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CardioPulmonary Vascular Disease > CVD & Electrolyte Imbalances > Flashcards

CVD & Electrolyte Imbalances Flashcards

1
Q

Where in the body is ADH produced & secreted

A

produced by magnocellular neurons in the hypothalamus; secreted by the posterior pituitary gland

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2
Q

ADH drives sodium & water reabsorption along which parts of the nephron?

A

TAL & CD

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3
Q

Hypernatremia is clinically defined as what?

A

Serum Na concentration > 145 mmol/L

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4
Q

What are the 3 main causes of Hypernatremia?

A

Diabetes Insipidus; Inadequate bodily fluid volume; hyperglycemia

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5
Q

How does hyperglycemia cause hypernatremia?

A

at high concentrations, glucose can act as an osmotic diuretic and trap free water in the lumen to be excreted through urine

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6
Q

What is the mechanism of Dehydration-induced Hypernatremia?

A

Hyperosmotic plasma relative to the renal luman; hyperosmotic urine

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7
Q

How does nephrogenic diabetes insipidus affect urine osmolarity?

A

the urine osmolarity does not change and will stay the same even if the water deprivation progresses

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8
Q

What are secondary causes of hypernatremia?

A

orthostatic hypotension; pneumonia; tachycardia

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9
Q

What is the drug of choice to treat central diabetes insipidus?

A

desmopressin

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10
Q

What drugs are 1st line for management of nephrogenic DI?

A

Thiazides; amiloride

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11
Q

What diseases have strong correlation w/ nephrogenic DI?

A

amyloidosis; sarcoidosis; SLE; malignancy; PKD; V2-receptor defects

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12
Q

How is hyponatremia clincialy defined?

A

serum Na concentration < 135 mM

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13
Q

What recreational drug has been shown to cause acute hyponatremia?

A

MDMA (Ecstasy)

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14
Q

How is factitious hyponatremia clinically defined?

A

Plasma osmolarity > 295 mOsm/Kg

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15
Q

What causes factitious hyponatremia?

A

hyperglycemia & mannitol; dilution of serum Na via osmosis

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16
Q

If a pt. has normal plasma osmolality but is hyponatremia what causes would be at the top of your DDx?

A

hyperproteinemia; hyperlipidemia;l bladder irrigation; pseudohyponatremia b/c Na serum con. is being displaced by increased occupancy of lipids and proteins both of which do not contribute to plasma osmolality

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17
Q

How is true hyponatremia clinically defined?

A

plasma osmolality < 280 mOsm/kg

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18
Q

What is happening with Hypotonic Hypervolemic Hyponatremia?

A

volume overload causes ECF to be hypotonic relative to the ICF; therefore water is going to move from the ICS to the ECS causing edema

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19
Q

What are the main causes of hypotonic hypervolemic hyponatremia?

A

CHF (decreased renal perfusion from low CO), Cirrhosis (vasodilation), Nephrotic syndrome (hypoalbuminemia), renal insufficiency (impairment of free water excretion)

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20
Q

What can cause hypotonic hyponatremia when ECF volume is normal?

A

SIADH, hypothyroidism; adrenal insufficiency

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21
Q

What are the clinical hallmarks of adrenal insufficiency?

A

hypotension or normal BP; skin hyperpigmentation (elelvatd MSH stimulates melanin synthesis in epidermal melanocytes) hyperkalemia (almost always due to hypoaldosteronism)

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22
Q

How do diuretics affect volume of the ECF?

A

decreases ECF volume

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23
Q

How will Insensible Loss & diaphoresis affect ECF?

A

it will decrease ECF

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24
Q

Secretory Diarrhea is caused by what pathogen and how will it affect the ECF volume?

A

cholera; will decrees ECF volume

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25
Q

normal plasma osmolarity is clinically defined as what?

A

Plasma osmolality: 280-295 mOsm/kg

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26
Q

What causes Plasma osmolality to be high and hyponatremic?

A

serum sodium levels are being diluted via reabsorption of water through the nephrons

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27
Q

what causes plasma osmolality to be normal and hyponatremic?

A

when molecules that do not participate in osmosis are increased in serum causing pseudohyponatremia

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28
Q

what causes plasma osmolality to be low and hyponatremic?

A

polydipsia & polyuria

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29
Q

Increased plasma volume of a substance not contributing to plasma osmolality is assoc. w/ what type of hyponatremia; what are common causes?

A

pseudohyponatremia: plasma level is normal; causes: proteinemia, hyperlipidemia, & bladder irrigation

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30
Q

Increased thirst causing water intoxication which overwhelms the body’s capacity to excrete water; this is characteristic of which type of hyponatremia?

A

true hyponatremia caused by primary polydipsia and urine osmolality < 100 mM

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31
Q

Increased plasma osmolarity induced by a substance drawing water out of the cells is characteristic of what type of hyponatremia and what causes would be at the top of your DDx?

