urinary

Question 1

1. Define obstructive uropathy.

Answer 1

Anatomic changes in the urinary system caused by obstruction

Question 2

2. Be familiar with causes for obstructive uropathy.

Answer 2

Kidney stones, compression from a tumour, inflammation

Question 3

3. Describe the two most damaging effects of urinary tract obstruction.

Answer 3

Stasis of urine, with increases possibility of infection and stone formation

Progressive dilation of the renal collecting ducts and tubules (hydronephrosis) (glomerular filtration continues, so pressure builds up, first in renal pelvis, and then in tubules)

Question 4

4. Describe compensatory hypertrophy and hyperfunction.

Answer 4

If one kidney is obstructed, the body can compensate: in the unobstructed kidney the size of individual glomeruli and tubules is increased, (but not the total number of functioning nephrons). In this way, the unobstructed kidney can make up for the reduction in function of the obstructed kidney

Question 5

5. Define “calculi”.

Answer 5

Kidney stones

Question 6

6. What are the most common kidney stones composed of and where can they be located?

Answer 6

Calcium salts (oxalate or phosphate) due to factors including high urine calcium, caused by hyperabsorption of calcium from the intestines or hyperparathyroidism

Question 7

7. What are 2 disorders that can lead to the formation of calcium oxalate or phosphate kidney stones?

Answer 7

Hyperabsorption of calcium from the intestines or hyperparathyroidism

Question 8

9. Describe the two types of pain that can be experienced as a result of kidney stones and give the probable location of the stone for each type of pain.

Answer 8

Renal colic – excruciating pain in the flank and abdomen caused by a 1-5 mm stone moving into the ureter and stretching it

Dull, deep, mild to severe ache – in flank or back caused by a stone in the renal pelvis or calyces

Question 9

10. Know the term renal colic.

Answer 9

Type of pain you get when urinary stones block part of your urinary tract

Question 10

11. How are urinary calculi treated?

Answer 10

Removing stones, managing pain, reduction of further formation through increasing fluid flow and altering diet

Question 11

12. To what is lower urinary tract obstruction primarily related?

Answer 11

Storage of urine in the bladder or emptying of urine through the bladder outlet

Question 12

13. Describe neurogenic bladder – what does the type of dysfunction depend upon?

Answer 12

Bladder dysfunction caused by neurologic disorders. The type of dysfunction (whether incontinence or functional obstruction) depends upon where damage has occurred in the nervous system

Question 13

14. Name two physical obstructions of the lower urinary tract.

Answer 13

Scarring of the urethra (infection, surgery) & enlarged prostate

Question 14

15. Define glomerulonephritis. What is the most common contributing factor?

Answer 14

Inflammation of glomerulus caused by immunologic responses, infection, diabetes mellitus

Hypertension

Question 15

16. Identify the two common immune mechanisms that can lead to glomerulonephritis, and a common disease that is associated with each.

Answer 15

Type 2 (antibody reacting against antigen within the glomerulus – goodpasture syndrome)

Type 3 (deposition of circulating antibody/antigen complexes into the glomerulus – post streptococcal glomerulonephritis)

Question 16

17. Describe the series of steps in the development of glomerulonephritis as caused by these immune mechanisms.

Answer 16

Antibodies activate complement proteins, which summon macrophages and neutrophils, which secrete compounds that damage the glomerular cells. This increases glomerular permeability, which allow proteins and RBC to escape into filtrate. Proteinuria and/or hematuria develops

Question 17

18. Define: glomerular filtration rate. How is it usually estimated?

Answer 17

Production of filtrate by the glomerulus

Perfusion of the kidney, state of the tubules, post-kidney obstruction, insulin

Question 18

19. Describe nephritic syndrome, naming the disorder that is the usual cause.

Answer 18

Sudden excretion of blood cells, protein, diminished GFR, oliguria

Caused by inflammation that blocks the glomerular capillary lumen and damages the capillary wall (associated with postinfectious glomerulonephritis)

Question 19

20. Describe nephrotic syndrome, naming a disorder that can be the cause.

Answer 19

Massive proteinuria: excretion of 3.5 g or more of protein/day in urine, lipiduria

