APII_Exam 1 Flashcards
(604 cards)
1
Q
what are the function of the kidneys
A
-excretion of waste: urea, cratinine
-excretion of foreign chemicals: drugs, toxins
-secretion/metabolism/excretion of hormones: erthryopoetic facotr
-regulation: acid base balance
-gluconeogensis: from amino acids
-controls arterial pressure
-regulation of water and electrolyte secretion
2
Q
what are some waste products the kidneys excrete
A
urea
creatinine
bilirubin
hydrogen
3
Q
what are some foreign chemicals the kidney excretes
A
drugs
toxins
pesticides
food additives
4
Q
what are some hormones the kidneys secrete/metabolize/excrete
A
renal erythropoietin factor
vitamin D3
renin
5
Q
what do kidneys perform gluconeogenesis with
A
amino acids
6
Q
what does excess BUN indicated
A
kidney disease
7
Q
what is a normal BUN level
A
20
8
Q
what is a byproduct of proteins being broken down
A
urea
9
Q
what is 100% excreted by the kidneys
A
creatinine
10
Q
what type of metabolism is creatinine metabolized from
A
muscle metabolism
11
Q
what time of metabolism is urea metabolized from
A
protein metabolism
12
Q
what type of metabolism is uric acid metabolized from
A
nucleic acid metabolism
13
Q
what type of metabolism is bilirubin metabolized from
A
hemoglobin metabolism
14
Q
what is the byproduct of ammonia
A
is all of urea excreted in urine
15
Q
what is byproduct of RBC breakdown
A
bilirubin
16
Q
how long does a RBC live for
A
120 days
17
Q
what is RBC broken down into
A
heme and globin
then into bilirubin
18
Q
is bilirubin conjugated or nonconjugated when it is first formed
A
non conjugated
19
Q
where is bilirubin conjugated
A
liver
20
Q
after bilirubin is conjugated where does it go
A
into bile which then goes into the bowel
21
Q
what makes urine yellow
A
bilirubin
22
Q
once liver detoxifies blood, where does part of the waste go
A
kidneys to be excreted
23
Q
what drug class is commonly excreted through kidney
A
antibiotics
24
Q
what is a common issue with halothane
A
nephrotoxic and HEPATOtoxic
25
what hormones are produced in the kidney
vitamin D3
renal erythropoetic factor
renin
26
what hormones are metabolized and excreted in the kidney
most peptide hormones such as insulin, angiotensin II
27
what hormone stimulates RBC production from kidney
renal erythropoetic factor
28
what causes pink puffer COPD
polycythemia from low O2 levels in blood which stimulates kidney to make more RBCs
29
what allows absorption of Ca in digestive tract and puts calcium into bone
vitamin D3
30
how does erythropoietin stimulate RBC production
stimulates erythrocyte production in the bone marrow
31
what ion metabolism is vitamin D3 important in
phosphate
32
what are the only means of excreting non-volatile acids
kidneys
33
how does the kidney regulate the body fluid acidity
bicarbonate
34
what is the carbonic acid formula
h2o + co2 <---> H2CO3 <---> HCO3 + H
35
what is carbonic acid
H2CO3
36
how is most CO2 carried in the blood to the lungs
bicarbonate
37
what actually drives respiration
H+ ions around pons in CSF
38
where does H+ have to be formed to be able to drive respiration
CSF from CO2
39
what does low and high bicarb mean
low= metabolic acidosis (high H+)
high= metabolic alkalosis (low H+)
40
why does high CO2 cause acidosis
creates H+ through carbonic acid equation thus a build up of excessive H+ ions
41
how is CO2 breathed off if carried through body as bicarb
combines with H+ to make carbonic acid which gets broken down into CO2 and water
42
what does the liver use for gluconeogenesis
glycogen
43
what does the kidney use for gluconeogenesis
amino acids
44
how does the kidney regulate arterial pressure
raas
prostaglandins (inflammatory)
bradykinin (inflammatory
controls extracellular fluid volume
45
raas, bradykinin, and prostaglandins are the _________________ function of the kidney
endocrine
46
what electrolytes balance the kidneys
Na
K
H+
Ca
Phos
Mg
47
with increased intake of Na, how many days does it take the kidneys to balance the Na level
4-6 dyas
*8 days on the graph*
48
what part of the kidney has no glomeruli
medulla
49
what surrounds kidney and provide protection
capsule of the kidney
50
where are nephrons found in the kidney
renal pyramids
51
are nephrons located in teh medulla and the cortex?
