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Urogenital Pharmacology > Electrolytes And Acid Base Disturbance > Flashcards

Electrolytes And Acid Base Disturbance Flashcards

1
Q

Isotonic hyponatremia is caused by……, hypertonic hyponatremia by…..
Their management is…..

A

Hyperlipidemia
Hyperglycemia
Treat the cause

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2
Q

Describe initial management of hypotonic hyponatremia

A

Either:
1. Infuse 3% saline (1 to 2 mEq per kg per hr) the goal is inc by 6-8mEq per L. Consider desmopressin
2. Single IV bolus of 100 to 150 mL 3% saline over 20 minutes, with goal of inc Na by 2 to 3 mEq; check Na every 20 min, may repeat bolus if symptoms do not resolve.

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3
Q

Usually symptoms of hypotonic hyponatremia resolve after……

A

4-6 mEq/L inc in Na

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4
Q

When to stop infusion of 3% saline in hyponatremia? What’s next

A

Stop when symptoms improve, serum Na inc 10 mmol/L in total or reaches 130 mmol/L.
Switch to isotonic saline, maintain venous line, determine cause.

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5
Q

What is the rate of correction of hyponatremia?

A

6-10 mEq/L in 1st 24 hrs, less than or equal to 18 mmol/l in 48 hrs

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6
Q

….may be needed in patients with concurrent symptomatic volume overload

A

Loop diretics

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7
Q

Rapid correction of hyponatremia can result in……,its risk factors are…….

A

Osmotic demyelination (central pontine myelinosis)
Liver disease, malnutrition, serum sodium less than 120 mEq/L for more than 48 hrs, development of hyoernatremia during management.

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8
Q

Describe management of hyponatremia >48 hrs if:
1. Hypovolemic
2. Euvolemic
3. Hypervolemic

A
  1. 0.9% solution NaCl to restore blood pressure
  2. Free water restriction, demeclocycline (SIADH), V2R blocker
  3. Free water and Na restriction, loop diuretics, V2R blocker
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9
Q

List drugs inducing SIADH

A

TCA, SSRI, oxytocin, carbamazepine, diuretics, opioids and vincristine

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10
Q

List advetse effects of vaptans

A
  1. Polyuria, thirst, hypernatremia
  2. Safety in hepatic cirrhosis (?)
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11
Q

Define goals of hypernatremia management

A

In acute, correct serum Na at an initial rate of 1-2 mEq/L (for 2-3 hr)(max total: 12 mEq/L)
In chronic, with no or mild symptoms, corrected at a rate not to exceed 0.5 mEq/L/h with a total of 8-10 mEq/d for fear of brain edema (e.g. 160 mEq/L to 152 mEq/L)
The target Na level is 145 mEq/L

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12
Q

What is the type of fluid used in hypernatremia with:
1. Hypovolemia
2. Euvolemia
3. Hypervolemia

A
  1. Isotonic saline before free water administration
  2. Hypotonic fluids (e.g.D5W)
  3. Comination of diuretics & D5W infusion
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13
Q

List causes of hyperkalemia

A

*Inc exit from cells
Digitalis, B2Bs, acidosis, succinylcholine
*Defective renal excretion
Impaired renal func, hypoaldosteronism, K+ retaining diuretics, B1Bs, NSAIDs, ACEI, ARB

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14
Q

List causes of hypokalemia

A

*Inc entry into cells:
Insulin, epinephrine, alkalosis
*Inc K+ loss:
Hyperaldosteronism, K+-losing diuretics, liquorice (renal). Laxatives, severe diarrhea (extra-renal)

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15
Q

Mention precautions of KCl administration

A
  1. Oral K+ has gastric & esophageal irritant effect & should be given with plenty of fluid in sitting position
  2. IV K+ can cause phlebitis & should be given in large veins
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16
Q

Describe management of hyperkalemia

A

-IV Ca used in severe cases, it stabilizes myocardial membrane by opposing effect of hyoerkalemia on membrane potential
-Inc movement inti cells by insulin+glucose OR glucose, B2 agonist nebulizer (salbutamol), IV Na+ bicarbonate which inc influx of K+ (not preferred)
Removal of K+ from body by loop diuretics, cation-exchange resins, dialysis in resistant cases.

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17
Q

Describe mechanism of action of magnesium

A
  1. Natural physiological competitove of Ca: antagonist at L-Ca++ channels
  2. Antagonist of NMDA receptors: analgesic, anticonvulsant & sedatative properties
  3. Interferes with Ach relesae, muscle relaxation
  4. Dec release of CAs after sympathetic stimulus
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18
Q

List indications of magnesium

A
  1. Torasde de pointes & digitalis induced arrhythmia (IV)
  2. Hypomagnesemia associated with MI
  3. Refractory hypokalemia 2ry to hypomagnesemia
  4. Osmotic laxative & antacid (oral)
  5. Seizures in preeclampsia (IV)
  6. Adjuvant in anesthesia: analgesic, sedative
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19
Q

List adverse effects of magnesium

A
  1. Diarrhea, drowsiness, hypotension
  2. Asystole (rapid IV administration)
  3. Tetaogenic: category D (fetal skeletal abnormalities)
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20
Q

