NBS Exam 2 Flashcards
1
Q
Where does gas exchange first occur?
A
the respiratory bronchioles
2
Q
the right and left bronchi have how many main stem bronchi?
A
Right has 3, Left has 2
3
Q
constriction of bronchi is due to
A
PNS innervation / alpha adrenergic agonists
4
Q
dilation of bronchi are due to
A
SNS inntervation/B2 adrenergic agonists
5
Q
the diameter of bronchioles is dependent on what 2 main factors
A
lung volume and by local O2 and CO2 in the airways
6
Q
local hypocapnia causes
A
local bronchiolar constriction to direct ventilation away from alveolar regions with poor perfusion
7
Q
hypocapnia is
A
a state of reduced carbon dioxide in the blood
8
Q
Local hypercapnia/hypoxia causes
A
local bronchiolar dillation, directing airflow to alveolar regions with better prefusion
9
Q
pores of Kohn are important for
A
exchange of gasses btw alveoli via diffusion, and for the spread of Type II pneumocytes and macrophages btw alveoli
10
Q
bronchiolar veins are an example of a
A
Right to Left shunt
11
Q
what percent of the atmospheric air is O2
A
20.93
12
Q
define O2 capacity
A
max amount of O2 combined w/ Hb at high PO2 = 1.39ml O2/gm Hb
13
Q
define O2 saturation
A
the percent of capacity that is occupied by O2
14
Q
define O2 content is (C o2)
A
(PO2s) + ([Hb]saturation*1.39)
15
Q
what factors cause a right shift in the Hb binding curve
A
increasing Temp, 2,3BPG, CO2, and H+
Decreasing pH
16
Q
right shift favors the ___ of O2
A
unloading of O2 (lower affinity)
17
Q
left shift favors the ____ of o2
A
loading of O2 (higher affinity)
18
Q
CO2 + H20 –>
A
H2CO3 –> H+ +HCO3-
19
Q
most of the CO2 that the body transports is carried as
A
HCO3=
20
Q
distral straight tubule is the same as the
A
Thick ascending limb
21
Q
FF (filtration fraction)
A
GFR/RPF
22
Q
Acetazolamide is
A
an carbonic anhydrase inhibitor leading to diuresis
23
Q
Furosemide
A
inhibits the NKCC co transporter –> leading to diuresis. loop diuretic
24
Q
chlorthiazide
A
inhibits the Na/Cl- cotransporter –> leading to diuresis. Type of diazide diuretic
25
Amiloride
sparing diuretic, inbitis the Na+ channel and inhibits K+ secretion
26
the macula densa senses
NaCl
27
calculate reabsoprtion
Filtration - excretion
28
clearance eqn
Clearance = [X}in urine * Urine flow rate / concentration C in arterial plasma
29
the Clearance of PAH is equal to
Renal plasma flow
30
what do you use to calculate the Renal plasma flow? why?
the clearance of PAH since PAH is completely cleared from the plasma in a single pass
31
normal GFR
120 ml/min
32
how do you calculate GFR?
Clearance of Inulin. You can also use creatinine.
33
what is filtration fraction
it is the fraction of the renal plasma flow that becomes glomerular filtrate
34
calculation of FF is
GFR / RPF = Cinulin/Cpah
35
normal plasma flow rate
600
36
RBF normal value?
1.2 L/min
37
when Na/Cl is high within the thick ascending limb, what transporter is responsible for the movement of Na/Cl into the macula densa?