YES in both
52
what is the flow of urine
nephron (renal pyramid)
papilla
minor calyx
major calyx
renal pelvis
ureter
53
what is in between the renal pyramids
renal columns
54
where is hydronephrosis found
underneath the renal capsule
55
what surrounds the kidney
fat
56
what is normal GFR per min and per day
125 ml/min
180L/day
57
how many times per day is plasma volume filtered
60x
58
does albumin or other proteins get filtered
NO
59
what is the filtration fraction equation
GFR / renal plasma flow= 0.2 (.20 x plasma filtered)
60
what is role of renal columns
extension of renal cortex that gives stability to kidney
61
what drives renal filtration
renal blood supply
62
what do renal arteries/veins branch out into
interlobular arteries and veins
63
what do interlobular arteries/veins branch into
arcuate arteries/veins
64
when does interlobular turn into arcuate
at turn of renal pyramid at the top
65
what branches off arcuates
interlobular
66
what branches off interlobular
afferent arterioles
67
what do interlobulars form
spiralling affect around nephron
68
how many glomerulus does a nephron have
1
69
what does glomerulus look like
bundle of vessels
70
what encases the glomerulus
bowmans capsule
71
what is the filtration apparatus of the kidney
glomerulus
72
what brings blood to the glomerulus and what artery does it come from
afferent arteriole brings it in
branches off interlobular artery
73
what takes blood away from the glomerulus
efferent arteriole
74
why does the glomerulus coil
increases surface area
75
what attaches to bowman's capsule carrying filtration content away
proximal tubule
76
what does proximal tubule turn into
descending loop of henle
77
finish the sequence--
proximal tubule-loop of henle--
distal tubule
78
where does collecting duct terminate
renal papilla
79
what does efferent arteries rap around
loop of henle
80
when does efferent arteriole attach to arcuate vein
after it wraps around loop of henle
81
what is ascending loop of henle attached to
descending loop and distal tubule
82
what is descending loop of henle between
proximal tubule and ascending loop
83
what does the distal tubule feed into
juxtaglomerular apparatus
84
what does juxtaglomerular apparatus dump into
connecting duct which dumps into collecting duct which dumps into papilla
85
do nephrons replace themselves
no
1.2 million nephrons per kidney
lose 1% per year after 40
86
what is glomerulus always in and what is loop of henle always in
g=cortex
LoH= medulla
87
which loop of henle has important function with water
-juxtamedullary- concentrate urine (pull water into back system)
88
what are portions of ascending/descending loop of henle
thick and thin
89
what are two types of nephrons
cortical and juxtamedullary
90
where are all glomeruli vs all loop of henle
glomeruli= cortex
loop of henle= medulla
91
which nephron has shorter loop of henle
cortical
92
which nephron has longer loop of henle
juxtamedullary
93
should there be protein or glucose in the urine
NO
94
what are systems of peripheral nervous system
ANS
Somatic
95
what is the receptor and neurotransmitter of somatic motor
Ach
nicotinic
96
what is the receptor and neurotransmitter of sns
epi/norepi- ,
alpha 1,
alpha 2,
beta 1,
beta, 2,
beta 3,
97
role of alpha and beta receptors
alpha 1= constrict
alpha 2= inhibit constriction
beta 1= increases HR
beta 2= inhibit response
beta 3= neutralizer
98
role of nicotinic vs muscarinic
N= muscular
M= organs/glands
99
how many neurons does a response have to go through
2 neurons
100
what is the receptor and neurotransmitter of pns
ach
nicotinic= n1, n2
muscarinic= m1, m2, m3
101
does sns have long or short pre ganglionic
short
102
does sns have long or short post ganglionic
long
103
does pns have long or short pre ganglionic
long
104
does pns have long or short post ganglionic
short
105
what are muscarinic receptors usually on
glands and organs
106
what is neurotransmitter for preganglionic in pns or sns
acetylecholine
107
by default what are all receptors in 1st synapse in pns or sns
nicotinic
108
what are neurotransmitters and receptors post ganglionic for pns (second synapse)
cholinergic (nicotinic/muscarinic)
Ach
109
what are neurotransmitters and receptors post ganglionic for sns (second synapse)
adrenergic receptors (alpha/beta)
epi/norepi
110
what nicotinic receptor is post ganglionic in somatic nerve
N1
111
what is the bladder muscle
detrusor muscle
112
what are receptor sites on bladder and nerves that synpase with them
M3- PNS- Pelvic nerve
Beta 3- SNS- hypogastric
113
what is the external sphincter in
urogenital diaphragm
114
what separates internal from external sphincter in male
prostate
115