Describe management of hypo- & hypermagnesemia

A

Hypo: diet rich in Mg, correct hypocalcemia & hypokalemia + adding K+ sparing diuretics
Hyper: IV Ca++, diuretics, dialysis

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21
Q

List drugs causing hypocalcemia

A
  1. Corticosteroids, tetracycline, iron, quinolones (dec Ca absorption)
  2. Phenytoin, phenobarbital, rifampin (inc vit D metabolsim)
  3. Mithramycin
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22
Q

List steps of management of symptomatic acute hypocalcemia

A
  1. Supportive management (IV fluid replacement, oxygen, monitoring)
  2. Calcium infusion drips should be started at 0.5 mg/kg/hr and inc to 2 mg/kg/hr
  3. Doses of 100-300 mg elemental calcium
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23
Q

Mention calcium preparations & the amount of elemental Ca in each
They are given in…..

A

10 mL calcium gluconate contain 90 mg elemental Ca
10 mL of CaCl contain 272 mg
In 50-100 mL of D5W should be given over 5-10 min

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24
Q

Management of hypoparathyroidism is……., while that of 2ry hyperparathyroidism is……

A

Vitamin D (0.5-2 mcg) calcitriol of 1-alpha-D3
Calcium + vitamin D

25
Q

Drugs which are avoided in hypocalcemia are……..

A

Frusemide (not thiazide), tetracyclines, quinolones, Al antacids, cholestyramine

26
Q

……inc level of PTH &…..is a diuretic avoided in hypercalcemia

A

Lithium
Thiazide

27
Q

List immediate therapy for hypercalcemia

A
  1. Volume expansion with isotonic saline
  2. Salmon calcitonin
  3. Bisphosphonates
  4. Hemodialysis
  5. Prevent recurrence
  6. Disease-specific approach
28
Q

With respect hypercalcemia, Glucocorticoids are used in…….., calcimimetics are used in……..

A

Hypervitaminosis D, sarcoidosis, lymphoma (inc calcitriol)
Parathyroid carcinoma, hemodialysis, 2ry hyperparathyroidism

29
Q

GR: Loop diuretic therapy is not recommended in hypercalcemia

A

Bec of potential complications & availability of drugs that inhibit bone resorption which is primarily responsible for hypercalcemia.

30
Q

List side effects of bisphosphonates

A
  1. Flu-like symptoms (fever, arthralgia, myalgia, fatigue, bone pain) & uveitis
  2. Hypocalcemia, hypophosphatemia, impaired renal function, nephrotic syndrome
  3. Osteonecrosis of jaw & atypical femur fracture
31
Q

Describe management of hyperphosphatemia

A
  1. Phosphate binders
  2. Inc renal excretion by saline + loop diuretics in normal renal function
  3. Manage the cause
32
Q

List the phosphate binders & the risks associated with each

A
  1. Almunium-containing PB: risk of dementia, anemia, osteomalacia
  2. Calcium-containing PB! risk of hypercalcemia
  3. Phosphate binders that contain no aluminum of Ca (Sevelamer)
33
Q

What is the MOA of tenapanor?

A

An inhibitor of Na/H exchanger isoform 3 that acts locally in gut to reduce absorption of Na & PO4- -

34
Q

Describe management of different types of alkalosis

A

1.Chloride-responsive alkalosis: IV isotonic NaCl + KCl, if diuresis is needed: K+ sparing diuretic
2.Cholride responsive metabolic alkalosis: K+ sparing diuretics
3.Specialized therapy in all types:
a. IV HCl in severe metabolic alkalosis (pH more than 7.55) or CI to fluid therapy
b. Dialysis

35
Q

General managemt of metabolic acidosis

A

IV HCO3- 50-100 mmol at a time with monitoring ABG
Dialysis if severe

36
Q

Describe management of renal tubular acidosis

A
  1. Type 1, severe with hypokalemia, treat hypokalemia
  2. Type 2, in PCT with HCO3 loss & hypokalemia: treat K & thiazide
  3. Type 3, aldosterone def or resistance: fludrocortisone
37
Q

Bicarbonate is used in……., its adverse effects are……..

A

Cardiac arrest & metabolic acidosis
Aggravated CHF, Cerebral Hge, edema, hypernatermia, hypocalcemia, hypokalemia

38
Q

When administering bicarbonate monitor…….

A

Potassium & calcium

39
Q

Mention precautions of bicarbonate administration

A
  1. Edematous or Na-retaining states: CHF, renal impairment, cirrhosis, HTN, corticosteroids
  2. May cause hypokalemia
  3. Used cautiously in peotic ulcer & edema
  4. Avoid extravasation (cellulitis, tissue necrosis)
  5. Check compatilibilty before adding drugs
40
Q

Urine moves from kidney to urinary bladder by……

A

Persitaltic waves (contractions)

41
Q

Nerve of micturation is……., describe effects of parasympathetic on urination

A

Pelvic nerve
1. Contraction of bladder wall (mainly trigone)
2. Relaxation of internal urethral sphincter causing emptying of bladder

42
Q

Symapthetic reaches bladder through….., mention its actions.

