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URN 2 - Potassium

memorize.ai (lvl 286)

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Amiloride, Triamterene

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6 years ago

Date created

Mar 1, 2020

Cards (49)

Section 1

(49 cards)

Amiloride, Triamterene

Front

name 2 ENaC blockers

Back

K+ loss is due to improper renal function

Front

what does hypoK+ w/ a high FEK+ (>10%) indicate

Back

< 3

Front

in the absence of aldosterone related pathology, describe the TTKG in hypokalemia

Back

10%

Front

normal FEK+

Back

ENaC, Na/K ATPase

Front

what 2 channels does Aldosterone directly upregulate?

Back

prevent hypoglycemia

Front

in a patient w/ hyperK+, why administer glucose prior to admin IV insulin?

Back

H+/K+ exchanger; H+ moves in/out according to gradient and K+ is exchanged (be able to connect this concept to why organic acidosis effects no change in [K+])

Front

through what channel does alkalosis and acidosis effect transcellular shifts in [K+]? how?

Back

Flat P, prolonged PR, Wide QRS, Peaked T

Front

describe EKG changes assocd w/ HyperK+

Back

proportion of the filtered load that is excreted

Front

what is fractional excretion?

Back

dec Na/K ATPase activity

Front

what effect does hypoK+ have on Na/K ATPase

Back

osmotic diuresis -> high flow rate + high Na+ delivery -> increased K+ secretion -> hypoK+

Front

how does uncontrolled DM effect [K+] secretion

Back

AR inherited mutation effecting a malfunctioning NaCl symporter in DCT (thiazide diuretic sensitive channel)

Front

describe Gitelman Syndrome

Back

mutation effecting a malfunctioning NKCC cotransporter in the TAL (loop diuretic sensitive channel)

Front

describe Bartter syndrome

Back

improper aldosterone response retaining K+ in the presence of hyperK+

Front

what does hyperK+ w/ a low FEK+ (<10%) indicate

Back

K+ loss is extrarenal (proper renal function)

Front

what does hypoK+ w/ a low FEK+ (<10%) indicate?

Back

no change in [K+]

Front

what effect does organic acidosis (lactic acidosis, ketoacidosis) have on [K+]

Back

low T wave w/ added U wave

Front

describe EKG abnormalities assocd w/ HypoK+

Back

Alkalosis, Kussmal Respirations, Irritable, Weakness/fatigue/lethargy, hyporeflexia, thready pulse, hypoactive bowels (ileus), nausea, vomiting

Front

list some clinical features of HypoK+

Back

Inorganic (hyperchloremic, nongap) metabolic acidosis is due to a physical loss of HCO3- via RTA or diarrhea

Front

what is an inorganic metabolic acidosis

Back

aldosterone activity (conservation of K+ at cortical collecting duct)

Front

what does TTKG (transtubular K+ Gradient) indicate? what is normal?

Back

reabsorption took place

Front

what does a low FE indicate

Back

1. stabilize membrane excitability (if EKG changes present) 2. increase ICF [K+] shift 3. removal of excess K+ 4. limit intake of K+

Front

4 tier treatment of hyperK+

Back

inc Na/K ATPase activity

Front

what effect does hyperK+ have on Na/K ATPase

Back

Beta2 mediated hepatocyte and myocyte uptake of K+

Front

what effect does the SNS have on K+

Back

ECF shift of [K+]

Front

what effect does inorganic acidosis have on [K+]

Back

> 10

Front

in the absence of aldosterone related pathology, describe the TTKG in hyperkalemia

Back

1. Cation exchange resins (prevent GI K+ absorption) 2. diuretics 3. dialysis

Front

in a patient w/ hyperK+, how could you remove excess K+?

Back

renal outer medullary K+ channels; luminal membrane of principle cells in the cortical collecting duct

Front

what does ROMK stand for and where can you find them?

Back

ENaC, ROMK

Front

(2) apical ion channels of principle cells of the cortical collecting duct

Back

1. muscle twitches, hyperreflexia 2. EKG changes (wide QRS) 4. low BP 3. abdominal cramping 4. Diarrhea

Front

describe some clinical features of a patient presenting w/ HyperK+

Back

hypoK+ due to extrarenal losses

Front

what does hypoK+ w/ a 24hr U[K+] << 15mmol/day indicate

Back

ICF shift of [K+]

Front

what effect does alkalosis have on [K+]

Back

1. Aldosterone 2. High distal Na+ delivery 3. High urine flow rate (washout) 4. High [K+] in tubular cells 5. Metabolic Alkalosis

Front

(5) physiologic factors that stimulate distal K+ secretion

Back

hypoK+ due to renal loss

Front

what does hypok+ w/ a 24hr U[K+] >> 15mmol/day indicate

Back

1. Transcellular shifts (minutes) 2. Renal Excretion (hrs)

Front

2 mech of K+ balance

Back

15mmol/day

Front

what is a normal 24hr u[K+] (mmol/day)

Back

marked leukocytosis or thrombocytosis

Front

consider pseudohyperK+ in patients w/ .....

Back

low total body K+ (serum [K+] may be w/in normal range due to compensatory transcellular shifts)

Front

describe the total body K+ in a patient w/ DKA (diabetic ketoacidosis)

Back

inc Na/K ATPase activity

Front

what effect does Insulin have on Na/K ATPase

Back

administer IV CaCl2 (gluconate)

Front

if EKG changes are present in a patient w/ HyperK+, how would you stabilize membrane excitability?

Back

AG = ([Na+])-([Cl-]+[HCO3-]) = 10 mEq/L

Front

how is Anion Gap calculated? what is a normal anion gap?

Back

ECF to ICF

Front

insulin effects a transcellular shift of K+ from to _

Back

1. Metabolic Acidosis 2. Hyperglycemia 3. B-blocker 4. Digitalis (Na/K ATPase inhib) 5. cell lysis

Front

what are some (5) pathophys that effect an ECF shift of [K+]

Back

AD inherited mut 16p13 effecting ENaC upregulation (pseudohyperaldosteronism)

Front

describe Liddle Syndrome

Back

1. Insulin (preceded by glucose) 2. B2 agonist (albuterol) 3. NaHCO3 (if acidosis assocd HyperK+)

Front

in a patient w/ HyperK+, how would you increase ICF [K+] shift?

Back

ENaC blockers

Front

what class of diuretic are Amiloride and Triamterene

Back

Alkalemia, Insulin, B-agonist

Front

3 pathophys that effect hypoK+ via [K+] ICF shift

Back

little to no reabsorption

Front

what does a high FE indicate

Back

proper renal function in the presence of hyperK+

Front

what does hyperK+ w/ a high FEK+ indicate

Back