NKCC (Na, K, 2Cl)
38
primary mechanism of tubuloglomerulae feedback : Na/cl control through the macula densa
increase in chloride from the macula densa --> increase in Ca+ movement into the macula densa --> increasein ATP and a decrease in NO. This leads ultimately to the constriction of the afferent arteriole and a decrease in GFR
39
secondary mechanism of tubuloglomerular feedback
Cl- in the macula densa communicates with the JG cells. The JG cells will stop secreting renin, leading to a decrease in aldosterone and angiotensin and thus a vasodillation. Vasodillation will increase GFR to restore
40
decreased NaCl leads to
vasodillation of the afferent arteriole to increase GFR
41
sympathetics lead to
AA constriction through NE release on alpha-1 adrenoreceptors. decrease in GFR and RBF
42
Angiotensin II at low physiologcal cocentrations
constriction of both afferent and efferent, but more of an effect on the efferent so increased GFR but decreased RBF
43
Angiotensin II at high concentrations
constriction of both afferent and efferent, leading to decreased GFR and RBF
44
Endothelin I
potent vasoconstricor that decreases GFR and RBF. comes from the mesangial cells
45
Adenosine
constriction of the afferent arteriole leading to a decrease in RBF and GFR
46
Prostaglandins
occur due to a result of some negavity. They are relased when sympathetic outflow is high
47
what causes the release of prostaglandins
when sympathetic outflow is high, dehydration, stress, ANGII
48
what is significant about prostaglandins
they are the escape from constrictor mechanisms
49
PGs do what
PG release PGI2, PGE2 and PGE1 which all help to prevent ischemic damage leading to an increase in RBF with no real change in GFR
50
nitric oxide and bradykinin
dillation of afferent and efferents leading to an increase in GFR and RBF
51
bradykinin stimules
release of NO and PG
52
ANP
from stretch receptors in the atrium which leads to dillation of the afferents and constriction of the efferents leading to an increase in GFR
53
renin
converts angiotensinogen and converts it to angiotensin I
54
calculate reabsoprtion
amount filtered - amount excreted
55
The net reabsorbed is
(GFR)(concentration in the plasma) - (Urine flow rate) (concentration in the urine)
56
if the ratio of Cx : C inulin is greater than one
then the substance is secreted
57
If the ratio of Cx:Cinulin is less than one then
the substance is reabsorbed
58
what are the 4 transporters in the early proximal tubule that i should care about
1- the NHE3 on the apical side that exchanges H+ out for Na+ in.
2- the AE1 on the basolateral side that exchanges a HCO3- to the blood for a Cl-
3- the NBC1 ont he basolateral side that puts Na and HCO3- into the blood
4: the SGLT 2 ont he apical membrane that brings glucose in with a high capacity but a low affinity
59
how does most of the Na/Cl come into the cells
through a transcelluar route (2/3!)
60
What is the important exchanger in the 2nd half of the PCT
The anion chloride exchanger which sits on the apical side of the cell and pumps anions out and Cl- in. This is how we excrete a lot of the drugs we take.
61
the high number of Na/K ATPases in the PCT function to
pump alot of sodium into the blood thus taking H20 with it through squaporin channels
62
Test Q* define glomerulotubular balance
as GFR increases, the oncotic forces increase in the efferent arteriole which then asserts a high oncotic force to bring H20 back in
63
is the thick ascending limb permeable to water?
NO!
64
the thick ascending limb has what notable transporters
NKCC Na in, 2Cl- in, K in.
65
where do you find the NKCC
the NKCC can be found in the Thick ascending limb and is responsible for the uptake of Na and Cl in the macula densa
66
the diluting segment of the nephon is
the thick ascending limb since it is taking ions in but leaving the water in the tubule
67
what important transporter is found in the early DCT?
The Na+/Cl- transporter which brings Na and Cl into the cell.
68
what drug blocks the NKCC
Furosimide
69
what kind of drugs will block the Na/Cl co transporter in the early DCT?
thiazide
70
what are the main cell types that are found in the late DCT, collecting tubule and collecting duct?