what receptor is on internal sphincter
alpha 1 -SNS- Hypogastric
116
what receptor is on external sphincter
somatic- pudenal
117
what muscle is voluntarily controlled in urethra
external sphincter
118
do women have an internal sphincter
Yes, but does not have constricting ability like males do
119
is male internal sphincter voluntarily controlled
NO
females is
120
what is the sensory nerve attached to the bladder and how does it sense things
pelvic- baroreceptors- senses stretch
121
what regions do nerves come out of that innervate bladder and urethral muscles
sacral and thoracic region
122
how does empty bladder signaling work
baroreceptors signal slowly which causes beta 3 to neutralize contraction and alpha 1 to constrict internal sphincter for urine to collect- m3 is also inhibited in bladder to stop contraction and nicotinic signals external sphincter to constrict
123
what receptor neutralizes contraction of the bladder
Beta 3
124
full bladder signaling
stretched bladder activates baroreceptors on pelvic sensory nerve which goes to pons (micturition center) which signals m3 (detrusor muscle to constrict), beta 3 is inhibited to bladder can constrict, alpha 1 is inhibited so internal sphincter can relax, and pudendal signals external sphincter to relax and let urine out
125
what nerve does sensation to urinate come from and where does it go to in the brain
pelvic sensory- pons
126
when does voiding reflex happen
after initiation- to completely empty bladder
127
how does voiding reflex work
baroreceptors keep signaling via pelvic nerve to have pelvic motor nerve to to keep detrusor muscle (m3) to constrict
128
what are the 4 mechanisms of urine formation
filtration
reabsorption
secretion
excretion
129
filtration, reabsorption, excretion of water
180
179
1
130
filtration, reabsorption, excretion of sodium
25
560
25
410
150
131
filtration
reabsoprtion
excretion
of glucose
180
180
0
132
filtration, reabsorption, excretion of creatinine
1.8
0
1.8
133
is any creatinine reabsorbed
NO
134
what is equation for excretion
excretion=filteration-reabsorption + secretion
135
how much renal plasma is filtered
20%
136
what is normal Renal blood flow, GFR and reabsorption
RBF= 625 ml/min
GFR= 125ml/min
reabsorption= 124ml/min
137
how much blood goes to kidney per minute
1.1 liter- only 50% is filtered, the rest is for kidney itself
138
what is gfr in ml/min and l/day
125 ml/min and 180/day
139
should albumin/amino acids/rbc be in urine
No should be filtered
140
who is more likely to develop proteinuria
diabetic patients
141
what are tiny holes inside endothelium of glomerulus that filter
fenestrations
142
what has negatively charged heparin sulfates that repels proteins and amino acids back into circulation
basement membrane
143
what is found in epithelium that has smaller holes than fenestrations
split pores
144
what is a split pore in
podocytes
145
when basement membrane is damaged, what happens
proteinuria
146
what is not a very accurate proteinuria test
dipstick
147
what is the equation for net filtration pressure
net filtration pressure = glomerular hydrostatic pressure- bowman's capsule pressure- glomerular oncotic pressure
148
what is normal met filtration pressure
10
(60-32-18)
149
what pressure push opposite of glomerular hydrostatic pressure
glomerular colloid osmotic and bowman's capsule pressure
150
how does glomerular colloid osmotic pressure cause pressure
draws water/proteins back into glomerulus against glomerular hydrostatic pressure
151
how does bowman's capsule cause pressure
funneled to pushes pressure upward
152
does net filtration rate = GFR
NO
153
what is normal GFR
125ml/min
154
what is kf a measure of
measure of surface area and permeability
-more surface area= bigger glomerulus=more filtering
155
what is kf
filtration coefficient
156
what diseases cause reduced kf and GFR
HTN
DM
Obesity
glomerulonephritis
157
what does cast noted mean in UA
tubular necrosis
158
does bowman's capsule pressure regulate gfr
no- changes because of ghp and gcop
159
what has most significant/important effect on gfr
GHP
160
what can influence bchp beside gcop and ghp
obstruction- stones, bph (urine backs all the up into bowman's pressure which increases pressure)
161
what influences glomerular hydrostatic pressure
arterial pressure, afferent/efferent arteriole resistance
162
what does increased afferent arteriole resistance do to ghp
decreased ghp thus decreasing gfr
decreased flow
163
when efferent arteriole resistance is increased what happens
fluid backs up, increasing ghp and gfr
164
where does angiotensin II constrict
efferent arteriole- backs up blood so ghp and gfr increase
165
what does increased ghp cause
