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urinary Flashcards

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1
Q
  1. Define obstructive uropathy.
A

Anatomic changes in the urinary system caused by obstruction

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2
Q
  1. Be familiar with causes for obstructive uropathy.
A

Kidney stones, compression from a tumour, inflammation

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

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)

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4
Q
  1. Describe compensatory hypertrophy and hyperfunction.
A

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

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5
Q
  1. Define “calculi”.
A

Kidney stones

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

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

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

Hyperabsorption of calcium from the intestines or hyperparathyroidism

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8
Q
  1. 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.
A

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

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9
Q
  1. Know the term renal colic.
A

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

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10
Q
  1. How are urinary calculi treated?
A

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

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11
Q
  1. To what is lower urinary tract obstruction primarily related?
A

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

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12
Q
  1. Describe neurogenic bladder – what does the type of dysfunction depend upon?
A

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

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13
Q
  1. Name two physical obstructions of the lower urinary tract.
A

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

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14
Q
  1. Define glomerulonephritis. What is the most common contributing factor?
A

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

Hypertension

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15
Q
  1. Identify the two common immune mechanisms that can lead to glomerulonephritis, and a common disease that is associated with each.
A

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)

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16
Q
  1. Describe the series of steps in the development of glomerulonephritis as caused by these immune mechanisms.
A

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

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17
Q
  1. Define: glomerular filtration rate. How is it usually estimated?
A

Production of filtrate by the glomerulus

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

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18
Q
  1. Describe nephritic syndrome, naming the disorder that is the usual cause.
A

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)

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19
Q
  1. Describe nephrotic syndrome, naming a disorder that can be the cause.
A

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)

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20
Q
  1. Define BUN – identify and explain the two facts that it reveals about the state of the kidney.
A

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)

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21
Q
  1. Identify and explain the one fact that the level of creatinine in the plasma reveals about the state of the kidney
A

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

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22
Q
  1. Define AKI (include BUN and plasma creatinine), including whether it is reversible.
A

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.

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23
Q
  1. What do the letters in “RIFLE” represent in terms of acute kidney injury?
A

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

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24
Q
  1. List the 3 causes of AKI – identify the most common one.
A

Prerenal acute kidney injury (most common)

Postrenal acute kidney injury

Intrarenal acute kidney injury

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25
Q
  1. What is prerenal AKI caused by? Be familiar with conditions that could lead to this.
A

– 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

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26
Q
  1. 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 …)
A

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

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27
Q
  1. With what does postrenal AKI usually occur? Give an example of one condition that would lead to this.
A

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

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28
Q
  1. From what does intrarenal AKI usually result? Be familiar with events/conditions that would lead to this.
A

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

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29
Q
  1. What is vital in the treatment of AKI?
A

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

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30
Q
  1. What is the primary goal of therapy for AKI? What 3 areas of concern are addressed? What may finally be necessary?
A

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

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31
Q
  1. Define chronic kidney disease, and be familiar with diseases/conditions which are risk factors.
A

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

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32
Q
  1. What are the two greatest risk factors for CKD?
A

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

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33
Q
  1. What criteria is used to assess the stage of CKD?
A

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&raquo_space; GFR > 90

2 = kidney damage with mild decrease in GFR&raquo_space; GFR = 60 – 89

3 = moderate decrease in GFR&raquo_space; GFR 30 – 59

4 = severe decrease in GFR&raquo_space; 15 – 29

5 = kidney failure&raquo_space; GFR < 15 or dialysis

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34
Q
  1. What does the intact nephron hypothesis propose, and what is the significance to the appearance of CKD manifestations?
A

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

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35
Q
  1. Define azotemia.
A

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

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36
Q
  1. Define uremic syndrome (uremia).
A

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

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37
Q
  1. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: sodium,
A

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.

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38
Q
  1. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: potassium,
A

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.

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39
Q
  1. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: creatinine and urea
A

Creatinine and urea levels in the plasma increase as GFR decreases

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40
Q
  1. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: pH,
A

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

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

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.

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42
Q
  1. Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: proteins and fat.
A

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.

43
Q
  1. Define anasarca.
A

A general accumulation of fluid in body cavities and tissues

44
Q
  1. Describe the effects (and their causes) on each of the following body systems: cardiovascular
A

Cardiovascular system –

Major cause of death in CKD

Excess sodium and water lead to hypertension

Excess LDL leads to increased atherosclerosis

45
Q
  1. Describe the effects (and their causes) on each of the following body systems: pulmonary
A

Complications associated with fluid overload

Acidosis results in Kussmaul respirations

46
Q
  1. Describe the effects (and their causes) on each of the following body systems: hematologic
A

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

47
Q
  1. Describe the effects (and their causes) on each of the following body systems: immune
A

Overall suppression by high levels of urea and metabolic wastes.

48
Q
  1. Describe the effects (and their causes) on each of the following body systems: neurologic
A

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

49
Q
  1. Describe the effects (and their causes) on each of the following body systems: gastrointestinal.
A

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

50
Q
  1. Name 4 means to evaluate CKD.
A

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

51
Q
  1. Name 4 means to treat CKD.
A

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

52
Q
  1. What are 2 reasons for the necessity of correct pH in the body?
A

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

53
Q
  1. What is the relationship between excitement of the nervous system and pH?
A

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

54
Q
  1. Be familiar with how the three compensatory mechanisms – chemical buffers – manage changes in arterial blood pH in order to maintain homeostatic equilibrium.
A

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.