Hypoalbuminemia, edema (hallmark manifestation), hyperlipidemia

Result is a group of manifestations that includes thrombotic complications, increased risk of infection

Caused by increase in glomerular permeability (injury to podocytes), as a result of specific diseases (diabetes mellitus, SLE, minimal change disease)

Question 20

21. Define BUN – identify and explain the two facts that it reveals about the state of the kidney.

Answer 20

Blood urea nitrogen: concentration of urea in the blood

Glomerular filtration (because urea is filtered at the glomerulus, as the amount of blood that is filtered drops, BUN rises) & urine-concentrating capacity (because urea is reabsorbed from the nephron, if flow through nephron slows down, tubule is able to reabsorb more urea back into the blood)

Question 21

22. Identify and explain the one fact that the level of creatinine in the plasma reveals about the state of the kidney

Answer 21

Plasma creatinine concentration: creatinine is produced by the muscles, is filtered at the glomerulus, and never reabsorbed. Therefore, the plasma creatinine concentration only indicates the amount of filtration that is occurring at the glomerulus (GFR). If the glomerular filtration rate decreases, the plasma creatinine concentration increases

Question 22

23. Define AKI (include BUN and plasma creatinine), including whether it is reversible.

Answer 22

Sudden (less than two days) decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood (increased BUN and plasma creatinine)

Unlike chronic kidney disease/failure, it is potentially reversible, if can correct the cause before permanent kidney damage has occurred.

Question 23

24. What do the letters in “RIFLE” represent in terms of acute kidney injury?

Answer 23

: Risk – Injury – Failure – Loss – End stage disease

Question 24

27. List the 3 causes of AKI – identify the most common one.

Answer 24

Prerenal acute kidney injury (most common)

Postrenal acute kidney injury

Intrarenal acute kidney injury

Question 25

28. What is prerenal AKI caused by? Be familiar with conditions that could lead to this.

Answer 25

– the decrease in GFR is caused by renal hypoperfusion Lowered perfusion may be due to renal vasoconstriction, hypotension, hypovolemia, hemorrhage or inadequate cardiac output. – Some drugs that cause intense vasoconstriction in kidney can also lead to AKI

Question 26

29. Why is the ratio of BUN to creatinine in the serum higher than normal with prerenal AKI (hint: remember that urea is also absorbed in the nephron, and slowing down the rate of flow of filtrate through the nephron would increase this rate of absorption …)

Answer 26

urea increases disproportionately to creatinine due to enhanced proximal tubular reabsorption that follows the enhanced transport of sodium and water

Question 27

30. With what does postrenal AKI usually occur? Give an example of one condition that would lead to this.

Answer 27

Usually occurs with urinary tract obstruction that affects both kidneys (e.g., prostatic hyperplasia)

Question 28

31. From what does intrarenal AKI usually result? Be familiar with events/conditions that would lead to this.

Answer 28

Usually results from tubular necrosis as a result of occurrences ischemia associated with prerenal failure Sepsis nephrotoxic effects of drugs, etc. Lower than normal BUN to serum creatinine ratio

Question 29

33. What is vital in the treatment of AKI?

Answer 29

determine and correct the cause of the kidney injury (e.g., improve perfusion, stop toxic drugs, etc.)

Question 30

34. What is the primary goal of therapy for AKI? What 3 areas of concern are addressed? What may finally be necessary?

Answer 30

to maintain life until renal function has been recovered 1. Supplement kidney function 2. Treat infections 3. Maintain nutrition Continuous renal replacement therapy (basically 24 hr hemodialysis) or hemodialysis may be required

Question 31

35. Define chronic kidney disease, and be familiar with diseases/conditions which are risk factors.

Answer 31

A progressive deterioration of kidney function. Not reversible. Defined by kidney damage or a GFR less than 60 ml/min/1.73 m2 (1.73 m2= avg person) for 3 months or longer. (normal ≥90 ml/min) Risk factors associated with CKD include hypertension, diabetes mellitus (these two are the greatest risk factors), chronic glomerulonephritis, obstructive uropathies, etc

