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Semester 1 TxWes > A/P Final > Flashcards

A/P Final Flashcards

1
Q

What is the relationship of pressure to speed in the CV system?

A

The higher the pressure, the faster blood can move, the lower the pressure, the slower blood moves

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1
Q

What is the surface area of the lungs?

A

70 square meters

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2
Q

What is the surface area of the circulatory system?

A

500 or more square meters

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3
Q

In the body, what swaps in the V = IR equation?

A

V = pressure
I = flow
R = resistance

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4
Q

What is the formula for conductance? Explain the relationship

A

1 / R (resistance). Conductance is the inverse of resistance, if resistance is high, conductance is low, if resistance is low, conductance is high

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5
Q

Where is blood flow control dictated?

A

At the local level of the capillary

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6
Q

What effect does parallel systems have on pressure?

A

The more series in parallel, the lower pressure will be

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7
Q

What is the relationship to cross-sectional area and blood vessels in the body?

A

As you go from the large single vessels to the numerous smaller ones, cross sectional area increases

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8
Q

What is the formula for velocity of blood flow?

A

Blood flow / cross sectional area
Aorta (CSA of 2.5) 5 / 2.5 = 2 L/min
Vena Cava (CSA of 8) 5 / 8 = 0.625 L/min

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9
Q

Why is pulse pressure wider in the large arteries, especially relative to the Aorta?

A

Because the large arteries are “stiffer”

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10
Q

What is the pressure range of the LA?

A

0 - 2

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11
Q

What is the pressure range of the LV?

A

0 - 120

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12
Q

What is the pressure range of the Aorta?

A

80 - 100

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13
Q

What is the pressure range of the large arteries?

A

80- 120

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14
Q

What is the pressure range of the small arteries?

A

60 - 100

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15
Q

What is the pressure range of the arterioles?

A

20 - 60

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16
Q

What is the pressure range of the capillaries?

A

0 - 30

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17
Q

What is the pressure range of the veins?

A

0 - 5 ish

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18
Q

What is the pressure range of the RV?

A

0 - 20

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19
Q

What is the pressure range of the pulmonary arteries?

A

15 - 30 ish

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20
Q

Why does pressure start to drop in the small arteries?

A

Branching and blood flow resistance increases

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21
Q

What determines pressure in the capillaries at a systemic level?

A

The pressure in the vessels upstream

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22
Q

What would happen upstream of arteriolar squeeze? Downstream?

A

It would increase pressure upstream, and decrease it downstream

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23
Q

What is Delta P?

A

The change in pressure

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24
Q

What happens with a high Delta P? Low?

A

High = more driving pressure meaning more blood flow can occur
Low = less driving pressure and less flow occurring

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25
Q

What is the MOA of edema in CHF in terms of pressure?

A

With higher venous pressure, fluid can get pushed (filtered) into the ISF, but it can’t be reabsorbed because of the higher pressure. So Delta P here is smaller.

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26
Q

What drives CO?

A

Tissue demand

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27
Q

What is the highest point of resistance in an artery? lowest?

A

Highest = the vessel wall
Lowest = the middle of the blood vessel (blood isn’t touching anything there)

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28
Q

What makes up Poiseuille’s law in the body?

A

The constant of pie, Delta P and radius, an increases in any of these would lead to more flow. Flow is inverse to blood viscosity and length of the tube, increase any of these and there will be less flow

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29
Q

What is the formula to determine vascular resistance?

A

Rearrange V = IR -> R = Delta P / Flow
If resistance goes up, either flow is going down, Delta P goes up

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30
Q

What drives the biggest change in flow of a blood vessel?

A

Radius or circumference of the vessel

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31
Q

What is the pressure on the afferent end of the arteriole? Efferent end?

A

30 and 10

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32
Q

Which vessels have the most resistance in the body?

