physiology Flashcards

1
Q

what is osmolarity?

A

the concentration of osmotically active particles present in a solution

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2
Q

what is the difference between osmolarity and osmolality?

A

osmolarity = units of osmol/L
osmolality = units of osmol/kg water

both can be used interchangeably

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3
Q

hypo vs hypertonic?

A

hypo = more water
hyper = less water

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4
Q

do males or females have higher total body water?

A

males
(males 60% of body weight, females 50%)

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5
Q

what is insensible loss of water?

A

loss of water there is no control over- e.g. via skin and lungs

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6
Q

what is sensible loss of water?

A

loss of water where there is some physiological control e.g. sweat, faeces, urine

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7
Q

are sodium ions in higher concentration inside or outside the cells?

A

outside is higher (140) than inside (10)

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8
Q

are potassium ions in higher concentration inside or outside the cells?

A

inside is higher (140) than outside (4.5)

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9
Q

what is the osmotic concentration of both intra and extracellular fluid (ICF and ECF)?

A

300 mosmol/l (osmolarity)

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10
Q

what happens to ECF and ICF osmolarity in gain or loss of water?

A

similar changes in both ECF and ICF

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11
Q

what happens to ECF and ICF osmolarity in gain or loss of NaCl?

A

ECF NaCl gain = increased ECF osmolarity, decreased ICF

ECF NaCl loss = decreased ECF, increased ICF

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12
Q

what happens to ECF and ICF osmolarity in gain or loss of isotonic fluid?

A

no change in osmolarity, change in ECF volume only

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13
Q

what happens if there is a change in potassium concentration in the plasma?

A

muscle weakness –> paralysis
cardiac irregularities –> cardiac arrest

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14
Q

how is salt imbalance manifested?

A

changes in extracellular volume

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15
Q

what are the 10 functions of the kidney?

A
  • Water balance
  • Salt balance
  • Maintenance of plasma volume
  • Maintenance of plasma osmolarity
  • Acid-base balance
  • Excretion of metabolic waste products (e.g.)
  • Excretion of exogenous foreign compounds (e.g.)
  • Secretion of renin (control of arterial blood pressure)
  • Secretion of erythropoietin (EPO; RBC production)
  • Conversion of vitamin D into active form (Calcitriol: Ca2+ absorption in GI tract)
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16
Q

what is the primary function of the kidney?

A

to regulate the volume, composition and osmolarity of the body fluids

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17
Q

what is the functional unit of the kidneys?

A

nephrons- each kidney has 1 million +

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18
Q

what are the functional mechanisms of the nephron?

A
  1. Filtration
  2. Reabsorption
  3. Secretion
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19
Q

what is the difference between efferent and afferent?

A

efferent = away from (e for exit)
afferent = towards

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20
Q

what are the 2 types of nephron?

A

juxtamedullary (20%)
cortical (80%)

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21
Q

which type of nephron had a bigger loop of henle?

A

juxtamedullary

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22
Q

what surrounds the glomerulrus?

A

bowman’s capsule

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23
Q

what do granular cells in the juxtaglomerular apparatus do?

A

produce and secrete renin

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24
Q

what is urine?

A

modified filtrate of the blood

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25
Q

how much of the plasma that enters the glomerulus is filtered?

A

20%

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26
Q

is filtration a passive or active process?

A

passive

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27
Q

what are the 4 forces comprising net filtration pressure?

A

glomerular capillary pressure
capillary oncotic pressure
bowman’s capsule hydrostatic (fluid) pressure
bowman’s capsule oncotic pressure

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28
Q

what is GFR and what is a normal GFR?

A

GFR = rate at which protein-free plasma is filtered from the glomeruli into the Bowman’s capsule per unit time

normal = 125ml/min

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29
Q

what affect does arterial bp have on GFR?

