Hypokalemia causes (Dr.

Fazaar)

decreased K intake

stool, urine, sweat

increased K loss

gastro urinary skin plasmapheresis and dialysis

K translocation (or redistribution)

High Insulin activate sodium potassium pump so alot of the potassium moves in to the cell.

HIgh beta adrenergic activtiy (like stress, myocardial infarction, headtrauma) that will move potassium
into the cell

Albuterol, dobutamine, terbutaline

Hypothermia

ALKALOSIS

hypomagnesemia

genetic disorder (barter, gitelman and liddle syndrome)

drugs (antipsychotics, fungal)

intoxication (heroine, barium)

measurement problem

if >30 mmol/day - renal disease

<30 mmol/ day -diarrhea

Spot urine analysis

- potassium/creatine = >1.5 =kidney problem if ,1.5 no kidney problem

Low potassium in blood, high in urine and acidosis = diabteic ketoacidosis or renal tubular acidosis

Low potassium in blood, high in urine and and alkalosis= diuretics, primary aldosterinism, gitelman
syndrome, bartter syndrome, renovascular disease

if no kidney problem

Low potassium in blood, low in urine and acidosis = diarrhea

Low potassium in blood, low in urine and alkalotic= vomiting

Symptoms

-muscle weakness

-heart problem

Hypokalemia (Osmosis)

-ICF(98%, 150 mEq/L)

- ECF (2%, 4.5 mEq/L)

electrochemical gradient >>>>> sets resting membrane potential >>> needed for contraction of smooth,
cardiac & skeletal muscle

External K balance

-excrete most of whats taken in

kidney 9most)

gi tract sweat

External Balance shift - increase K excretion results to decrease in blood

-intake

Low intake (anorexia, prolonged fasting, specific diets)

Excretion

- 67% reabsorbes in PCT, 20% thick ascending limb

-alpha intercalated cells - reabsorbs

-prinicpal cells- excrete

-Aldosterone increases number of sodiuam in principal cells

Primary hyperaldosteronism- less K is retined more excreted

Loss of GI secrections

-due to vomiting and diarrhea

vomiting- direct losses of K is minimal but the stomach acid lost will result to metabolic alkalosis
Diarrhea -more lossess

Internal balance shift - K moves into the cells

- Excess insulin -insulin activate sodium potassium pump

-alkalosis - blood too alkaline (high in pH and decreased hydrogen ion)

-so hydrogen ion will move out from the cell in exchange of K moves in to the cell, resulting to less K in
blood

RESPIRATORY 9because co2 is lipid soluble so no hypokalemia

-ccertain catecholamines (beta 2 adrenergic stimulates Na and K pump; agonists)

(alpha adrenergic stimualtes calcium dependent K channels; anntagonists)

less reactive to stimuli if K is decreased

Diminished contractions of

1. smooth muscle - constipation

2. skeletal muscle - weakness, cramps, flaccid paralysis

3. respiratory muscles0 resouratiry depressiin

4. cardiac muscls

Diagnosis

- low potassium 9,3.5

- electrocardiogram

Treatmenat

noramlike K levels- treat underlying causes

use K sparring

Hyperkalemia
-over potassium of blood

electrochemical gradient >>>>> sets resting membrane potential >>> needed for contraction of smooth,
cardiac & skeletal muscle

External Balance shift (kidney, sweat, GI, diet)

(50-150 mEq/l consume diet)

-decrease k excretion - inceasesd in blood

potassium is excreted in the renal tubule

Internal Balance shift (sodium potassium pump)

3 sodium out; 2 K in

-K pulls out of cells results in increased in blood

1. Insulin deficiency= insulin bind in the cell membrane, that will stimulate sodium potassium up

2, Acidosis -too acidosis , higher hydrogen ions and low ph

-exchage hydrogen ions enter cellss and potassium exits the cells

Respiratory acidosis- lipid soluble an Co2 so no hyperkalemia

Metabolic acidosis from organic cells (like ketoacidosis and lactic acid)