Question 32

36. What are the two greatest risk factors for CKD?

Answer 32

hypertension, diabetes mellitus (these two are the greatest risk factors)

Question 33

37. What criteria is used to assess the stage of CKD?

Answer 33

Five stages are recognized, as defined by decreasing GFR, indicating increasing levels of kidney damage, ending in kidney failure (<15 ml/min) (requiring dialysis or transplantation) 1 = kidney damage with normal or increased GFR >> GFR > 90 2 = kidney damage with mild decrease in GFR >> GFR = 60 – 89 3 = moderate decrease in GFR >> GFR 30 – 59 4 = severe decrease in GFR >> 15 – 29 5 = kidney failure >> GFR < 15 or dialysis

Question 34

38. What does the intact nephron hypothesis propose, and what is the significance to the appearance of CKD manifestations?

Answer 34

proposes that the unaffected nephrons are capable of hypertrophy and hyperfunction in their rates of filtration, reabsorption and secretion, in order to make up for the declining GFR symptoms of CKD do not actually become apparent until renal function declines to less than 25% of normal

Question 35

39. Define azotemia.

Answer 35

increased levels of serum urea and other nitrogenous compounds. Can be asymptomatic (depending upon extent).

Question 36

40. Define uremic syndrome (uremia).

Answer 36

the systemic signs and symptoms associated with the accumulation of nitrogenous wastes and toxins in the plasma brought about through kidney failure

Question 37

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: sodium,

Answer 37

Sodium – Ultimately, the kidney loses its ability to regulate sodium and water, and both are retained, contributing to edema (“anasarca” = a general accumulation of fluid in body cavities and tissues) and hypertension.

Question 38

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: potassium,

Answer 38

Potassium – Although initially, the kidney can adapt its potassium excretion to lower GFR, in later stages, potassium is not secreted sufficiently and can increase to life-threatening levels.

Question 39

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: creatinine and urea

Answer 39

Creatinine and urea levels in the plasma increase as GFR decreases

Question 40

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: pH,

Answer 40

Metabolic acidosis: The kidney’s ability to secrete hydrogen ions and reabsorb bicarbonate ions is decreased.

Question 41

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: calcium,

Answer 41

Calcium: less calcium is absorbed from the GIT. WHY??. This is detected by the parathyroid gland, which then increases levels of PTH, which results in loss of calcium from the bone, increasing the risk of bone fracture.

Question 42

41. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: proteins and fat.

Answer 42

Proteins and fat: advanced CKD causes decreases in amount of proteins (loss of muscle mass and serum proteins). There is also a shift in the ratio of LDL/HDL, with more LDL, causing increased atherosclerosis.

Question 43

42. Define anasarca.

Answer 43

A general accumulation of fluid in body cavities and tissues

Question 44

43. Describe the effects (and their causes) on each of the following body systems: cardiovascular

Answer 44

Cardiovascular system – Major cause of death in CKD Excess sodium and water lead to hypertension Excess LDL leads to increased atherosclerosis

Question 45

43. Describe the effects (and their causes) on each of the following body systems: pulmonary

Answer 45

Complications associated with fluid overload Acidosis results in Kussmaul respirations

Question 46

43. Describe the effects (and their causes) on each of the following body systems: hematologic

Answer 46

Anemia (why?), impaired platelet function (possibly due to uremia)

Question 47

43. Describe the effects (and their causes) on each of the following body systems: immune

Answer 47

Overall suppression by high levels of urea and metabolic wastes.

Question 48

43. Describe the effects (and their causes) on each of the following body systems: neurologic

Answer 48

Numerous effects of uremic toxins, including both peripheral and central nervous systems: restless leg syndrome, headache, impaired concentration – with later stages, seizures and coma

Question 49

43. Describe the effects (and their causes) on each of the following body systems: gastrointestinal.

Answer 49

Anorexia, vomiting, possibly due to breakdown of urea by intestinal bacteria. Ulceration and bleeding of GI tract

Question 50

44. Name 4 means to evaluate CKD.

Answer 50

• Elevated serum creatinine and BUN levels • Protein in the urine, particularly albumin • Confirmed by renal biopsy