A

vasoconstriction –> decreased glomerular capillary bp –> decreased net filtration pressure –> decreased GFR

vasodilation is the opposite so:
vasodilation –> increased glomerular capillary bp –> increased net filtration pressure –> increased GFR

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30
Q

describe myogenic autoregulation of the kidneys

A

if vascular smooth muscle is stretched (arterila bp increased) it contracts constricting arteriole

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31
Q

describe tubuloglomerular feedback autoregulation of the kidneys

A

involves juxtaglomerular apparatus, if GFR rises, more NaCl flows through the tubule leading to constriction of afferent arterioles

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32
Q

what cells sense salt content of tubular fluid?

A

macula densa cells

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33
Q

name some examples where GFR would increase

A

decreased capillary oncotic pressure e.g. severe burns
change in surface area available for filtration

34
Q

name some examples where GFR would decrease

A

increased bowman’s capsule fluid pressure e.g. kidney stone

increased capillary oncotic pressure e.g. diarrhoea

35
Q

what is inulin clearance equal to?

A

GFR (use clinically to determine GFR)

36
Q

what is the clearance for substances that are filtered, completely reabsorbed and not secreted?

A

0

37
Q

for substances that are filtered, secreted and not reabsorbed what is the clearance in comparison to GFR?

A

clearance>GFR

38
Q

what is reabsorbed in the proximal tubule?

A

Sugars
Amino acids
Phosphate
Sulphate
Lactate

39
Q

what is secreted in the proximal tubule?

A

H+
Hippurates
Neurotransmitters
Bile pigments
Uric acid
Drugs
Toxins

40
Q

what is the difference between primary and secondary active transport?

A

primary- energy directly required to move substrate against its conc. gradient

secondary- carrier modules transported coupled to an ion in its gradient

41
Q

how does isosmotic fluid reabsorption occur across proximal tubule epithelium?

A

leaky epithelium
standing osmotic gradient
oncotic pressure gradient

42
Q

where are all glucose and amino acids absorbed? what happens if it can’t all be absorbed here?

A

proximal tubule - if there is too much to be absorbed here (above transport maximum) excess is excreted in urine

43
Q

what is the flow of the loop of henle?

A

opposing flow in the 2 limbs - countercurrent flow

44
Q

what is reabsorbed in the ascending limb of the loop of henle?

A

Na+ and Cl-
(impermeable to water)

45
Q

describe the triple co-transporter pump in the loop of henle

A
  1. Solute removed from lumen of ascending limb (water cannot follow)
  2. Tubular fluid is diluted and osmolality of interstitial fluid is raised
  3. Interstitial solute cannot enter the descending limb
  4. Water leaves the descending limb by osmosis
  5. Fluid in the descending limb is concentrated - can then go up ascending limb
46
Q

what is the purpose of countercurrent multiplication?

A

to concentrate medullary interstitial fluid allowing kidney to produce different volumes and concentrations of urine according to amounts of circulation ADH

47
Q

what are the 2 components of the countercurrent system?

A

loop of henle + vasa recta

48
Q

what is the structure of the vasa recta capillaries?

A

hairpin loop structure

49
Q

what hormone promotes water reabsorption across the distal tubule and collecting duct?

A

ADH

50
Q

what hormone increases Na+ reabsorption and promotes H+ and K+ secretion in the distal tubule and collecting duct?

A

aldosterone

51
Q

what hormone decreases Na+ reabsorption in the distal tubule and collecting duct?

A

atrial natriuretic hormone (peptide - ANP)

52
Q

what happens in the presence of maximal plasma ADH in the collecting duct?

A

water moves from the collecting duct lumen along the osmotic gradient into the medullary interstitial fluid (rebsorbed), enabling hypertonic urine formation

(small amounts of concentrated urine)

53
Q

what happens in the presence of low plasma ADH in the collecting duct?

A

low water permeability (water can’t be reabsorbed) = hypotonic urine

(large volumes of dilute urine)

54
Q

what causes increased ADH release?

A

decreased arterial pressure

55
Q

what is ADH also known as?

A

vasopressin - causes arterial and venous vasoconstriction

56
Q

where is aldosterone secreted?