A

Arterioles

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33
Q

What are the 4 starling forces? Give numbers as well

A

Hydrostatic pressure in the capillary (pushing fluid out) 30 mmHg
Hydrostatic pressure outside the capillary in the ISF (sucking fluid out of the capillary) -3 mmHg
Capillary oncotic pressure (protein pressure, sucking water into the capillary) 28 mmHg
ISF oncotic pressure (protein pressure suck water into the ISF) 8 mmHg

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34
Q

Why is water filtered at the beginning of the capillary and reabsorbed at the end?

A

A high delta P favors filtration, low favors reabsorption

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35
Q

What happens to pressure as it flows through high resistance vessels?

A

Pressure drops

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36
Q

What is the mean capillary pressure?

A

17.3 mmHg

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37
Q

What is the net filtration pressure? What does this mean?

A

0.3 mmHg, this means we slightly favor filtration

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38
Q

How much fluid is lost due to the net filtration pressure, and what happens to it?

A

1 - 2 L into the ISF, but it is scavenged by the lymphatic system and dumped back into the Vena Cava

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39
Q

What components make up the capillary oncotic pressure? Fraction of the total?

A

Albumin - 21.8 / 28 or 22 mmHg (4.5 g/dL)
Globulins - 6 / 28 or 6 mmHg (2.5 g/dL)
Fibrinogen - 0.2 / 28 or 0.2 mmHg (0.3 g/dL)

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40
Q

If you have CHF, the higher venous pressure means less fluid will be reabsorbed, and more gets pushed into the ISF, why is there no immediate edema in early stages of CHF?

A

The lymphatic system can increase its capacity to suck up fluid 20 fold, allowing it to suck up a lot of water

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41
Q

What is the permeability of compounds compared to? General trends?

A

The standard permeability of water, which is 1. The larger you are, the harder it is for you to cross a capillary

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42
Q

How do kidneys regulate RBC manufacture?

A

By erythropoietin release, if oxygen tension is low, EP is released to make the bone marrow grow more RBCs. If oxygen tension is high, EP release is slowed to decrease RBC production

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43
Q

What is the difference in split points of arteries vs veins in the kidney?

A

Renal artery -> segmental arteries, -> interlobar arteries -> arcuate arteries -> interlobular arteries -> afferent arterioles
Veins are the reverse, interlobular -> arcuate -> interlobar -> segmental -> Renal vein

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44
Q

Describe the basic setup of a nepron

A

Afferent arteriole -> glomerular capillary bed -> efferent arteriole -> peritubular capillaries

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45
Q

What is the term for deep peritubular capillaries? How many are there?

A

Vasa Recta, 5% of total PTCs

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46
Q

What occurs in the peritubular capillaries?

A

The bulk of reabsorption

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47
Q

What organs are the right kidney in contact with? Left?

A

R = liver
L = stomach, spleen and pancreas

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48
Q

What nerve controls bladder emptying?

A

Pudendal nerve

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49
Q

What is the supporting structures of the glomerulus?

A

The podocytes

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50
Q

What category of cell are the podocytes? What is their function?

A

Endothelial cells, and the slit pores of the podocytes are - charged to repel - charged proteins. Negative ions are still allowed in

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51
Q

What are the large openings on the endothelial layer of the glomerulus? Function?

A

Fenestrations, allows small things like water, glucose and ions to move with little to no resistance

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52
Q

What is the GFR?

A

125 ml/min

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53
Q

What is secretion?

A

Specifically placing something in the urine to be excreted, usually involves a transporter to move it from the capillary into the urine.

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54
Q

What is the formula to determine excretion?

A

Excretion = Filtration - reabsorption + secretion

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55
Q

What is the average reabsorption rate?

A

124 ml/min

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56
Q

What is the net filtration pressure in glomerulus? What is different about it relative to a normal capillary?

A

10 mmHg, and the starting pressure, which is 60 mmHg, double what is in a standard capillary

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57
Q

What is the relationship to BP in the capillary to filtration rate?

A

The higher the BP, the higher filtration will be, the lower it is, the lower filtration will be

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58
Q

What would happen to filtration if you squeezed the afferent arteriole?