A

factitious hyponatremia; causes: hyperglycemia

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32
Q

What type of hyponatremia is assoc. w/ the following characteristics:
decreased oncotic pressure resulting in markedly increased vasodilation and decreased arterial blood volume

A

Hypotonic Hyponatremia assoc. w/ cirrhosis

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33
Q

What type of hyponatremia is assoc. w/ the following factors:
a primary defect in NaCl reabsorption int he medullary TAL

A

hypotonic hyponatremia induced by sodium wasting syndrome; Parameters: decreased ECF & urine osmolaity > 100 mmol/L & Urine Na > 20 mmol/L

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34
Q

Describe the mechanism of Cerebral Edema?

A

rapid decrease in plasma osmolality drives water into the surrounding tissues; this causes tissue volume overload and edema to occur

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35
Q

What structure in the brain is most affected by cerebral edema?

A

the pons

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36
Q

How is the brain going to respond to cerebral edema and why is this important to consider in clinical settings?

A

The body’s natural response is going to be to drive osmolytes out of the tissue and back into the plasma causing acute hypernatremia to occur; therefore if hyponatremia is corrected too fast w/ IV hypertonic saline, then this can lead to osmotic demyelination syndrome

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37
Q

What symptoms are associated w/ osmotic demyelination syndrome?

A

quadriparesis, diplopia, loss of consciousness

38
Q

Mild-moderate hyponatremia is clinically defined how and what are common symptoms?

A

Mild: 130-135; Moderate: 121-129; HA nausea, fatigue

39
Q

Severe hyponatremia is clinically defined how and assoc. w/ what symptoms?

A

<120 meq/L; seizures, coma, respiratory arrest

40
Q

What is the appropriate treatment for mild and severe hyponatremia?

A

isotonic saline; do not correct Na > 10 meq/L in a 24 hr. period

41
Q

what medications are appropriate for treating SIADH?

A

vasopressin receptor antagonists; furosemid; salt tablets

42
Q

The world health organization recommends a daily potassium intake of how much?

A

3510 mg/day

43
Q

what tissue in body stores the most potassium?

A

skeletal muscle

44
Q

Hyperkalemia is clinically defined by what parameter?

A

> 5 mmol/L

45
Q

What are the main causes of hyperkalemia?

A

rhabdomyolysis; hemolysis; burns; strenuous exercise; sepsis; hypertonicity; insulin deficiency; metabolic acidosis

46
Q

What drugs can induce hyperkalemia?

A

digoxin; BBs; succinylcholine; arginine; K-sparing diuretics

47
Q

What is the mechanism of strenuous exercise-induced hyperkalemia?

A

Constant Repetition of APs to maintain muscle contraction will cause excessive efflux of K

48
Q

What cautions concerning strenuous exercise should you counsel a pts. with h/o CVD?

A

Right after exercise there will be a rapid drop in serum K to replenish K stores in skeletal muscle tissues which puts everyone with or without h/o CVD at increased risk for arrhythmias & cardiac arrest but more so for those w. h/o CVD

49
Q

What are drugs that decrease K excretion?

A

ACE inhibitors; trimethoprim; NSAIDs; spironolactone; triamterene; pentamidine

50
Q

what diseases are assoc. w/ hyperkalemia?

A

End stage AIDS, Diabetic nephropathies; Sickle cell disease, metabolic acidosis; cirrhosis

51
Q

EKG should be considered for hyperkalemia if serum levels exceed what parameter?

A

K > 6 mEq/L

52
Q

What types of arrhythmias are assoc. w/ hyperkalemia?

A

sinus bradycardia, sinus arrest; VTach & V. fib.; Asystole

53
Q

What are different interventions that can be applied in severe cases of hyperkalemia?

A

intravenous Ca; Insulin and glucose; Inhaled Beta agonists; sodium bicarbonate (more appropriate for metabolic acidosis); hemodialysis

54
Q

What affect does exogenous Ca have on the heart?

A

stabilizes myocyte membranes by slowing down conduction

55
Q

What effects do insulin and beta agonists have on the heart?

A

displaces K from myocytes

56
Q

What drugs are used to decrease to K serum?

A

Patiromer (Veltassa) bind K+ in GI lumen increasing its excretion; Sodium Zirconium cyclosilicate; Kayexalate (Na polystyrene sulfonate) exchanges plasma K for lumenial GI Na

57
Q

What are some of the causes of Hypokalemia?

A

Type IV renal tubular acidosis; metabolic & respiratory alkalosis; licorice; Cushing Syndrome; hyperaldosteronism; thyrotoxicosis

58
Q

How are extrarenal vs. renal induced hypokalemia discerned?

A

24 hr. Urine: <30 mmol (extrarenal); > 30 mmol (renal)

59
Q

A urine K to creatinine ratio higher than 13meq/g indicates what?

A

renal potassium wasting

60
Q

What does the transtubular potassium gradient assess?

A

values > 2 indicate renal loss; values < 6 indicate inappropriate renal response to hyperkalemia

61
Q

Unlike TPP, FHPP typically presents at ages younger than 20 and what else?

A

not caused by hyperthyroidism; genetic autosomal dominant inheritance pattern

62
Q

what drugs are typically first line for hypokalemia in pts. w/ comorbidities?