A

adrenal cortex

57
Q

what type of hormone is aldosterone?

A

steroid

58
Q

when is aldosterone secreted?

A
  1. In response to rising [K+] or falling [Na+] in the blood
  2. activation of the renin-angiotensin system
59
Q

when is renin released from granular cells in JGA?

A
  • reduced pressure in afferent arteriole
  • macula densa cells sense reduces amount of NaCl in distal tubule
  • increased sympathetic activity resulting from reduced arterial bp
60
Q

what is the treatment of fluid retention associated with congestive heart failure?

A

loop diuretics + ace inhibitors

61
Q

when is ANP released?

A

when atrial muscle cells are mechanically stretched due to an increase in the circulating plasma volume

62
Q

what is the name of the involuntary urinary reflex babies have before they gain voluntary control?

A

micturation reflex

63
Q

what is the pH of arterial blood?

A

7.45

64
Q

what is the pH of venous blood?

A

7.35

65
Q

how do the kidneys control levels of HCO3-?

A
  • variable reabsorption of filtered HCO3-
  • can add new HCO3- to the blood
66
Q

what is the vast majority of H+ secretion used for?

A

HCO3- reabsorption to prevent generation of acidosis

67
Q

what are the 3 criteria for normal acid base balance?

A
  1. Plasma pH close to 7.4 (range 7.35 – 7.45)
  2. [HCO3-]p close to 25 mmol/l (range 23 – 27)
  3. Arterial PCO2 close to 40 mmHg (range 35 – 45)
68
Q

what is respiratory acidosis?

A

Retention of CO2 by the body

E.g. chronic bronchitis
chronic emphysema
airway restriction (bronchial asthma, tumour)
chest injuries
respiratory depression

69
Q

how is respiratory acidosis compensated?

A

Since the respiratory system is the cause the renal system must compensate
blood PCO2 drives H+ secretion by the kidney
Therefore, CO2 retention stimulates H+ secretion into the filtrate

70
Q

what is respiratory alkalosis?

A

Excessive removal of CO2 by the body

E.g. Low inspired PO2 at altitude (hypoxia stimulates peripheral chemoreceptors, hyperventilation lowers PCO2)

Hyperventilation (causes include fever, brainstem damage)

Hysterical overbreathing

71
Q

how do the kidneys compensate for respiratory alkalosis?

A

Excessive removal of CO2 reduces H+ secretion into the tubule

72
Q

what is metabolic acidosis?

A

Excess H+ from any source other than CO2

  • Ingestion of acids or acid-producing foodstuffs
  • Excessive metabolic production of H+ (e.g. lactic acid during exercise or ketoacidosis)
  • Excessive loss of base from the body (e.g. diarrhoea – loss of HCO3-)
73
Q

what causes metabolic acidosis compensation?

A

respiratory system - decreased plasma pH stimulates peripheral chemoreceptors increasing ventilation, lowering H+

74
Q

what system compensates for respiratory acidosis and alkalosis?

A

renal system

75
Q

what system compensates for metabolic acidosis and alkalosis?

A

respiratory system

76
Q

what is metabolic alkalosis?

A

Excessive loss of H+ from the body

E.g.
- Loss of HCl from the stomach (vomiting)
- Ingestion of alkali or alkali-producing foods
- Aldosterone hypersecretion (causes stimulation of Na+/H+ exchange at the apical membrane of the tubule; acid secretion)

77
Q

what is the ion indication of respiratory acidosis?

A

pH < 7.35 and PCO2 >45 mmHg

78
Q

what is the ion indication of respiratory alkalosis?

A

pH > 7.45 and PCO2 < 35mmHg

79
Q

what is the ion indication of metabolic acidosis?

A

pH < 7.35 and low HCO3-

80
Q

what is the ion indication of metabolic alkalosis?

A

pH > 7.45 and high HCO3-

81
Q

how is metabolic alkalosis compensated?

A

respiratory system slows ventilation due to pH increase, H+ rises