A
  1. Relaxes the baldder wall
  2. Closure of internal urethral sphincter
  3. Transmits pain sensation through sensory fibers
  4. VC
    Inhbit bladder evacuation
43
Q

IVP is maintained until volume….. then it rises sharply

A

400 ml

44
Q

At volume from 100 to 400 ml, IVP is……

A

10 cm/water

45
Q

Micturation reflex is………
Describe it mechanism

A

Sacral spinal automotic reflex
When the bladder is ditended & IVP inc this causes stimulation of stretch receptors in bladder wall & afferent discharge in parasympathetic nerves that enter the spinal chord in LHCs of S2,3,4.
1. Stimulation of efferent parasympathetic fibers in pelvic nerves leading to contraction of bladder wall & relaxation of internal urethral sphincter.
2. Inhibition of pudendal n. causes relaxation of the external urethral sphincter when starts bladder evacuation
In children it is only spinal mechanism

46
Q

List higher centers controlling micturation

A
  1. Brain stem centers Facilitatory center in pons, inhibitory center in medulla
  2. Centers in cerebral cortex mainly inhibitory
47
Q

Mention how the higher centers control micturation

A
  1. They keep micturation reflex partially inhibited all the time to prevent immediate evacuation of bladder when volume reaches 400 ml the volume at which micturation refkex is initiated in adults
  2. Feeling the desire to micturate when bladder is distended
  3. Sensory signals are sent from bladder wall to higher brain centers which are interpreted as sense if bladder fullness & need to micturate
  4. According to the surrounding conditions the brain can cause either facilitation or inhibition of reflex
48
Q

Mention response of higher centers when conditions are:
1. Suitable
2. Unsuitable

A
  1. Inhibitory cortical impulses continue, thus inhibit micturation reflex, helped by voluntary contraction of external sphincter & pelvic diaphragm. This process is limited till 600 ml then obligatory micturation.
  2. The normal cortical inhibitory effect disappears & micturation reflex is initiated.
49
Q

Describe mechanism of voluntary micturation

A

It can be voluntary initiated by relaxation of pelvic floor & perineal muscles and contraction of abdominal muscles which help expulsion of urine by inc intra-abdominal pressure.

50
Q

Describe cause & pathophysiology of atonic bladder

A

Destruction of sensiry nerve fiber from urinary bladder to spinal cord or interruption of sacral dorsal nerve roots as in tabes dorsalis
Prevent transmission of stretch signals from bladder, loss of urinary bladder sensation & loss of micturation reflex, bladder fills to a capacity and overflows a few drops at a time (overflow dribbling = retention with overflow)

51
Q

Describe cause & pathophysiology of automatic bladder bladder

A

It occurs if spinal cord is cut above sacral region as in spinal cord transection
There is disconnection of sacral micturation center from brain & micturation reflex still occurs but no longer controlled by brain (loss of voluntary control), refkex evacuation as soon as it reaches a critical capacity.

52
Q

List causes of AKI

A
  1. Severe reduction GF due to prerenal cause (acute curculatory failure), postrenal (complete prolonged obstruction of urethra or both ureters), renal (acute & rapidly progressive glomerulonephritis)
  2. Acute failure of tubular epithelium: acute tubular injury, acute papillary necrosis, acute pyelonephritis.
53
Q

What are effects of AKI

A
  1. Anuria or oliguria
  2. Generak edema & HTN due to salt & water retention
  3. Metabolic acidosis due to failure of excretion or secretion of H+ resulting from metabolism
  4. Inc level of urea, uric acid, creatininem phosphate, potassium
54
Q

GR: Occurrence of the following with CKD
1. Polyuria
2. Isothenuria
3. HTN
4. Osteomalacia

A
  1. Due to dec concentrating power of kidney
  2. Due to failure of concentrating & diluting mechanisms of the kidney
  3. Due to salt & water retention, inc renin secretion & inc Ang II.
  4. Dec formation of calcitriol dec intestinal absorption & its availability to bones, inc phosphate due to dec GFR & inc binding of phosphate with Ca in plasma.
55
Q

Terminal stage of CKD causes……

A

Uremia, uncompensated acidosis, coma & death

56
Q

Extra-renal pathological changes in kidney failure include:

A
  1. Fibrinous pericarditis & pleurisy
  2. Uremic pneumonitis
  3. Enterocolitis with ulceration
57
Q

Describe mechanism of peritoneal dialysis

A

Patient abdomen is filled & drained several times a day with a dialysis solution through a tube implanted in the abdomen. The body’s peritoneal membrane allows waste products & extra fluid to pass from blood to dialysis solution, then this solution is drained from abdomen.
This method is old & has many disadvantages

58
Q

Describe mechanism of hemodialysis

A

Blood is removed from the body & filtered through a membrane called a dialyzer or artificial kidney then filtered blood is returned to body. Patients with acute RF require treatment for only few days or weeks while chronic require it for life or until transplantation. Such patients undergo dialysis several times a week.

Urogenital Pharmacology (6 decks)

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