Principal cells, alpha intercalated cells and beta intercalated cells
71
AQP2 is found
on the apical side of principal cells of the late DCT and Collecting duct
72
AQP3 and AQP4 are found
on the basolateral side of principal cells in the late DCT and the collecting duct
73
alpha intercalated cells have what types of channels
secrete acid using an ATPase which exchanges H+ for K+, pumping H+ into the urine. They also have an ATP H+ pump to pump H+ into the urine. On the basolateral side they have an AE2 pump that pumps HCO3- into the blood in exchange for a cl-
74
Beta intercalated cells have what types of channels
Pendrin (Cl/HCO3), which pumps HCO3- into the urine in exchange for a cl
75
what is pendrin channel
in a b intercalated cell, it is responsble for pumping HCO3- into theurine in exchange for a cl-
76
what is the glucose maximum that can be reabsorbed
375 mg/min
77
angiotensin II
acts directly on PCT to increase Na+ and H20
78
Aldosterone
acts on the TAL, CT and DCT on the principal cells where it stimulates reabsoprtion of Na and loss of K+
79
Acute v chronic phase of aldosterone
acute phase (hours --> day): increase in the activity of the Na/K ATPase which decreases Na in the cell and drives the reabsoprtion of Na from the urine and secretion of K+. (saving Na and loss of K+)
Chronic: Na/K ATPase activity and # increase leading to high K+ in the cell and low Na+ putside. New K+ channels also get inserted on the apical side to pump it out and make the ATPase more efficient
80
Angiotensin acts on the
PCT
81
Aldosterone acts on the
DCT
82
ADH acts on the
DCT and mainly in the collecting duct
83
ADH is realeased from the
posterior pituitary
84
ADh binds to the
V2 receptor
85
V2 receptor increases
cAMP
86
increase in PKA (in relation to ADH) as a result of ADH causes
the insertion of aquaporin channels on the apical membrane leading to the absorption of H20 and the insertion of urrea channels which also helps bring H20 in
87
summary of ADH
vasoconstriction, insertion of AQP2 channels to increase H20 reabsoprtion, increase of urea uptake, stimulation of thirst, increase activity of the NKCC in the TAL
88
low BP causes the JG cells to
release renin with cleaves angiotensinogen into ANT I which then goes to the liver to become ANT II which is a vasoconstrictor leading to an increase in BP. Angtiotesin II also causes secretion of aldosterone which increases blood volume
89
PTH
inhibits Na+ and H20 reabsoption in the PT --> dumping volume. Inhibits phosphate reabsorption. It also increases bone resorption leading to an increase in Ca2+ resorption in the TAL &
90
prostaglandins
dilates renal blood vessels to maintain nutritive aspects
91
Natriuretic hormone
inhibits Na+ reabsoprtion --> dumping of fluid
92
Urodilatin
inhibits the reabsprtion of Na in the collecting duct
93
aldosterone
increases Na reabsoprtion in the loop of Henle, distal tubules and colelcting duct via Na/K ATPase
94
Carbonic anhydrase inhibitor
acetozolamide
95
diuretics that apply to the proximal and collecting duct often lead to
acidosis
96
diuretics that act in the collecting duct often lead to
alkylosis
97
Furosimide
diuretic that acts in the thick ascending limb to block the NKCC
98
chlorothiazide
blocks the apical Na/Cl transporter in the DCT
99
Amiloride
diuretic that acts int he collecting duct to inhibit the Na channel collecting duct
100
Spironolactones
block aldosterone leading to an increase in Na+
101
Hypoxic Hypoxemia
low Po2 stimulates breathing
102
anemic hypoxia. Cause?
low hb int he blood, but normal PO2
| -Can be from CO poisoning --> get no ventialtory response to CO2
103
stagnant hypoxia cause and response
low blood flow --> ventialtory response from the CB
104
Histotoxic hypoxia cause and response
low ATP production due to cyanide which will block the ETC
105
fixed acids are
sulfuric and phsophoric acids which result from metabolism of sulfur or phosphate containig AA
106
organic acids are
production of Lactic, pyruvic acid
107
amount of fixed acid
50-100 mm/day
108
alkylosis can lead to
hyperexcitablility
109
most powerful and important bufferig systems are
proteins
110
The 4 major physiochemical buffers are
bicarbonate, phosphate, ammonia and proteins
111
Step 1 in the 6 step mechanism: shortcut for converting pH to H+ ion
```
[H] = 80 -pH*XX
[H] = 24 *(PaCO2/HCO3-)
```
112
Buffering power pertains to what 2 things?