3. certain catecholamines

(epi- adrenaline norepi-noradrel

(beta 2 adrenergic stimulates Na and K pump; agonists) not working (HYPOKALEMIA) (Beta blockers or
beta 2 adrenergic antagonist)

(alpha adrenergic stimualtes calcium dependent K channels; antagonists) so more K moves out of the
cell (HYPERKALEMIA) (alpha adrenergic agonist)

4. Hyperosmolarity - water pulls out to the interstetial cells that increases the K concentration then
moves out to the cell

5. Cell lysis -severe burns, rhabdomyolysis, tumor lysis

cell dies and K will be out of the cell

6. Exercise strenous - cell works harder uses atp

-K channels open letting K go out to the cell

External

Repid, excessive intake

-intravenous fluids

-usually involves kidney

-unable to produce aldosterone (damo an aldosterone, increases sodium potassium pump)

more potassium then stimulate

addisson and hypoaldosteronism

drugs that can also decrease aldosterone

1. renin inhibitors

2. ace inhibitos

3. Angiotensisn II receptor antagonist

4. Selective aldosterone inhibitors /blocker

5. potasssium sparing inhibitors (

Acute kidney injury

-low glomerular filtration rate

-oliguria (<30ml/hr)

-hyperkalemia

-low na and high K in blood

results to intestinal cramping

Skeletal muscles

-weakness

-flaccid

Cardiac muscle

Diagnosis

- K in blood >5.5
-ECG peakd t wave st segmet depression, short QT interval

severe - prolonged pr interval, absent p wave, wide QRS complex

Treatment

-calcium - stabilize myocardial cell membrane

-insulin, glucose, B adrenergic agonists and sodium bicarbonate - swift K+ into the cells

-resins that bind K--- K elimination in GI tract (thru feces)

-potassium- wasting diuretics ---- K elimination in kidneys

- dialysis

-IV calcium gluconate - counteract the result of potassium ( excitability

Kayexalate (oral or enema) - release sodium and absorb potassiium for excretion thru feces

Hypocalcemia

-primarily stored in the skeletal system (99%)

0.99% Ca- ECF 0.01 ICF (organelles, mitochondria, smooth endoplasmic reticulum)

-more in ECF than ICF

-it is release whenever it is needed

-has inverse relationship with phosphate (Mg friend)

-has a sedative effect on nerve cells

-regulates muscles contraction and relaxation

-needed in blood clotting

-activates enzymes that stimulate chemical reaction

Calcium functions

Builds strong bones and teeth

Clotting of blood

Sends and receives signals

Squeezes and relaxes muscles

Releases hormones

Keeping a normal heartbeat

IONIZIED (not attached in proteins)

Bound (half) combined with protein

Complex (non protein substances) like citrate

Total calcium level – 2.12- 2.62 mmol/L

Calcium food sources

-yogurt

-buttermilk

-cheese

-milk

-broccoli

-mustard green

Regulatory Mechanism

- Parathyroid hormone (increasing the level of Ca)

- Calcitonin (thyroid hormone) decreasing the level of Ca
- Calcitroil (a metabolite of vit D) absorption of CA

HYPOCalcemia

-low calcium blood

<8.5 mg

-ion with 2 charge

-abundant metal in body

-calcium phosphate (hydroxyapatite)

High ICF ca – apoptosis programmed cell death

-ligand-gated –most cells –controlled by hormones and neurotansmitter

Voltage gated- muscle and nerve cells and controlled by electric membrane

Exit :

Atp dependent ca pump

And na and ca exchange

ECF

-diffusible

-not diffi

Diffusible – small; can easily pass thru membrane

-free ionized – neuron action potential, muscle contraction, hormone secretion blood clotting

-complexed- (bound to non protein) calcium oxalate small anion

-electrically neutral and not useful cellu

Not diffusible (large)

-albumin (too large not involve in cecullar)

Receptor Parathyroid cell (calcium sensing receptor)–makadto sa PTG- PTH –

Bones - release Ca – to the blood

kidney reabsorbs ca – caltriol

Gi absorb CA

2 Determinants – low ph, protein levels

Albumin has acidic amino acidic.