A

ACE inhibitors; ARBs; BBs; Potassium sparing diuretics

63
Q

what is the most appropriate treatment for hypokalemia in non-urgent situations/

A

oral potassium 40 - 100 mmol/day

64
Q

the majority of free ionized Ca is flittered through which part of the nephron?

A

PT; followed by TAL and then Distal nephron; 70;20;15

65
Q

What specialized receptors on Parathyroid gland cells can sense changes in serum Ca levels?

A

CaSRs

66
Q

How does PTH act on the GI to increase Ca reabsorption?

A

promotes synthesis of calcitriol (Vitamin D) which enhances Ca absorption

67
Q

Of all the Ca in luminal GI, the vast majority of it is reabsorbed where along the GI tract and via which receptors ?

A

duodenum & jejunum; through TRPV6

68
Q

How does PTH increase Ca reabsorption through the kidney?

A

increases distal nephron reabsorption of Ca through TRPV5 receptors

69
Q

How does PTH work on bone to increase Serum levels of Ca?

A

increases osteoclast activity

70
Q

How does Vitamin D increases Ca reabsorption through the nephron?

A

stimulates TRPV5 receptors in DCT & CD

71
Q

Describe how the mechanism of Ca self regulation works.

A

Ca ions can directly influence renal Ca reabsorption via CasR in all segments of the nephron

72
Q

Hypercalcemia induced by excess Ca intake is referred to as what?

A

Milk alkali syndrome

73
Q

What is the mechanism for sarcoidosis induced hypercalcemia?

A

increased endogenous production of Vitamin D: hypervitaminosis D

74
Q

what are the parameters for mild, moderate, & severe hypercalemia?

A

Mild: 11-11.5 mg/dL usually asymptomatic; Moderate: 12-14 mg/dL fatigue & muscle weakness; severe: > 14 mg/dL assoc. w/ neruopsych deficits, GI complications, & nephrolithiasis, shot QT syndrome, bradycardia

75
Q

What is mechanism for familila hypocalciuric hypercalcemia?

A

autosomal dominat; inactivates CaSRs in parathyroid gland thus increases the Ca amount to respond to high Ca

76
Q

What are appropriate treatments for mild to moderate cases of hypercalcemia?

A

calcitonin; bisphosphosphonates (inhibit Osteoclast mediated bone resorption); glucocorticoids: decreases synthesis of Vit. D.

77
Q

What are the common clinical manifestations of hypocalcemia?

A

Tetany: trosseau’s sign (carpal spasm), Chvostek’s sign (facial nerve tap elicits contraction of ipsilateral facial muscles); seizures; papilledema

78
Q

What are the main causes of Hypophosphatemia?

A

hyperparathyroidism; Vit. D deficiency; Rickest & osteomalacia asso. w/ renal phosphate wasting; fanconi syndrome; diarrhea, antacids; respiratory alkalosis; increased insulin secretion

79
Q

What does a 24 urine collection indicate?

A

Ph secretion < 100 mg (intestinal dysfunction); >100 mg: reduced renal absorption

80
Q

what are common causes of acute hyperphosphatemia?

A

tumor lysis syndrome; rhabdomyolysis

81
Q

What is a unique clinical manifestation of hyperphosphatemia?

A

pulmonary & cardiac calcifications

82
Q

How can hyperphosphatemia be treated?

A

Volume expansion will promote renal excretion; antacids will cause chelation limiting absorption in intestine; hemodialysis

83
Q

what part of the nephron reabsorbs the majority of Mg?

A

TAL; this is the one exception in which the PT is not the main player

84
Q

How does PTH affect magnesium serum levles?

A

it increases renal reabsorption

85
Q

what can impair magnesium reabsorption?

A

hypercalcemia due to activation of CaSR which decreases Mg reabsorption

86
Q

What are the main causes of intestine induced hypomagnesemia?

A

diarrhea; proton pump inhibitors; mutations to the renal and intestinal TRP receptors

87
Q

What are genetic diseases that cause hypomagnesemia

A

Glitelman syndrome: mutation of NCC channels
Barter’s syndrome: mutataed channel varies w/ each phenotype
autosomal recessive renal hypomagnesemia w/ hypocalcemia: mutation of TRVP6 receptors in small intestine

88
Q

what are drugs that can induce hypomanesemia?

A

loop & thiazide diuretics inhibit Mg reabsorption; Amphotericin B, aminoglycosides

89
Q

What is commonly given for reversing torsades de pointe?

A

IV magnesium

90
Q

If a pt’s K serum level is b/t 5.5 & 6.5 what would you expect to see on an EKG?`

A

peaked t-waves and QT interval shortening

91
Q

If a pt’s K serum level is b/t 6.5 & 7.5 what would you expect to see on an EKG?`

A

first-degree AV block, QRS widening, PR interval prolongation

92
Q

If a pt’s K serum level is >7.5 what would you expect to see on an EKG?`

A

Flattened or absent p-waves

CardioPulmonary Vascular Disease (7 decks)

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