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Physiology II > E1- Random > Flashcards

E1- Random Flashcards

1
Q

What type of cells secrete renin?

A

Granular/Juxtaglomerular cells

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2
Q

What type of cells contract in response to AT II?

A

Mesangial cells

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3
Q

What are the two main barrier to proteins?

A

Basal lamina and filtration slits

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4
Q

What is the effect of NSAIDs?

A

Inhibit synthesis of prostaglandins so there is no vasodilation to oppose alpha 1 (loss of protective affect on RBF)

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5
Q

What 5 types of transports occur in the PT?

A 
Primary active Na+, K+ pump
Secondary active Na+, glucose, AA symport
Tertiary active alpha-KG, PAH OAT
Na+, H+ antiport
Cl- paracellular transport
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6
Q

What hormone increases the activity of the Na+, H+ transporter?

A

AT II

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7
Q

In what part of the nephron does Mannitol work? (osmotic diuretic)

A

Proximal tubule

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8
Q

How does Mannitol work? (osmotic diuretic)

A

Blocks the reabsorption of H20, trapping it in the nephron lumen to then be excreted with Na+

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9
Q

What is the thin descending limb permeable to?

A

H20

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10
Q

What is the thick ascending limb permeable to?

A

NaCl

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11
Q

What is pattern of flow in the descending vasa recta?

A

H2O flows out

NaCl flows in

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12
Q

What is pattern of flow in the ascending vasa recta?

A

H2O flows in

NaCl flows out

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13
Q

What types of transports are in the LOH? (3)

A

Primary active Na+, K+ pump
NKCC2 transporter
Back flow of K+ –> paracellular Ca2+ reabsorption

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14
Q

In what part of the nephron does Furosemide work? (loop diuretic)

A

LOH

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15
Q

How does Furosemide work? (loop diuretic)

A

Inhibits the NKCC2 transporter and Ca2+ reabsorption

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16
Q

What hormone increases the activity of the NKCC2 transporter?

A

ADH/vasopressin

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17
Q

Is the early distal tubule permeable to H2O?

A

No

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18
Q

What determines the permeability of the late distal tubule and collecting duct to H2O?

A

ADH/vasopressin

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19
Q

What portion of the nephron is considered the diluting segment?

A

Early distal tubule

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20
Q

What type of transporter is in the early distal tubule?

A

NCC symport (Na+, Cl-)

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21
Q

In what part of the nephron does Chlorothiazide work? (thiazide diuretic)

A

Early distal tubule

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22
Q

How does Chlorothiazide work? (thiazide diuretic)

A

Inhibits the NCC symporter

Increases Calcium reabsorption in the distal tubule

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23
Q

What types of transporter are in the late distal tubule? (5)

A 
Primary active Na+, K+ pump
ENaC antiport
H+ uniport
H+,  K+ pump
Ca2+, Na+ pump
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24
Q

What hormone increases the activity of the Na+, K+ pump?

A

Aldosterone

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25
Q

What hormone increases the activity of the ENaC transporter?

A

Aldosterone

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26
Q

What hormone increases the activity of the H+ uniport?

A

Aldosterone

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27
Q

In what part of the nephron do Amiloride and Spironolactone work? (K+-sparing diuretics)

A

Collecting ducts

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28
Q

How do Amiloride and Spironolactone work? (K+-sparing diuretics)

A

Amiloride- Inhibits the ENaC antiport

Spiromolactone- Inhibits aldosterone

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29
Q

What part of the tubule adjusts the final concentration of urine?

A

Collecting duct

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30
Q

What porin inserts into the nephron cell when ADH levels are high to allow for the passage of H2O?

A

AQP2

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31
Q

What porins are always present that allow water to be reabsorbed?

A

AQP3

AQP4

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32
Q

What is the driving force for filtration?

A

P(GC)

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33
Q

If total urine flow is greater than 1100, is the subject in a positive or negative water balance?

A

negative

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34
Q

If total urine flow is less than 1100, is the subject in a positive or negative water balance?

A

positive

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35
Q

How are nephrons arranged?

A

In parallel

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36
Q

What two capillary beds are arranged in parallel?

A

Glomerular

Peritubular (cortical, vasa recta)

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37
Q

What autoregulation mechanism responds to changes in BP?