Question 51

45. Name 4 means to treat CKD.

Answer 51

Management includes dietary control to replace/restrict appropriate factors • Drugs to treat hypertension • Dialysis and renal transplantation

Question 52

1. What are 2 reasons for the necessity of correct pH in the body?

Answer 52

Hydrogen ion concentration very important for proper shape of proteins • Also involved in metabolic reactions

Question 53

2. What is the relationship between excitement of the nervous system and pH?

Answer 53

Decreasing pH depresses the nervous system / Increasing pH overexcites the nervous system

Question 54

3. Be familiar with how the three compensatory mechanisms – chemical buffers – manage changes in arterial blood pH in order to maintain homeostatic equilibrium.

Answer 54

Chemicals React to pH changes almost instantaneously: A drop in pH (as in acidosis) will move the reaction to the right, absorbing H+ ions, increasing pH back to normal levels. Conversely, an increase in pH (as in alkalosis) will move the reaction to the left.

Question 55

Be familiar with how the three compensatory mechanisms – the pulmonary – manage changes in arterial blood pH in order to maintain homeostatic equilibrium

Answer 55

Pulmonary Changes in ventilation work to change the partial pressure of arterial carbon dioxide, PaCO2. A drop in pH, for example, results in increased ventilation to blow off excess CO2. An increase in pH decreases ventilatory effort, which increases PaCO2 and lowers pH back to normal levels

Question 56

Be familiar with how the three compensatory mechanisms – renal systems – manage changes in arterial blood pH in order to maintain homeostatic equilibrium

Answer 56

Renal Renal mechanisms kick in after other compensatory mechanisms have been ineffective – generally after about 6 hours of sustained acidosis or alkalosis

Question 57

4. What is meant by the term, “a primary acid-base disturbance”?

Answer 57

A change in the normal amounts of acid or base in the body At the pH present in the body, bicarbonate (HCO3 - ) acts as a base. For metabolic causes of changes to the body’s pH, It’s all about the base At the pH present in the body, CO2 acts as an acid. For respiratory causes of changes to the body’s pH, it’s all about the acid

Question 58

5. Relate changes in the levels of bicarbonate and carbon dioxide to metabolic and respiratory acidosis and alkalosis.

Answer 58

a decrease in bicarbonate causes metabolic acidosis an increase in bicarbonate causes metabolic alkalosis An increase in carbon dioxide causes respiratory acidosis A decrease on carbon dioxide causes respiratory alkalosis

Question 59

What are the two causes of the decrease in bicarbonate that results in metabolic acidosis?

Answer 59

Increase in H+ & Actual loss of HCO3

Question 60

7. Be familiar with examples of conditions that can result in metabolic acidosis. (Explain why these conditions would result in metabolic acidosis – it will make it easier to remember them).

Answer 60

Nervous system depression (headache, lethargy, coma), Kussmaul respirations (deep and fast, as with exercise, but more laboured), anorexia, nausea, vomiting, diarrhea, abdominal discomfort

Question 61

9. Be able to calculate anion gap and know its significance.

Answer 61

Na - (Cl + HCO3) This value is called the “anion gap” and is known to be between 8-12 mEq/L. If the anion gap is significantly larger than 12 mEq/L, there are more metabolic acids than normal if there is metabolic acidosis, but the anion gap is normal, there must be loss occurring of HCO3 - from the body.

Question 62

Na - (Cl + HCO3) This value is called the “anion gap” and is known to be between 8-12 mEq/L. If the anion gap is significantly larger than 12 mEq/L, there are more metabolic acids than normal if there is metabolic acidosis, but the anion gap is normal, there must be loss occurring of HCO3 - from the body.

Answer 62

Excessive loss of metabolic acids & Gain in bicarbonate

Question 63

11. Be familiar with examples of conditions that can result in metabolic acidosis. (Explain why these conditions would result in metabolic acidosis – it will make it easier to remember them).

Answer 63

Nervous system excitement

Question 64

12. Be familiar with clinical manifestations of metabolic alkalosis (especially the underlined manifestations).

Answer 64

muscle cramps, hyperactive reflexes, confusion, convulsions) shallow/slow respirations

Question 65

13. What is the relationship between H+ and plasma calcium concentration? Why does this affect the activity of the nervous system?