1. concetration of the buffer
| 2. the zone of pH has to be +/- 1 to the proteins Pk
113
if the pk of a buffer is at 6.1, what pHs is it good at buffering?
5.1 --> 7.1
114
why is HCO3 considered to be an important buffer?
it cannot be saturated or pushed to one extreme ot the other since it is an open buffering system
115
is phosphate a powerful buffer?
No! While its pk is appropriate, there is no enough Pi in the ECF/plasma to be powerful.
116
the kidneys filter how much HCO3-/day
180 L/day * 24 mEq/L = 4320 mEq/Day
117
What is a system that generates NEW bicarbonate?
the phosphate buffer system and the Nh4/NH3 system
118
PTH does what to phosphate
PTH blocks the reabsoprtion of H2PO4 into the cell thus driving the excretion of phosphate and H+
119
does ammonium or ammonia predominate at acific pH
Nh4+ (which cannot move across the lipid bilayer)
120
what activates glutaminase
hydrogen
121
what does glutaminase do
it breaks down glutamine to Nh4+ and HCO3-
122
Where is NH4+ reabsorbed the most?
In the Thick ascending limb `
123
most prevalent species of ammonia in urine is
NH4+ since urine is acidic
124
calculate bicarbonate excretion
urine flow rate*urinary HCO3-
125
an increase in H+ in the intracellular fluid results in
an increase in activity of the Na/H exchanger, an increased afinity of the exchanger, increase in H+ ATPase and a stimulation of glutaminase to make ammonia, an increase in the Na+ absorption (Na+ in, H+ out)
126
describe the mechanism of volume based contraction alkylosis
When low blood volume --> angiotensinII is realsed to incresae Na+ absoprtion in the PCT (to bring H20 in with it). The increase in Na+ absorption causes the cell the excrete H+ --> alkylosis
127
being hypokalemic leads to
alkylosis
128
being hyperkalemic leads to
acidosis
129
part of the tubule that drives the steepest excretion of H+
CD and Late Distil Tubule
130
salicylic acid and treatment of overdose
salicilate causes the respiratory centers to increase ventilation which leads to an initial ventilation. This creates an alkilosis. The physicians then treat the alkalosis with acid, however the drug itself is an acid so this makes them much worse.
131
diarrhea leads to
an increase in HCO3- loss and thus acidosis. Also leads to an increase in Cl
132
carbonic anhydrase inhibitors
cant take the HCO3- back into the blood while you are conutously makng acid --> acidosis
133
ethylene glycol is metabolized to
OXALIC ACID
134
type I renal tubule acidosis
inability of the distal nephron to pump acid into the tubule and acidify the urine (further accentuating theproblem by reducing the ammonia trapping mechanism)
135
Type II renal tubule acidosis
inability of the proximal to reabsorb HCO3- in the proximal region
136
How do you differentiate Type I RTA
when NH4Cl challenge, you cannot excrete that excess acid that was given. A normalperson will have a urine pH below 5.5, but a person with Type I RTA will not have a urine pH below 5.5
137
How to you diagnose Type II RTA
No problem in acidifying the urine.. the urine will have a ph below 5.5
138
Type IV RTA
reduction in both K+ and H+ secretion by the collecting duct
139
Type 4 RTA will present with
urine ph below 5.5 since there is decreased ammonia in the urine to buffer he secreted H+
140
how does aldosterone affect Na, K and H
aldosterone increases reabsoprtion of Na+ and increases excretion of H+ and K+
141
effect of vomiting on blood ph
you are losing acid to you ca become alkylotic