increased GFR
166
what does kidney need a lot of oxygen/atp for
tubular reabsorption of sodium (active transport)
167
can you decrease renal blood flow and increase gfr
yes- constriction of efferent arterioles by angiotensin II
168
kidney consumes o2 at _____________ rate of brain but receives ______________ times the blood flow
twice
7
169
how much cardiac output goes to kidney
22%
170
what does sns do to gfr
vasoconstriction= increased resistance, decreased renal blood flow so decreased gfr
171
what does angiotensin II do to arterioles
increases efferent arteriole resistance, which backs blood up in glomerulus
172
overall what does angiotensin II to do gfr
holds at normal- since angiotensin II is indirectly released by renin (which is only released with low blood pressure) the gfr would already be low. So angiotensin II raises gfr but gfr was already low to begin with so it brings it to normal
173
how do prostaglandins/nitric oxide affect gfr
decreases resistance= increased blood flow= increased gfr/renal blood flow
174
how does ibuprofen affect kidneys
blocks prostaglandins- so afferent and efferent arterioles are not as dilate= decreased gfr
175
what is auto-regulator to stop complete vasoconstriction
endothelial derived nitric oxide
176
nitric oxide
vasodilator
makes o2 more soluble
177
how does endothelin impact gfr
decreases it by vasoconstriction (increased resistance)
178
what are autoregulation control of gfr/renal blood flow
myogenic mechanism- increase bp=increase calcium=increased contraction=increased increased resistance= decreased flow/gfr
macula densa feedback=
angiotensin II=
179
myogenic autoregulation
increase bp=increase calcium=increased contraction=increased increased resistance= decreased flow/gfr
180
where is macula densa
juxtaglomerular apparatus
181
what makes renin
juxtaglomerular cells
182
what cells line distal tubule
macula densa- come close to afferent and efferent arterioles
183
what does macula densa measure
sodium and chloride in distal tubule (which is urine)
184
when sodium chloride is decreased in macula densa, what happens
decreases afferent arterial resistance so more blood gets into glomerulus to filter more sodium/chloride out
185
what does low gfr cause sodium to be in distal tubule, low or high
low
more gets absorbed
186
how does angiotensis II affect GFR
decreased gfr= low macula densa nacl= increases renin= angiotensin II= increases efferent arteriole resistance= raises GFR
187
where does angiotensin II have effect on kidney
efferent arterioles
188
other factors that influence GFR
increase= fever, STEROIDS, hyperglycemia, high diet protein
decrease= age, low diet protein
189
what are the four mechanisms of urine formation
filtration
reabsorption
secretion
excretion
190
what kind of cells do aldosterone antagonists and sodium channel blockers work on
principal cells
191
what location do aldosterone antagonists and sodium channel blockers work
collecting duct
192
what is the equation for excretion
filtration - reabsorption + secretion
193
what is the equation for resborption
filtration- excretion
194
what is the equation for secretion
excretion - filtration
195
what is excretion
removing wastes and drugs
196
what is the process of filtered components going back into body
reabsorption
197
what is the process of stuff coming from body going into lumen to get excreted
secretion
198
is most of water reabsorbed or excreted from body
reabsorbed
199
why is Na so well reabsorbed
Na follows H2O
200
where does stuff that get filtered go to for excretion
lumen
201
where does the lumen lead to
collecting duct
202
what does the lumen connect
glomerulus and collecting duct
203
what is the filtered material in the lumen
urine
204
what are the ways molecules get reabsorbed into the body
active transport, passive transport (diffusion), osmosis
paracellular/transcellular paths
205
what is between the peritbular capillar and lumen
tubular cells
206
what do molecules have to pass through to be reabsorbed in the kidney
tubular cells
207
where do transporter mechanisms occur for reabsorption
tubular cells
208
what ions travel in paracellular path
Ca
Mg
209
what ions travel in the transcellular path
Na
K
Cl
210
what drives diffusion
concentration or electrical gradient
211
how can sodium move against concentration/electrical gradient
active transport
212
what are the 3 methods of transport sodium is reabsorbed in the kidney
diffusion
active transport
osmotic pressure
213
does secondary active transport use ATP
NO
gets energy from Na to move molecules
214
how does secondary active transport work
It takes advantage of a gradient that has already provided energy.