55
Q

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

A

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

56
Q

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

A

Renal

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

57
Q
  1. What is meant by the term, “a primary acid-base disturbance”?
A

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

58
Q
  1. Relate changes in the levels of bicarbonate and carbon dioxide to metabolic and respiratory acidosis and alkalosis.
A

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

59
Q

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

A

Increase in H+ & Actual loss of HCO3

60
Q
  1. 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).
A

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

61
Q
  1. Be able to calculate anion gap and know its significance.
A

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.

62
Q

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.

A

Excessive loss of metabolic acids & Gain in bicarbonate

63
Q
  1. 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).
A

Nervous system excitement

64
Q
  1. Be familiar with clinical manifestations of metabolic alkalosis (especially the underlined manifestations).
A

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

65
Q
  1. What is the relationship between H+ and plasma calcium concentration? Why does this affect the activity of the nervous system?
A

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.

66
Q
  1. What is hypercapnia?
A

a buildup of carbon dioxide in your bloodstream

67
Q
  1. What is the main cause for respiratory acidosis?
A

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

68
Q
  1. Be familiar with the clinical manifestations of respiratory acidosis.
A

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

69
Q
  1. What is the main cause for respiratory alkalosis?
A

a decrease in plasma pCO2 (hypocapnia)

Increased ventilation caused by pulmonary disease, congestive heart failure, high altitudes

70
Q
  1. Be familiar with the clinical manifestations of respiratory alkalosis.
A

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.

71
Q
  1. 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?
A

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

72
Q
  1. Define: compensation, partially compensated, fully compensated and corrected state, not compensated.
A

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

73
Q
  1. What is meant by a mixed acid-base imbalance?
A

more than one primary imbalance arises in the same person

74
Q
  1. Be familiar with the uses for sodium in the body.
A

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

75
Q
  1. Describe how sodium levels are regulated (with what compound’s levels are they associated? What hormones are involved?)
A

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)

76
Q
  1. 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.
A

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)

77
Q
  1. 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.
A

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)

78
Q
  1. What does SIADH stand for?
A

Syndrome of inappropriate antidiuretic hormone secretion

79
Q
  1. What is water intoxication?
A

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

80
Q
  1. Be familiar with the uses for potassium in the body.
A

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

81
Q
  1. Describe the two main mechanisms for regulation of potassium.
A

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+

82
Q
  1. Be familiar with, and able to apply, the causes of hyperkalemia.
A

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

83
Q
  1. What is the relationship between insulin and potassium?
A

(insulin promotes the entry of potassium into cells

84
Q
  1. What is the relationship between aldosterone and potassium?
A

undersecretion of aldosterone

85
Q
  1. What is the effect of hyperkalemia on neuromuscular excitability?
A

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

86
Q
  1. What is the most serious effect of hyperkalemia and what is this due to?
A

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

87
Q
  1. Describe 3 causes for hypokalaemia.
A

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).

88
Q
  1. What is the most serious effect of hypokalemia?
A

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

89
Q
  1. Be familiar with the uses of calcium in the body.
A

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

90
Q
  1. What is the relationship between calcium and sodium membrane transport?
A

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

91
Q
  1. Be familiar with the regulation of calcium.
A

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

92
Q
  1. What is the main cause of hypercalcemia, and to what is this due?
A

Due mainly to increased bone resorption (i.e., reabsorbing calcium from the bones) due to neoplasms or hyperparathyroidism

a result of overactive parathyroid glands

93
Q
  1. What is the effect of hypercalcemia on excitability of muscles and nerves?
A

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

94
Q
  1. Be familiar with manifestations of hypercalcemia (try to relate them to decreased nerve/muscle activity).
A

fatigue, weakness, lethargy, hypoactive reflexes (decreased neural excitability)

depression, bizarre behaviour

bradycardia/arrhythmias

nausea, vomiting, constipation (decrease in smooth muscle activity)

95
Q
  1. Name three causes of hypocalcemia. (Understand how alkalosis can cause hypocalcemia).
A

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)

96
Q
  1. What is the effect of hypocalcemia on excitability of muscles and nerves?
A

leads to increased excitability of both muscles and nerves

97
Q
  1. Be familiar with the clinical manifestations of hypocalcemia.
A

spasms, tetany

increased GI motility

cardiovascular dysrhythmias

98
Q
  1. What breathing pattern could produce tetany? Explain.
A

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

99
Q
  1. Be familiar with the uses of magnesium in the body.
A

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

100
Q
  1. What is the relationship between magnesium and calcium membrane transport?
A

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

101
Q
  1. What is the effect of hypermagnesmia on excitability of muscles and nerves?
A

Decreases excitability of both muscle and nerves

102
Q
  1. Be familiar with the clinical manifestations of hypermagnesmia.
A

Hypoactive reflexes

Muscle weakness

Bradycardia (slow HR), respiratory distress

Nausea, vomiting

103
Q
  1. What is the effect of hypomagnesmia on excitability of muscles and nerves?
A

Increases excitability of both muscles and nerves

104
Q
  1. Be familiar with the clinical manifestations of hypomagnesmia
A

Increased reflexes

Muscle cramps and convulsions

Tachycardia (increased HR)

Behavioural changes, irritability

Biology 2401 (30 decks)

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