A

BP in the glomerulus would drop, filtration would decrease

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59
Q

What would happen to filtration if you squeezed the efferent arteriole?

A

BP in the glomerulus would increase, filtration would increase

60
Q

What would happen to reabsorption if you squeezed the efferent arteriole?

A

Reabsorption would be favored because of the decreased hydrostatic pressure in the capillary

61
Q

What do most of our drugs target to manipulate glomerular BP?

A

The afferent arteriole

62
Q

Which vessel does the body use to modulate GFR? Which vessel would it use if it ONLY wanted to modulate GFR?

A

Modulate = afferent, if you just want to target GFR independent of other changes, you would modulate the efferent

63
Q

What happens to oncotic pressure as you move through the capillary?

A

As you go, it starts at 28 mmHg, then as filtration occurs and water leaves the capillary, the concentration of the protein increases, and oncotic pressure increases

64
Q

What occurs with a + reabsorption pressure and - filtration pressure?

A

Reabsorption is favored

65
Q

What is the net reabsorption pressure?

A

10 mmHg

66
Q

What is the formula for clearance?

A

Clearance = urine output x urinary concentration of the compound / plasma concentration of the compound

67
Q

What is the clearance rate of something that is filtered but not reabsorbed?

A

A high clearance rate

68
Q

What is the clearance rate of something that is filtered and reabsorbed?

A

A low clearance rate

69
Q

List the Renal vessels from renal artery to vein

A

Renal artery -> segmental artery -> interlobar artery -> arcuate artery -> interlobular artery -> afferent arteriole -> glomerular capillary -> efferent arteriole -> PTCs -> interlobular vein -> arcuate vein -> interlobar vein -> segmental vein -> renal vein

70
Q

What is the secondary function of the PTCs?

A

To provide the metabolic needs of the deeper parts of the kidneys via the vasa recta capillaries

71
Q

Describe the branching pattern of deep PTCs

A

DVR (descending vasa recta) = one vessel or branch
AVR (ascending vasa recta) = several ascending vessels or branches

72
Q

What creates the elevated hydrostatic pressure in the kidney? What allows release of this pressure if it gets too high?

A

The tough outer fibrous coating. The only exit point is the tubular system, so too high of pressure = increased UOP

73
Q

List the renal tubular structure

A

Corpuscle (Bowman’s capsul) -> PCT (proximal convoluted tubule) -> PST (proximal straight tubule) -> DTL (descending thin loop of Henle) -> ATL (ascending thin loop of Henle) -> TAL (thick ascending loop of Henle) -> MD (macula densa) -> DCT (distal convoluted tubule) -> CT (convoluted tubule) -> CCD (cortical collecting duct) -> oMCD (outer medullary collecting duct) -> iMCD (inner medullary collecting duct)

74
Q

How does the MD estimate GFR?

A

By counting Na, counts too few Na = low GFR, counts too much Na = high GFR

75
Q

How does the JGA affect GFR?

A

By dilating/constricting the efferent and afferent arterioles

76
Q

What system does the JGA use to cause constriction? Which vessel is it preferential to?

A

The renin system, and it can constrict both, but will preferentially constricts the efferent arteriole

77
Q

List these values: RBF, Hct, RPF, GFR and FF (under healthy conditions)

A

RBF (renal blood flow) = 1100 ml / min
Hct = 40% of RBF
RPF = 60% of RBF, or 660 ml / min
GFR = 125 ml / min
FF (filter fraction) = GFR / RPF or 125 / 660

78
Q

What is the highest resistance point in the kidneys?

A

The efferent arteriole

79
Q

Approximately how much reabsorption occurs in the PT?

A

~ 2/3 of total reaborption

80
Q

What is the clearance equation?

A

Cx = clearance
V = urinary flow rate
U = urinary concentration
Px = plasma concentration

Cx = V x U / Px

81
Q

What is the relationship to renal pressure and UOP?