215
what happens to gfr with hyperglycemia and hyperproteinemia
increases
216
how is glucose/amino acids reabsorbed in the kidney
secondary active transport
217
what is it called when a substance reaches its maximum rate of tubular transport in ALL nephrons
transport maximum
218
when the transport maximum is reached for all nephrons, what happens when more substance comes through
NOT reabsorbed- excreted
219
what is it called when transport maximum is exceeded in SOME nephrons
threshold
220
t or f- individual nephrons may have lower transport maximum's than others
True
221
what are some examples of substances that have a transport maximum
glucose
amino acids
phosphate
sulfate
222
what happens to lumen potential when sodium is reabsorbed
negative potential increases (since sodium is positive)
223
what happens to chloride and urea when sodium and water are reabsorbed in proximal tubule
increased concentration-->passive reabsorption due to concentration gradient
224
how much of all sodium is reabsorbed in proximal tubule
65%
225
what is reabsorbed in proximal tubule
sodium
chloride
potassium
bicarb
water
glucose
amino acids
226
where is most of sodium reabsorbed in kidney
proximal tubule
227
what is excreted out of proximal tubule
hydrogen
organic acids
bases
228
what are the byproducts of metabolism and are most toxic
hydrogen
organic acids
bases
229
what are kidneys key in balancing
balance fluid through sodium renetion
acid-base balance through h+ and bicarb
230
what is the thin descending loop of henle very permeable to
water 20%
231
which nephron is responsible for concentration of urine
juxtamedullary nephrons
232
which nephron absorbs most of water
juxtamedullary nephrons
233
where is 25% of sodium reabsorbed
thick ascending loop of henle
234
what is reabsorbed in the thick ascending loop of henle
sodium
chloride
potassium
bicarb
calcium
magnesium
235
what is the ratio of molecules for the transporter in the thick ascending loop of henle
1 sodium, 2 chloride, 1 potassium
236
is the proximal tubule isosmotic or hyposmotic
isomotic
237
is the thick ascending loop of henle isosomtic or hyposmotic
hyposmotic
238
what does the thick ascending loop of henle secrete
Hydrogen
239
what is the thick ascending loop of henle NOT premeable to
H2O
240
where is h2o not permealbe to in the kidney
thick ascending loop of henle, early distal tubule
241
where do loop diuretics work
thick ascending loop of henle
242
what are the loop diuretic examples
furosemide
bumetanide
ethacrynic acid
243
which transporter does the loop diuretic work on
1 na, 2 cl and 1 K transporter
"triple transporter"
244
what do loop diuretics bind up to have effect
2 chloride on triple transporter
245
when sodium-hydrogen exchanger in thick ascending loop of henle moves sodium into tubular cells, what does it initiate
triple transporter to move into tubular cell
246
what is the pathway of sodium when reabsorbed in the kidney
tubular lumen- tubular cell- renal interstitial fluid
247
what does loop diuretic cause excretion of from triple transporter
Na
K
Cl
248
are loop diuretics potassium sparing
NO. Loop diuretics cause potassium loss into the urine
249
where is 5% of sodium reabsorbed
distal convoluted tubule
250
what pump is responsible for sodium being reabsorbed in early distal tubule
sodium chloride transporter
251
in the sodium chloride pump on the early distal convoluted tubule, does chloride come into lumen or go into renal interstitial fluid
from tubular lumen into tubular cell then into renal interstitial fluid
252
what are the two types of transporters/exchangers on the early distal tubule and where are they located
sodium potassium exchanger- between renal interstitial fluid and tubular cells
sodium/chloride transporter- between tubular cells and tubular lumen
253
where do thiazide diuretics work
early distal tubule- on sodium chloride transporter
254
what does thiazide diuretic inhibit
sodium chloride transporter- so sodium stays in lumen and draws water into lumen for excretion
255
in early distal tubule, where does sodium and chloride travel from and to
from tubular lumen to tubular cell and then to renal interstitial fluid
256
what structure has a similar functional to the thick ascending loop of henle
early distal tubule
257
is the early distal tubule permeable to water
NO
258
where are macula densa located
early distal tubule
259
where does active reabsorption of sodium, chloride, calcium, and magnesium occur