Answer 65

Let’s look at the effect of an increase in H+ (decreased pH): This change in pH causes decreased binding of Ca2+ to plasma proteins, which releases free Ca2+ into the blood and thus the tissues. Free Ca2+ competes with Na+ in crossing cell membranes. If less Na+ can cross neuronal membranes, it will be more difficult for action potentials to occur = depression of the nervous system.

Question 66

14. What is hypercapnia?

Answer 66

a buildup of carbon dioxide in your bloodstream

Question 67

15. What is the main cause for respiratory acidosis?

Answer 67

impaired ventilation caused by depression of respiratory center, disorders of respiratory muscles or lung tissue, etc.

Question 68

16. Be familiar with the clinical manifestations of respiratory acidosis.

Answer 68

Nervous system depression (headache, lethargy, coma), Kussmaul respirations (deep and fast, as with exercise, but more laboured), anorexia, nausea, vomiting, diarrhea, abdominal discomfort. CO2 crosses blood brain barrier much more readily than bicarbonate ion, so has a direct effect on brain tissue. Capillaries dilate, resulting in headache and blurred vision

Question 69

17. What is the main cause for respiratory alkalosis?

Answer 69

a decrease in plasma pCO2 (hypocapnia) Increased ventilation caused by pulmonary disease, congestive heart failure, high altitudes

Question 70

18. Be familiar with the clinical manifestations of respiratory alkalosis.

Answer 70

Nervous system excitement (muscle cramps, hyperactive reflexes, confusion, convulsions) shallow/slow respirations CO2 crosses blood brain barrier much more readily than bicarbonate ion, so has a direct effect on brain tissue. Capillaries constrict, decreasing blood flow, resulting in dizziness and tingling of fingers and toes.

Question 71

19. What are the two compounds that balance to maintain correct pH, and what are the systems that control the amounts of each of these compounds?

Answer 71

The balance of pH is maintained by the correct concentrations of CO2 and HCO3 - The respiratory system controls the levels of CO2 The excretory system controls the levels of HCO3

Question 72

20. Define: compensation, partially compensated, fully compensated and corrected state, not compensated.

Answer 72

what is done to bring the pH back to normal levels one of the systems (respiratory or excretory) is attempting to rectify the disturbance, but has not yet been successful (pH is still abnormal), resulting in values for both systems that are outside normal ranges (in the same direction) pH level is within normal limits, but values for both systems are outside of normal limits (in the same direction) all values are within normal limits pH is abnormal. One system (the cause of the abnormal pH) is outside of normal limits. Other system is still within normal limits (has not yet begun to try to compensate

Question 73

22. What is meant by a mixed acid-base imbalance?

Answer 73

more than one primary imbalance arises in the same person

Question 74

23. Be familiar with the uses for sodium in the body.

Answer 74

Important for water balance, conduction of nerve impulses, regulation of acid-base balance, some biochemical reactions, membrane transport

Question 75

24. Describe how sodium levels are regulated (with what compound’s levels are they associated? What hormones are involved?)

Answer 75

Receptors that monitor sodium levels in body fluids have yet to be found. Sodium has the highest concentration of any ion in the ECF and so is responsible for osmotic pressure. Therefore, sodium levels are coupled with water levels in the body, and regulation of sodium levels is therefore coupled with blood pressure and volume Levels of sodium are controlled by hormones that control reabsorption of water and sodium in the kidneys (aldosterone, ADH, natriuretic hormones)

Question 76

25. What is the main effect of hypernatremia? a. Describe the three main causes of hypernatremia – understand and be able to apply the listed causes under each main cause. b. Be familiar with the overall clinical manifestations for hypernatremia, no matter what the direct cause is. c. Name the effect on blood volume as a result of each of the three ways that hypernatremia can occur. d. Understand the manifestations that result from each of these three ways.