A

Direct; if RBF goes up, UOP goes up, if RBF goes down, UOP goes down

82
Q

What is the relationship of charge and filterability?

A

+ = more filterable, - = less filterable

83
Q

What is the filtration coeffecient?

A

12.5 ml / min per 1 mmHg of pressure

84
Q

What 2 things can increase the filtration coefficient (kf)? Which is the primary modality?

A

Extreme infection or increased pressure, and the primary one is the severely increased pressure

85
Q

What is the relationship to plasma creatinine and GFR?

A

Linearly inverse, if you half GFR, plasma creatinine (over time) should double

86
Q

Where does most of the organic cation/anions secretion occur?

A

In the proximal tubule

87
Q

What is the rate of creatinine secretion?

A

0.1 to 0.15 mg / min

88
Q

Why is the creatinine blood test less accurate than inulin?

A

Because Inulin is ONLY filtered, no secretion giving a very accurate measure of GFR. Whereas there is a small amount of creatinine being secreted which changes the GFR measurement

89
Q

What compound can you use to measure RPF?

A

PAH, para-amino hippuric acid

90
Q

What changes after a nephrectomy? What stays the same?

A

Excretion rate of creatinine stays the same, 1.25 mg /min, plasma creatinine increases and GFR decreases

91
Q

What are the terms for the side of the tubular cell in contact with the tubule? ISF?

A

Tubule = apical membrane, tubular side, luminal side
ISF = basolateral membrane, interstitial side

92
Q

What is Na reabsorption linked with in the PT?

A

Glucose and AA reabsorption or the Na/H exchanger

93
Q

How does Cl get into the ISF in the PT?

A

It follows the + charge of Na, which is going into the tubular cell, then being pumped into the ISF

94
Q

What is the term for the massive movement of water and solutes in the PT called?

A

Bulk flow

95
Q

What drives Na into the tubular cell from the lumen in the PT?

A

The negative charge of the tubular cell (-70) attracts the Na in, and the lumen has a charge of -3, creating the gradient for Na to follow

96
Q

Where would you find the brush border?

A

Per lecture, isolate it to the basolateral membrane

97
Q

Why does Na/Cl concentration in the filtrate not change much throughout the tubule?

A

Because Na and Cl closely follow water, if it constantly follows water then the concentration won’t change. Whereas things like glucose get reabsorbed and stay reabsorbed, decreasing filtrate concentration. Inverse is true for creatinine, it stays behind, and as water leaves, the creatinine gets more concentrated

98
Q

What helps secrete protons in the PT?

A

The NHE (Na/H) pump

99
Q

How does the PT help regulate pH?

A

By secreting protons into the urine, it can combine with bicarb and then move into the tubular cell to then be reabsorbed

100
Q

Describe the cycle of reabsorbing bicarb

A

Bicarb is easily filtered, and we don’t want to waste it. The PT secretes protons into the lumen, which, along with the carbonic anhydrase enzyme, then combines with bicarb to form carbonic acid. CA then disassociates into H2O and CO2, both go into the tubular cell. In the cell, the carbonic anhydrase enzyme is present, and carries out the reaction in reverse, combining CO2 and H20 to make bicarb and H, the bicarb is then reabsorbed

101
Q

What is the only part of the tubule that as AA and glucose transporters?

A

The proximal tubule

102
Q

Where are the organic anion/cation transporters (OAT and OCT)?

A

The proximal tubule

103
Q

What is the difference between SGLT and GLUT?

A

SGLT is on the apical (luminal side) membrane, and gets glucose out of the lumen and into the tubular cell. GLUT is on the basolateral side (ISF side) to get glucose into the ISF to be reabsorbed

104
Q

What is the difference between SGLT 1 and 2? Which one do we prefer to use?

A

1 = low capacity high affinity, reabsorbs 10% of our glucose at a 2:1 ratio of Na to glucose, it is high affinity to make sure it grabs any glucose that SGLT 2 misses. Uses a lot of energy
2 = high capacity, low affinity, this means there needs to be a lot of glucose present for it to work. reabsorbs 90% of our glucose at a 1:1 ratio of Na to glucose. More energetically favorable, making it the preferred method to move glucose

105
Q

What happens if SGLT 2 fails?