Glumate and aspartate – carboxyl group

Alkalosis- high ph – few protons ( less hyrdrogen ions)

More bound and less free ionized

Hypoalbuminea or false hypocalcemia- less bound; same free ionized hormonally regulated

Less ca entering the blood (HypoPTHoidsm ) surgical removal or autpommune destruction, congenital
def, and mg def

Low vit d- def diet malab, cirrhosis lack

Too much excretion of blood- kidney failure, ca excreted in urine

Tissue injury- burns, rabdomyolysis and tumorlysis; nagiging insoluble

Other inflamm- acute pancreatitis

Hypocalcemia- too many blood transfusions; Citrate and EDTA( ethylene diamine tetraacetic acid)

Neuron- resting state of sodium channel stabilized by CA

- Low ca and na channels unstable and cell depolarizes more easily and cell more excitable

Results to

-tetany- involuntary muscle contration

-chvosteks sign

Trousseau sign

Diagnosis

-low ca in blood <8.5

-EC prolonged ST segment prolonged Qt Arrythtmia

Lab test

Treatment- normalize Ca, calcium gluconate

-High parathyroid hormone secretion

-low parathyroid

Ca 2.12- 2.62 mmol

Bound to albumin + free (most important)

Nephrotic syndrome - proteins are secreted from the kidney

Malnutrition - not eating enough proteins

High PTH -secreted in PT gland, regulate calcium level

- try to increase Ca to normal level

HIGH PTh secondary hyperparathyroidsim (HIGH PTH

- vit D deficiency

- renal disease

-acute pancreatitus

-acute respiratory alkalosis

-sepsis

Low PTH - hypaPTH

-surgery

-thyroidectomy

-radical neck dissection

-surgery

-autoimmune diseases

-HIV

-genetic diseases (diGeorge syndrome)

-hypomagnesemia

-Medications (Biphosphonates and denosumab) side effect low amount of ca in the blood

Phenytoin- epileptic drug

Cisplatin- common cause hypomagnesimea

Foscarnet- herpes

Chelators- citrate (binding calcium)

PTH - to increase calcium; activate kidney para sa Vit D

-distal tubule in kidney (PTH) does not allow Ca to be excreted (hence ca stay in the body)

- Calcitriol (active form of vit D) absorbs in the intestine that is important in absorption of Ca

- VIT D (food, sun)

loss of Albumin 1g/dl =0.2 mmol/L

Symptoms

Acute

chronic

Acute= Dangerous common

muscle, nerves

-tetany

- chvostek sign contraction of facial muscles provoked by lightly tapping over the facial nerve anterior to
the ear as it crosses the zygomatic arch

-trousseau sign - by placing a blood pressure cuff on the patient's arm and inflating to 20 mm Hg above
systolic blood pressure for 3-5 minutes abduction and reflexion

-perioral lip twitching/ spasm

-paresthesia

-muscle weakness and spasm

-laryngospasm

-bronchospam

-ground mal, petit mal, focal

-high speak in EEG

heart -Qt prolongation

-papilledema (eyes)

Chronic

-calcific deposition (parkinsons, dementia, ectopic calcifaction, very dry skin, cataract)

Treatment
Hypocalcemia treatment

With no sysmptom but acute drop of Ca free < 0.8 mmol, QT prolongation

No Syomtoms >0.8 mmol Calcium carbonate 1500mg

-IVF - tetany, carpopedal spasms and seizures, sudden hypocalcemia

1g calcium gluconate (90mg of elemental calcium) put it in 50 ml 5% glucose in 10 mins increase in 3hrs
until stable if not slow continuous ca infusion, 1mg/kg/hr

orally (no symptom) calcium carbonate (1500mg)