A

Myogenic

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38
Q

What autoregulation mechanism responds to changes in salt load?

A

Tubuloglomerular feedback

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39
Q

What are the characteristics of the perfect GFR marker>

A

Freely filtered, but neither reabsorbed nor secreted

40
Q

What two things can be used to measure GFR?

A

Inulin clearance and creatine clearance

41
Q

What can be used to measure RPF?

42
Q

If the clearance of a substance is greater than the clearance of creatine, thus greater than GFR, was the substance secreted or reabsorbed?

43
Q

If the clearance of a substance is less than the clearance of creatine, thus less than GFR, was the substance secreted or reabsorbed?

A

Reabsorbed

44
Q

If the clearance ratio of a substance to the clearance of inulin is zero, then what must also be true?

A

The substance must also be a GFR marker

45
Q

If the clearance ratio of a substance to the clearance of inulin is less than 1.0, then what must also be true?

A

The substance is not filtered, or is filtered and reabsorbed

46
Q

If the clearance ratio of a substance to the clearance of inulin is more than 1.0, then what must also be true?

A

The substance is filtered and secreted

47
Q

What does it mean if the transport rate is positive?

A

Some material was removed from the filtrate by reabsorption

48
Q

What does it mean if the transport rate is negative?

A

Some material was added to the filtrate by secretion

49
Q

What does it mean if the tubular fluid to plasma ratio equals zero?

A

The substance has been exactly proportional to the reabsorption of water

50
Q

What does it mean if the tubular fluid to plasma ratio is less than 1?

A

The reabsorption of the substance has occurred to a greater extent than water

51
Q

What does it mean if the tubular fluid to plasma ratio is greater than 1?

A

The reabsorption of the substance has occurred to a lesser extent than water OR there has been a net secretion of the substance

52
Q

If you increase GFR, will the /Tm be reached at higher or lower plasma concentrations?

53
Q

What can cause hyperosmotic volume contraction?

A

Very low levels of ADH
Ineffective ADH
(dehydration, DM insipidus)

54
Q

Is plasma osmolality high/low in hyperosmotic volume contraction?
Is urine osmolality high/low in hyperosmotic volume contraction?

A 
Plasma = high
Urine = low
55
Q

What is the cause of low ADH in neurogenic diabetes insipidus?

A

Hypothalamic-pituitary injury

will respond to exogenous ADH agonist- desmopressin

56
Q

What is the cause of low ADH in nephrogenic diabetes insipidus?

A

Renal origin, kidney is unable to respond to ADH or desmopressin
Plasma ADH is high since Hypothalamic-pituitary are functioning normally

57
Q

What can cause hyposmotic volume expansion?

A

SIADH

Acute water load

58
Q

What electrolyte imbalance is seen with SIADH?

A

Hyponatremia (euvolemia)

59
Q

Is K+ higher inside/outside the cell?

Is Na+ higher inside/outside the cell?

A 
K+ = inside
Na+ = outside
60
Q

Alpha1 activation has what effect on K+?

A

Shift of K+ out of cells

Hyperkalemia

61
Q

Beta2 activation has what effect on K+?

A

Shift of K+ into cells

Hypokalemia

62
Q

Insulin activation has what effect on K+?

A

Dietary shift of K+ into cells after a meal

Hypokalemia

63
Q

Aldosterone activation has what effect on K+?

A

Shift of K+ into tubule cells for excretion

Hypokalemia

64
Q

Besides alpha1 activation, what else can cause a K+ shift out of cells?

A

Hyperosmolarity and exercise

65
Q

What is is effect of a hyperkalemic state on pH?

A

Acidosis

Hyperkalemic state, K+ moves into the cells, this stimulates the movement of H+ out of the cells

66
Q

What is is effect of a hypokalemic state on pH?

A

Alkalosis

Hypokalemic state, K+ moves into the cells, this stimulates the movement of H+ out of the cells

67
Q

What is an example of a volatile acid?

A

Respiratory CO2

68
Q

What is the fist line of defense against pH change?

69
Q

What determines the effectiveness of a buffer?

A

Concentration

pK (most effective within +/- one unit

70
Q

What is the most important buffering system in the ECF.

A

Bicarbonate

71
Q

What is normal ratio of HCO3- to dissolved CO2?