A

SGLT-1 can pick up the slack a bit, increasing its ability to grab total luminal glucose from 10% up to 35%

106
Q

Why is GFR higher than 62.5 in someone who donated a kidney?

A

The nephron can undergo physiologic hypertrophy of the nephrons, increasing GFR past baseline.

107
Q

Where does the bulk of transporter function for pH occur?

A

PT

108
Q

Where are the 3 areas of the kidney that can make bicarb? Precursor molecule?

A

PT (proximal tubule) TAL (thick ascending loop of Henle) and DCT (distal convoluted tubule). Precursor = Glutamine

109
Q

What does glutamine give you?

A

2 bicarbs and 2 ammonium ions

110
Q

What are the 2 primary urinary buffers?

A

Bicarb and phosphate

111
Q

What effect does renin have on aldosterone?

A

Increases circulating aldosterone

112
Q

What does angiotensin II do in the proximal tubule?

A

Binds to the AT1 receptor, speeding up the Na/K pump. Na leaves the tubular cell, allowing more Na to come in from the lumen via the NHE pump and pumping more H into the lumen. Water follows the Na, so we conserve water and Na

113
Q

Describe how Ca usually likes to be reabsorbed

A

Na goes into the tubular cell of the PT, Cl follows Na, and Ca follows the Cl. Once in the tubular cell, Ca can be pumped via an atp pump, via a 3 Na / 1 Ca exchanger

114
Q

How much Ca do we filter? Why?

A

About 60%, because of the 2+ charge on Ca, it will hang out close to large negatively charged things, like protein which can’t be filtered. So the Ca that is too close to proteins, won’t be filtered.

115
Q

What releases para thyroid hormone?

A

The lateral sides of the parathyroid gland

116
Q

How does PTH help increase blood calcium?

A

3 methods; increase Ca absorption in the gut by activating vitamin D (cholecalciferol) into active vitamin D (1,25 Dihydroxy-cholecalciferol). It also acts on tubular cells in the PT to increase Ca reabsorption. 3rd, is to upregulate osteoclast activity (break down bone) and downregulate osteoblasts (bone making cells) to release calcium and phosphate from bone.

117
Q

How much water is reabsorbed in the DTL?

A

20%

118
Q

Generally, what is the trend of water vs solute movement in the tubule?

A

As you go “down”, water moves and solutes stay behind, as you go “up”, water stays behind (sort of) and solutes move

119
Q

Why would a high flow rate of the AVR reduce interstitial osmolarity?

A

Because if you go too fast, there isn’t time for the salts in the AVR to move into the interstitial space

120
Q

Where are most ions moved out of the lumen?

A

In the TAL, via the NK2CC transporter, Mg and Ca are reabsorbed here as well

121
Q

What is the primary source of dissolved renal substances?

A

Ions/solutes reabsorbed in the TAL

122
Q

What is a unique feature of the tubular cells in the TAL?

A

They have K channels on the tubular side of the cell, normally you only have K channels on the luminal side

123
Q

What drives cation reabsorption in the TAL?

A

Potassium leaking into the lumen, the now + lumen drives the cations into the ISF

124
Q

What happens to H, Na, K and Cl in the TAL?

A

K comes in, and can either go into the ISF or the lumen
Na comes in, and gets pumped into the ISF via an Na/K pump
Cl goes into the ISF via a channel
H gets pumped into the lumen in exchange for Na

125
Q

Where is the diluting segment found? What creates this?

A

Distal tubule, the action of the TAL, we reabsorb so many ions that osmolarity drops significantly, and is the only part of the tubule where the lumen is significantly more dilute than its environment

126
Q

What primarily moves in the DT?

