into cortisone?

Back 34

11-beta-hydrogenase

Front 35

what prevents the conversion of cortisol to cortisone

Back 35

licorice and obviosly a deficeincy in 11-beta-hydroxysterone. causing a hypokalemic hypertensive syndrome

Front 36

Pseudohyperaldosteronism (AD) aka

Back 36

Liddle’s Syndrome (AD):

Front 37

Liddle’s Syndrome (AD): aka

Back 37

Pseudohyperaldosteronism (AD)

Front 38

mutation of epithelial Na
channel (ENaC/amiloride sensitive channel) increasing its activity

Back 38

AD Liddles/pseudohyperaldosteronism

Front 39

Improve with drugs that block ENaC

Back 39

AD Liddles/pseudohyperaldosteronism

Front 40

the aldosterone levels and renin levels are ------ in psuedoaldosteronisms/Liddles which is an entity involving an increase in Enac activity

Back 40

renin and aldosterone levels are low

Front 41

triamterene can treat what disease with low renin and aldosterone levels that causes a hypokalemic HTN syndrome

Back 41

increased ENaC Liddle/psudohyperaldosteronism

Front 42

Magnesium depletion (impairs renal K conservation – unclear mechanism)

SO in someone with low magnesium causeing a secondary low in K what is there BP

Back 42

Normotensive

Front 43

are patients with Mg depletion causiing hypokalemia normotensive?

Back 43

yup

Front 44

name the two syndromes alongside RTA that causes a normotensive Hypokalemia

Back 44

Barters-AR and gittlemans

Front 45

Barters and Gittlemans cause

Back 45

a normotensive low K state

Front 46

Autosomal recessive, salt wasting syndrome, with hypokalemia and hypomagnesemia as well as high levels of renin and aldo

Back 46

Bartter’s Syndrome AR

Front 47

what are the renin/aldo levels in the salt, K and Mg wasting BArrters AR

Back 47

High as hell

Front 48

NKCC2 malfunction, in this AR with high renin and aldo and low mg/k

Back 48

Barters AR

Front 49

acts like a loop diuretic since there is malfunction of the NKCC2

Back 49

Bartters AR

Front 50

chloride urine levels in BArters AR

Back 50

High because it blocks the NKCC2, remember renin and aldo levels are also high here

Front 51

hypercalcemia is associated with what AR salt wasting hypoK/Mg normotensive syndrome

Back 51

Gittlemans since it acts like a thiazide

Front 52

acts like a thiazide

Back 52

gittlemans

Front 53

measure of net K secretion

Back 53

Transtubular K Gradient

Front 54

Transtubular K Gradient normal circumstances

Back 54

6-8

Front 55

To exonerate the kidney:
in hypokalemia: what must the ttk be?

Back 55

less than two

Front 56

to exonerate the kidney in hyperkalemia what must the TTK be

Back 56

greater than 7

Front 57

(Uk/Pk)/(Uos/Pos) =

Back 57

TTK =

Front 58

TTK = ?

Back 58

(Uk/Pk)/(Uos/Pos) =

Front 59

TTK = ?

Back 59

(Uk/Pk)/(Uos/Pos) =

Front 60

Urine K concentration is low in

Back 60

extrarenal loss and high in renal loss. i.e. it should be less than 20 in extrarenal loss and greater than 40 in renal loss

Front 61

what is the TTK in renal loss

Back 61

high greater than areound 4-6

Front 62

what is the TTK in extrarenal loss?

Back 62

low, less than about 2-4

Front 63

For each mEq decrease in serum K, total body
K has decreased by

Back 63

100-200mEq/L

Front 64

Hyperkalemia should suggest impairment in

Back 64

renal K excretion

Front 65

“spaghetti” legs

Back 65

Hyperkalemia

Front 66

paralysis of diaphragm

Back 66

Hyperkalemia

Front 67

slower rise in Na influx

Back 67

Delayed depolarization of Hyperkalemia

Front 68

More rapid repolarization is seen in

Back 68

hyperkalemia because there is an increased permiability to K

Front 69

Decreased magnitude of RMP makes a cell

Back 69

more excitable and this is seen in hyperkalemia

Front 70

a cell is more excitable because

Back 70

of a decrease in RMP associated with hyperkalemia

Front 71

Peaked narrow T waves reflect

Back 71

rapid repolarization seen in hyperkalemia

Front 72

rapid repolarization seen in hyperkalemia is reflected by

Back 72

Peaked narrow T waves

Front 73

Shortened QT interval

Back 73

reflects rapid repolarization seen in hyperkalemia

Front 74

reflects rapid repolarization seen in hyperkalemia

Back 74

Shortened QT interval

Front 75

Widened QRS reflects

Back 75

delayed depolarization in hyperkalemia

Front 76

delayed depolarization in hyperkalemia is reflected by

Back 76

Widened QRS

Front 77

sine wave pattern

Back 77

hyperkalemia

Front 78

Eventual sine wave pattern, ventricular fibrillation

Back 78

hyperkalemia

Front 79

flattened P wave

Back 79

hyperkalemia

Front 80

prolonged PR interval

Back 80

hyperkalemia

Front 81

Impairs urinary acid excretion

Back 81

hyperkalemia

Front 82

hyperkalemia impars urinary excretion of what

Back 82

acid

Front 83

why does hyperkalemia Impair urinary acid excretion

Back 83

it decreases the collecting duct H/K, it decreases amoniagenesis, Causes Type IV renal tubular acidosis (RTA)

Front 84

decreases amoniagenesis

Back 84

hyperkalemia

Front 85

Causes Type IV renal tubular acidosis (RTA)

Back 85

hyperkalemia

Front 86

hyperkalemia can cause what type of RTA

Back 86

type IV

Front 87

Stimulates aldosterone secretion

Back 87

hyperkalemia

Front 88

Pseudohyperkalemia is caused by what?