early distal tubule
260
what is actively reabsorbed in early distal tubule
sodium
chloride
potassium
magesium
261
what is called the diluting segment
early distal tubule
262
what is the macula densa responsible for
Na Cl balancing
263
what part of tubule is not very permeable to urea
early and late distal tubule/collecting tubule
264
what does permemability of water in late distal tubule/collecting tubule depend on
ADH
265
where are principle cells located
late distal tubule/collecting tubule
266
another name for ADH
vasopressin
267
where are type a intercalated cells located
late distal tubule/collecting tubule
268
what do intercalated cells play a role in
acid base balance
269
what is an important role of principal cells
what are the types of leaky channels in principal cells
270
in the principal cell, when sodium potassium exchanger puts sodium into renal interstitial fluid (blood), what does that cause
sodium leaky channel brings in sodium from tubular lumen
271
what is renal interstitial fluid
blood
272
in the principal cell, when sodium potassium exchanger puts potassium from renal interstitial fluid in the cell, what does that cause
potassium leaky channel to take potassium from inside cell and put into tubular lumen
273
what does the principal cell work primarily off of
sodium potassium transporter
leaky channels- k and na
274
what are some aldosterone antagonists
spironolactone, eplerenone
275
what are some sodium channel blockers
amiloride, triamterene
276
how do aldosterone antagonists work
bind sodium potassium transporter between renal interstitial fluid and tubular cell, so sodium isn't pulled from cell into interstitial fluid, so then sodium leaky channel doesn't bring sodium from tubular lumen into cell. Sodium stays in tubular lumen and draws water into tubular lumen
277
what cell does aldosterone have greatest impact on
principal cell
278
what does aldosterone stimulate
sodium potassium exchanger- so more sodium is reabsorbed
279
what are the potassium sparing diuretic classes
aldosterone antagonists- sprinolactone
sodium channel blockers- amiloride
280
where do sodium channel blockers work
blocks leaky channels on principal cells (which are in late distal tubule/collecting tubule)
281
what do the type a intercalated cells help with
acidosis- help to decrease h and save bicarb
282
what do the type b intercalated cells help with
alkalosis- increase h and decrease bicarb
283
where are the intercalated cells a-b found
late distal tubule/collecting tubule
284
where does adh act
medullar collecting duct
285
what is reabsorbed in medullary collecting duct
sodium
chloride
water
urea
bicarb
286
what is secreted into medullary collecting duct
hydrogen
287
what is peritubular capillary reabsorption
pressure needed to move from interstitial fluid into capillary
288
when is aldosterone produced
low bp, or low extracellular fluid
289
how does aldosterone work
acts on sodium potassium exchanger to increase sodium moving from principal cell into interstitial fluid
290
what cell does aldosterone work in
principal cell
291
what are the factors that increase aldosterone secretion
angiotensin II
increased potassium
adrenocorticotrophic hormone (acth)
292
where is aldosterone secreted from
adrenal cortex
293
what are factors that decrease aldosterone secretion
atrial natriuretic factor
increased na concentration
294
why does increased potassium increase aldosterone
too high potassium= sodium-potassium exchanger isn't pumping enough potassium out- so it releases to pump more potassium out and more sodium in
295
what is the permissive role of acth
release aldosterone
296
what does high atrial natriuretic factor mean
too much fluid
297
what is the opposite of renin
atrial natriuretic factor
298
what does angiotensin II stimulate the release of
aldosterone
299
where does angiontensin II directly increase sodium reabsorption
proximal, loop, distal, and collecting tubules
300
what does angiotensin II do to the efferent arterioles
constricts them
301
what happens when angiotensin II constricts efferent arterioles
-decreased peritubular capillary hydrostatic pressure
-increases filtration fraction which increases peritubular colloid osmotic pressure
302
what is the important thing to remember with angiotensin II
vasoconstriction
303
what are the pumps that angiotensin II affects on tubular cells to increase sodium reabsorption