72
Q

What causes metabolic disturbances?

A

Changes in HCO3-

73
Q

What causes respiratory disturbances?

A

Changes in CO2 (must be compensated for by kidneys)

74
Q

What are causes of Metabolic acidosis?

A 
Ingestion of acid
Formation of non-volatile acids (lactic acids)
Diabetic ketoacidosis
Loss of HCO3- (diarrhea)
Renal HCO3- recovery reduced 
Excretion of NH4+ reduced
75
Q

What are causes of Metabolic alkalosis?

A

Antacid abuse
ECF volume contraction (vomiting, diuretics)
Hyperaldosteronism

76
Q

What can cause of Respiratory alkalosis?

A

Hyperventilation

  • high altitude
  • anxiety
  • hypoxemia
77
Q

What can cause of Respiratory acidosis?

A

COPD
Asthma
Airway obstruction

78
Q

What is the Mass Action Rule?

A

Every 10 increase in CO2 results in a 1 increase in HCO3-

Every 10 decrease in CO2 results in a 2 decrease in HCO3-

79
Q

What parts of the nephron do not change transport on the face of increased or decreased total body K+?

A

PT and LOH

80
Q

Why is metabolic alkalosis maintained even when vomiting has stopped?

A

ECF volume contraction increases H+ loss via RAAS

critical factor is elevated aldosterone

81
Q

What is the treatment of metabolic alkalosis?

A

Saline

Corrects fluid volume deficit and then adjusts RAAS, leading to the excretion of HCO3-

82
Q

Why will saline not work to treat metabolic alkalosis caused by aldosterone excess? (Conn syndrome)
What is the appropriate treatment?

A

ECF volume is already expanded

Remove tumor or aldosterone antagonist- Spirolactone

83
Q

What type of acidoses have a normal anion gap?

A

Simple HCO3- loss: Diarrhea or Renal Tubular Acidosis

Cl- increases to meet the drop in HCO3-

84
Q

What type of acidoses have an increased anion gap?

A

Excess of non-volatile acids
(fixed acids liberate H+ which is buffered by HCO3- w/o changing the Cl- levels)

Lactic acidosis
Ketoacidosis
Renal failure- phosphoric sulphuric
Salicylate poisoning- aspirin 
Ethylene glycol poisoning
Methanol poisoning
85
Q

What type of RTA is due to impaired H+ secretion by H+-ATPase in the distal nephron?

A

Type 1 (distal)

86
Q

What are the characteristics of Type I (distal) RTA?
Hyperkalemia/Hypokalemia
Normal anion gap/Increased anion gap

A

Hypokalemia

Normal anion gap

87
Q

What type of RTA is due to a defect in the Na+-H+ exchanger in the proximal tubule, leading to the imparement of H+ secretion and HCO3- reabsorption?

A

Type II (proximal)

88
Q

What are the characteristics of Type II (proximal) RTA?
Gain or loss of HCO3-
Normal anion gap/Increased anion gap

A

Loss of HCO3-
Normal anion gap
(in severe cases may also lead to hypokalemia)

89
Q

What type of RTA is due to a defect in urinary acidification due to inhibition of renal glutaminase, which impairs formation of NH4+?

90
Q

What are the characteristics of Type IV RTA?
Hyperkalemia/Hypokalemia
Gain or loss of HCO3-
Normal anion gap/Increased anion gap

A

Hyperkalemia
Impaired HCO3- generation
Normal anion gap

91
Q

What RTA is associated with a aldosterone deficiency?

92
Q

How does diabetic ketoacidosis cause volume depletion?

A

Ketoacids acidify blood, deplete HCO3-
Plasma glucose increases
Glucose acts as an osmotic diuretic and increases urine flow

93
Q

Would you expect to see hyperkalemia or hypokalemia in a diabetic ketacidosis pt?

A

Hyperkalemia

94
Q

What hormone will be elevated in a pt with diabetic ketacidosis?
What hormone will be decreased?

A

Elevated plasma glucose makes the blood hyerposmotic leading to increased ADH
ANP

95
Q

Although vomiting can initiate metabolic alkalosis, what can maintain it?

A

Volume contraction and hypokalemia

Volume contraction stimulates aldosterone which increases alkalosis and K+ loss

Physiology II (3 decks)

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