Back 88

Hemolysis, Leukocytosis, Thrombocytosis

Front 89

Hemolysis, Leukocytosis, Thrombocytosis may cause what?

Back 89

Pseudohyperkalemia

Front 90

Mutation subunit calcium channel

Back 90

Hyperkalemic periodic paralysis

Front 91

the Hyperkalemic Disorders of External Balance are

Back 91

Excessive Intake, Hypoaldosteronism, Potassium secretory defect, Pseudohypoaldosteronism

Front 92

Hypoaldosteronism does what to renal excretion of K

Back 92

it decreases it

Front 93

what are the three causes of hypoaldosteronism that leads to a decrease in K excretion?

Back 93

Addison’s disease, Type IV renal tubular acidosis, Medications which inhibit aldosterone

Front 94

what RTAs cause hyperkalemia

Back 94

I and IV

Front 95

Major causes of hypoaldosteronism which leads to hyperkalemia

Back 95

primary (addisons) Congenital adrenal hyperplasia and heparan.

Front 96

heparin

Back 96

suppresses aldosterone secretion

Front 97

Hyporeninemic hypoaldosteronism which causes hyperkalemia is most commonly caused by

Back 97

*Diabetes mellitus – most common

Front 98

Besides diabetes mellitis what else causes hyporeninemic hypoaldosteronism

Back 98

beta-blockers, cycloposrine, and NSAIDS and HIV

Front 99

beta-blockers, cycloposrine, and NSAIDS and HIV

Back 99

Besides diabetes mellitis what else causes hyporeninemic hypoaldosteronism

Front 100

Renal secretory defects causing hyperkalemia

Back 100

Renal transplant, Interstitial nephritis, Systemic lupus erythematosus, Sickle cell disease, Amyloidosis, Obstructive nephropathy

Front 101

KCl, Penicillin,
Polycitrate all do what

Back 101

cause hyperkalemia because they contain K

Front 102

Inhibit renin
release and therfore cause hyperK

Back 102

Metoprolol,
Atenolol

Front 103

Inhibits aldoster
one synthase and can cause hyperkalemia

Back 103

Heparin sodium

Front 104

Inhibit Na/K ATPase causing hyperkalemia

Back 104

Calcineurin inhibitors, Cyclosporine, Tacrolimus

Front 105

Inhibit renin release causing hyperkalemia

Back 105

NSAID and COX-2 inhibitors

Front 106

Block ENaC and can cause hyperkalemia

Back 106

Trimethoprim, Pentamidine, Amiloride, Triamterene

Front 107

Genetic disorders causing hyperkalemia

Back 107

Pseudohypoaldosteronism type Pseudohypoaldosteronism type II (Gordon
syndrome)

Hyperkalemic periodic paralysis

Front 108

What are the two different mutations seen in pseudohypOraldosterone type I which causes hyperkalemia.

Back 108

ENaC – hypofunction or Mutation of mineralcorticoid receptor

both reulting in salt wasting, hyperkalemia and metabolic alkalosis

Front 109

ENaC – hypofunction

or

Mutation of mineralcorticoid receptor

Back 109

psuedohypOaldosteronism I

Front 110

present in infancy with salt wasting, hyperkalemia and metabolic acidosis is psudohyporaldosteronism I caused by

Back 110

ENaC – hypofunction or Mutation of mineralcorticoid receptor

Front 111

AD gordons syndrome AKA

Back 111

psuedoHypeOaldosteronism II AD

Gain of function of NaCl cotransporter DCT

Front 112

Gain of function of NaCl cotransporter DCT

Back 112

Treatment: hydrochlorthiazide and this is PsudoHypoaldosteronism II gordons AD

Front 113

which pseudohypoaldosteronism presents with HTN

Back 113

gordons type II with the gain of function in NaCl cotransporter DCT

Front 114

Antagonizes cardiac conduction abnormalities of hyperkalemia

Back 114

Calcium

Front 115

while calcium can be administered to antagonize conduction abnormalities of hyperkalemia what does it do to the plasma K levels

Back 115

nothing

Front 116

Can be repeated in 35
minutes

Back 116

calcium can be administered to antagonize conduction abnormalities of hyperkalemia what does it do to the plasma K levels? NOthing

Front 117

calcium does what to the RMP

Back 117

decreases it by making it less negative

Front 118

Most rapid way to decrease plasma K

Back 118

insulin

Front 119

Ion exchange resin
that Works in the intestine to lower K in hyperkalemia

Back 119

Sodium polystyrene sulfonate

Front 120

Very effective – 200-300
mEq K removed via this mech

Back 120

dialysis

Front 121

Avoid multiple medications that raise K in order to prevent hyperkalemia i.e.

Back 121

use of nonsteroidal antiinflammatory agents
in someone on an ACE inhibitor