sodium-potassium-exchanger
sodium-hydrogen-exchanger
sodium-bicarb-transporter
304
what do ace inhibitors, arbs and renin inhibitors decrease
decreases:
aldosterone
sodium reabsorption
efferent arteriolar resistance
305
what is a renin inhibitor example
aliskirin
306
where is ADH secreted from
posterior pituitary gland
307
what does adh increase permeability to and where does it do this
water- distal and collecting tubules
308
what is an important controller of extracellular fluid osmolarity
ADH
309
what hormone allows for differential control of water and solute secretion
ADH
310
what is the most important renal action of adh
increase water permeability in distal tubule/collecting tubule
311
what does adh attach to on tubular cell
V2 receptor
312
when adh binds to v2 receptor, what happens
increases formation of cAMP
313
what does camp activate after creation by adh
protein kinase
314
what does protein kinase stimulate prodction of
protein phosphorylation
315
what does protein phosphorylation stimulate to move to lumen side
aquaporin 2
316
where does aquaporin 2 attach to
wall of tubular cell on the tubular lumen side
317
where are aquaporin 3 and 4 found
tubular cell wall on interstitial fluid side
318
what is the gateway for water to flow from tubular lumen into interstitial fluid
aquaporins
319
what does anp increase excretion of
Na
320
what are the 3 things anp inhibits
sodium reabsorption
renin release
aldosterone formation
321
what impact does anp have on gfr
increases
322
what is an example of osmotic diuretic
mannitol,
isosorbide,
urea,
glycerin
323
how does diabetes cause diuresis
osmosis
water follows glucose
324
does an increase or decrease of unreabsorbed solutes in tubules decrease water reabsorption
increase
325
what tests measure plasma concentration of waste products
BUN
creatinine
326
what measures urine concentrating ability
urine specific gravity (1-2)
327
what measures albumin excretion
microalbuminuria
328
what describes rate at which substances are removed from plasma
clearance
329
what is the volume of plasma completely cleared of a substance per min by kidney
renal clearance
330
clearances of different substances
glucose- 0
albumin- 0
sodium- 0.9
urea- 70
inulin- 125
creatinine- 140
pah-600
331
what should renal clearance be equal to
GFR
332
what does efferent arteriole turn into
vasa recta- which wraps around loop of henle
333
what is between the bowman's capsule and the descending loop of henle
proximal convoluted tubule
334
what is the between the ascending loop of henle and the collecting duct
distal convoluted tubule
335
what gets reabsorbed in proximal convoluted tubule
sodium
chloride
potassium
glucose
amino acids
urea
water
bicarb
336
where do juxtaglomerular nephrons lie
in cortex but near medulla
337
which nephrons concentrate urine
juxtamedullary nephrons
338
what is main thing loop of henle reabsorbs
water
339
what is reabsorbed at thick ascending loop of henle
na, cl, k, bicarb, ca, mag
340
where is the sodium potassium exchanger located in the nephron
collecting duct
341
where is the sodium chloride transporter found in nephron
distal convoluted tubule
342
how does sodium potassium exchanger work in dct
sodium is moved from dct to blood
potassium is moved from blood to dct
343
what is reabsorbed from late distal convoluted tubule
sodium
chloride
potassium
bicarb
water (adh)
344
what is reabsorbed from collecting duct
sodium
chloride
bicarb
urea
water (adh)
345
what are parts of nephron where things are primarily secreted
proximal convoluted tubule
346
how is creatine removed from body
urine
347
what is the byproduct of breakdown of muscle and protein
creatinine
348
what is secreted into proximal convoluted tubule (lumen)
hydrogen, organic acids, bases, creatinine, drugs
349
what is secreted into distal convoluted tubule
hydrogen
potassium
350
what are the types of diuretics
osmotic
loop
thiazide
potassium sparing
carbonicanhydrase inhibitors
351
where is most (65%) of sodium reabsorbed from in kidney
proximal convoluted tubule
352
where is a high concentration of sodium bicarb reabsorbed from
proximal convoluted tubule
353
what does the triple transporter transport and where does it do so
thick ascending loop of henle
Sodium
2 chloride
potassium
354
where is 25% of sodium reabsorbed from in kidney
thick ascending loop of henle
355
what is reabsorbed in the early distal convoluted tubule
sodium
chloride
calcium
magesium
356