A

Na, Cl and Ca into the tubular cell from the lumen, then you have an Na/K pump on the basolateral membrane, and a Na/Ca exchanger on the basolateral membrane as well (pumps Ca into the ISF, Na into the tubular cell). There is a Ca atp pump into the ISF as well, but like the heart, the exchanger does most of the work here

127
Q

What do thiazide diuretics block?

A

The Na/Cl co transporter in the DT

128
Q

What does PTH do in the DT?

A

Governs how many channels are present in the wall to reabsorb calcium from the lumen.

129
Q

How would you manipulate Na in the DT to increase Ca reabsorption?

A

Reduce intracellular Na concentration, if there is less Na, then the Na/Ca exchanger will speed up, sending Ca into the ISF and bring Na into the tubular cell. An easy way to do this is blocking the Na/Cl cotransporter

130
Q

What is the chronic effect of elevated PTH, increased osteoclast and decreased osteoblast activity?

A

Osteoporosis

131
Q

What are the 2 main cell types in the DT? Basic function of each?

A

Principal cells = manage potassium levels
Intercalated cells = pH or Acid/Base management

132
Q

What does aldosterone do? Where does it work?

A

In the principal cells of the DT. It speeds up the basolateral Na/K pump, putting Na into the ISF, K into the tubular cell. Then the luminal Na/K channels let more Na in, and allow K to leave. Overall effect, is conservation of water and Na, while wasting K

133
Q

What does high aldosterone do to Na/K? Low?

A

High = waste K, hold onto Na
Low = hold onto K, waste Na

134
Q

What effect does Aldosterone have on the channels of the principal cells?

A

It dictates how many Na channels we have, more aldosterone = more Na channels, less = less channels. No change in K channels though

135
Q

Where is aldosterone produced?

A

The adrenal glands, specifically, in the Zona glomerulosa

136
Q

What are the layers of the adrenal gland (outer to inner)?

A

Zona glomerulosa, Zona fasciculata, Zona reticularis and the Medulla

137
Q

Where are cortisol and androgens made?

A

The adrenal glands, specifically the zona fasciculata and zona reticularis

138
Q

Where are catecholamines produced?

A

The adrenal glands, specifically the medulla

139
Q

Why would excess cortisol waste potassium? What is the bodies defense against this?

A

Cortisol looks very similar to aldosterone, if there’s enough cortisol (or other cholesterols) it can actually bind to the aldosterone receptor. The principal cells have an enzyme, 11-beta HSD that will break down non-aldosterone steroids to prevent them from binding to the intracellular aldosterone receptor

140
Q

What is the relationship of K to aldosterone?

A

If K increases, aldosterone increases to try and waste K. If K decreases, aldosterone decreases to try and hold onto K

141
Q

What happens if you inhibit Na reabsorption before you hit the DT?

A

The excess Na in the lumen floods into the principal cell, leading to a greater loss of potassium because the Na/K pump on the basolateral membrane speeds up. This is why diuretics like lasix make us waste so much K, we hold onto a lot more Na.

142
Q

What do type A and B intercalated cells do? Which is more active?

A

A = get rid of protons (the more active of the two)
B = get rid of bicarb

143
Q

WHAT DOES EFFING AVP STAND FOR

A

Arginine Vasopressin

144
Q

How does AVP/ADH/vasopressin work?

A

It binds to the V2 receptor on the basolateral membrane of the intercalated cell. This mobilizes type 2 aquaporins (AQP-2) to go to the apical membrane and allow water in. AVP also modulates how much Urea is coming back in.

145
Q

What does V1 do? V2?

A

V1 = modulate vascular resistance
V2 = modulate water reabsorption

146
Q

How do aldosterone and AVP work on the collecting ducts?

A

Aldosterone has no effect. AVP can still cause water retention.

147
Q

Where are the osmoreceptors located and how do they work?

A
148
Q

What makes ADH unique relative to other compounds that modulate water/ion movement in the kidneys?

A

ADH ONLY changes water reabsorption, every other compound deals with volume and salts

Semester 1 TxWes (7 decks)

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