Answer 76

Intracellular dehydration cell shrinking Loss of both water and sodium, but more water than sodium: (symptoms of dehydration) = hypovolemia (manifestations include hypotension, weight loss, tachycardia, weak pulse) DI or decreased intake of water = blood volume doesn’t change (no loss of salt) = none of symptoms caused by changes in blood volume Retention of both water and sodium, but more sodium than water = hypervolemia (manifestations include weight gain, bounding pulse, increased blood pressure) Hypernatremia (hypovolemic (loss of...)) = More water than sodium e.g., a lot of watery diarrhea or the production of a lot of urine (as in osmotic diuresis that occurs with uncontrolled diabetes mellitus) Hypernatremia (hypervolemic (gain of...)) More sodium than water e.g., 1) too rapid IV delivery of sodium bicarbonate (in order to correct acidosis, for example), without allowing enough time for the kidney to get rid of the extra sodium 2) too high secretion of aldosterone (more sodium than normal is reabsorbed)

Question 77

26. What is the main effect of hyponatremia (on slide 7)? a. Describe the three main causes of hyponatremia – understand and be able to apply the listed causes under each main cause. b. Be familiar with the overall clinical manifestations for hyponatremia, no matter what the direct cause is. c. Name the effect on blood volume as a result of each of the three ways that hyponatremia can occur. d. Understand the manifestations that result from each of these three ways.

Answer 77

Cell swelling Most seriously affected are cells of the brain and nervous system (in addition to cell swelling, membrane potential is also altered), causing neurological alterations: confusion, depressed reflexes, seizures, coma (think of someone who is inebriated) Loss of both sodium and water, but more sodium than water = hypovolemia (manifestations include hypotension, weight loss, tachycardia, weak pulse) SIADH or excessive intake of water = blood volume doesn’t change significantly (no loss of salt) = none of symptoms caused by changes in blood volume. Retention of both sodium and water, but more water than sodium = hypervolemia (manifestations include weight gain, bounding pulse, increased blood pressure) Hyponatremia (hypovolemic (loss of...)) = More sodium than water e.g., too low secretion of aldosterone (more sodium than normal is lost from the body, due to aldosterone not causing its reabsorption) Hyponatremia (hypervolemic (gain of...)) = More water than sodium e.g., edema causing diseases (fluid moves out of the blood into the tissues, causing edema. The body compensates for the drop in blood volume by releasing both aldosterone and ADH, which replaces more of the water than the sodium in the blood)

Question 78

27. What does SIADH stand for?

Answer 78

Syndrome of inappropriate antidiuretic hormone secretion

Question 79

28. What is water intoxication?

Answer 79

drinking too much water in too short a period of time leads to these neurological symptoms

Question 80

29. Be familiar with the uses for potassium in the body.

Answer 80

Important for fluid balance, nerve impulse conduction, some biochemical reactions

Question 81

30. Describe the two main mechanisms for regulation of potassium.

Answer 81

By the kidney (main source of loss from the body): negative feedback release of aldosterone occurs in relation to serum potassium levels (the transporter is the same one that brings sodium into the body). There is also a H+/K+ transporter in tubule cells that responds to serum potassium levels. Shifts across body cell membranes – a H+/K+ transporter in body cell membranes causes exchange of these ions. ECF levels rise with acidosis / fall with alkalosis. Insulin also causes the uptake of K+

Question 82

31. Be familiar with, and able to apply, the causes of hyperkalemia.

Answer 82

Excess potassium ions in the blood Usually by renal disease (kidney loses ability to excrete K+ ) increased intake (rare by oral route, more likely through too rapid IV) a shift from intracellular to extracellular (changed cell permeability caused by trauma (e.g., burns), acidosis, hypoxia, etc.) insulin deficits (insulin promotes the entry of potassium into cells) undersecretion of aldosterone

Question 83

33. What is the relationship between insulin and potassium?

Answer 83

(insulin promotes the entry of potassium into cells

Question 84

34. What is the relationship between aldosterone and potassium?

Answer 84

undersecretion of aldosterone

Question 85

35. What is the effect of hyperkalemia on neuromuscular excitability?

Answer 85

Decrease in neuromuscular excitability has several effects, including paresthesias with mild attacks, ranging to loss of muscle tone and paralysis with more severe attacks

Question 86

36. What is the most serious effect of hyperkalemia and what is this due to?

Answer 86

Most serious effect is on the heart: the decrease in membrane excitability produces changes in the conduction and repolarization of electrical signals in the heart. Severe hyperkalemia can cause ventricular fibrillation or cardiac arrest

Question 87

37. Describe 3 causes for hypokalaemia.

Answer 87

excessive loss of potassium (diuretics, increased aldosterone (and cortisol, which can also activate aldosterone receptors, so stress can cause hypokalaemia) secretion) inadequate intake (frequent cause) (fad diets) increased entry into cells (ECF hypokalaemia) (drugs, insulin).

Question 88

39. What is the most serious effect of hypokalemia?

Answer 88

most serious effects involve the heart. Alterations in contraction pattern of the heart may cause arrhythmias.

Question 89

40. Be familiar with the uses of calcium in the body.

Answer 89

Important for many enzyme reactions, muscle contraction, release of neurotransmitters, blood clotting

Question 90

41. What is the relationship between calcium and sodium membrane transport?

Answer 90

alters neuromuscular excitability by altering the cell membrane permeability. (calcium stabilizes the cell membrane and blocks sodium transmission)

Question 91

42. Be familiar with the regulation of calcium.

Answer 91

through Vitamin D and parathyroid hormone, absorption/secretion by bones, kidney, GIT

Question 92

43. What is the main cause of hypercalcemia, and to what is this due?

Answer 92

Due mainly to increased bone resorption (i.e., reabsorbing calcium from the bones) due to neoplasms or hyperparathyroidism a result of overactive parathyroid glands

Question 93

44. What is the effect of hypercalcemia on excitability of muscles and nerves?

Answer 93

leads to decreased excitability of both muscles and nerves (remember: calcium blocks sodium movement across neuronal membrane)

Question 94

45. Be familiar with manifestations of hypercalcemia (try to relate them to decreased nerve/muscle activity).

Answer 94

fatigue, weakness, lethargy, hypoactive reflexes (decreased neural excitability) depression, bizarre behaviour bradycardia/arrhythmias nausea, vomiting, constipation (decrease in smooth muscle activity)

Question 95

46. Name three causes of hypocalcemia. (Understand how alkalosis can cause hypocalcemia).

Answer 95

Due to decreased PTH, kidney disease, alkalosis (alkaline pH in plasma causes increased binding of calcium ions to proteins, thus decreasing the amount of free calcium)

Question 96

47. What is the effect of hypocalcemia on excitability of muscles and nerves?

Answer 96

leads to increased excitability of both muscles and nerves

Question 97

48. Be familiar with the clinical manifestations of hypocalcemia.

Answer 97

spasms, tetany increased GI motility cardiovascular dysrhythmias

Question 98

49. What breathing pattern could produce tetany? Explain.

Answer 98

Low levels of carbon dioxide cause tetany by altering the albumin binding of calcium such that the ionized (physiologically influencing) fraction of calcium is reduced; one common reason for low carbon dioxide levels is hyperventilation. Low levels of magnesium can lead to tetany

Question 99

50. Be familiar with the uses of magnesium in the body.

Answer 99

Important as a cofactor in many intracellular enzymatic reactions Important role in nerve conduction Important role in smooth muscle contraction and relaxation (high levels Mg inhibit calcium transport into the cell and release from SR

Question 100

51. What is the relationship between magnesium and calcium membrane transport?

Answer 100

calcium decreases magnesium absorption by a nonspecific reduction in membrane permeability to solutes that induce net water flow

Question 101

52. What is the effect of hypermagnesmia on excitability of muscles and nerves?

Answer 101

Decreases excitability of both muscle and nerves

Question 102

53. Be familiar with the clinical manifestations of hypermagnesmia.

Answer 102

Hypoactive reflexes Muscle weakness Bradycardia (slow HR), respiratory distress Nausea, vomiting

Question 103

54. What is the effect of hypomagnesmia on excitability of muscles and nerves?

Answer 103

Increases excitability of both muscles and nerves

Question 104

55. Be familiar with the clinical manifestations of hypomagnesmia

Answer 104

Increased reflexes Muscle cramps and convulsions Tachycardia (increased HR) Behavioural changes, irritability