where is 5% of sodium reabsorbed from
distal convoluted tubule
357
in the sodium potassium exchanger in the collecting duct, what is also secreted into collect duct with potassium
hydrogen
358
where is 1-2% of sodium reabsorbed from
collecting duct
359
t or f- osmotic diuretics last a long time
False
360
how do osmotic diuretics work
mannitol is a salt- increases concentration of particles in lumen so then water wants to go into lumen to be where the large concentration of particles are. Once in the lumen, osmotic diuretics won't get reabsorbed into blood
361
where does osmotic diuretics work
proximal convoluted tubule
362
what transporter do loop diuretics work on
triple transporter
363
what do loop diuretics prevent from being transported
2 chlorides
so then sodium and potassium also stay in lumen
364
which diuretic may cause hypokalemia
loop diuretics
365
what other ions can loop diuretics have an effect on after a period of time
Ca
Mg
366
what ions are transported paracellularly from lumen to blood
Ca
Mg
367
what are all of the things loop diuretics can increase excretion of
sodium
chloride
potassium
water
calcium
magnesium
368
what can loop diuretics be used to treat
pulmonary edema
cirrhosis
acute renal failure
369
what are examples of thiazide diuretics
hydrochlorothiazide, chlorothiazide
370
where do thiazide diuretics work
distal convoluted tubule
371
what transporter do thiazide diuretics work on
sodium chloride transporter-
stops sodium from being reabsorbed
372
what do thiazide diuretics increase reabsorption of
Ca
urea
373
what do thiazide diuretics decrease reabsorption of (and therefore increase excretion)
mg
Na
Cl
374
what drugs increase reabsorption of urea in distal convoluted tubule
thiazide diuretics
375
when are thiazide diuretics contraindicated and why
gout
they cause reabsorption of urea in proximal convoluted tubule
376
which diuretics are used to treat hypertension, edema, and renal stones
thiazide diuretics
377
why does thiazide diuretics not have a lot of effect on sodium
because they act in distal convoluted tubule where only 5% of sodium is reabosrbed
378
where do potassium sparing diuretics work
mostly collecting duct
379
why are potassium sparing diuretics often used with other diuretics
because they work in areas where only 1% of sodium is reabsorbed, they aren't as effective as other diuretics
380
which diuretic class potentiates other diuretics
K sparing
381
what are the two types of potassium sparing diuretics
sodium channel blockers- amiloride
aldosterone antagonists- spironolocatone
382
what channel does sodium channel blocking diuretics block
sodium leaky channel- so sodium can't get out of lumen and into cell
383
what happens to potassium with sodium channel blocking diuretics
potassium stays in cell and goes into blood
384
where does aldosterone antagonist have effect and on what transporter
collecting duct- on sodium potassium exchanger
385
what does aldosterone increase the number of
sodium potassium exchanger- so more sodium gets out of cell into blood
386
how does spironolactone work
on sodium potassium exchanger in collecting duct- keeps sodium in lumen and potassium in blood
387
what are the uses of potassium sparing diuretics
primary and secondary aldosteronism
resistant hypertension
heart failure
hypertension (na channel blockers)
388
what is ph range for hydrogen
7.2-7.4
389
what are the body fluid chemical buffers that play a role in hydrogen ion regulation
bicarb
ammonia
phosphate
proteins
390
how do lungs play a role in hydrogen regulation
increased hydrogen= increased ventilation to increase co2 exhalation
391
how do kidneys regulate hydrogen ions
secrete H
reabsorb bicarb
generates new bicarb
392
what is the most important extracellular fluid buffer
bicarb
393
what kind of buffers are phsophate and ammonia
renal tubular buffers
394
what is the intracellular buffer
proteins (Hgb)
395
what does phosphate and hydrogen form
phosphuric acid
396
what does ammonia and hydrogen form
ammonium
397
what does proteins and hydrogen form
hydrogen-hemoglobin
398
why does hydrogen have to be buffered instead of excreted
fixed amount of hydrogen that can be directly excreted from kidneys
399
what is the most important kidney hydrogen buffer system
bicarb
400
what is pk
concentration of hydrogen at a certain ph
401
what does the effectiveness of the bicarbonate buffer system depend on
concentration of reactants
pk of system
ph of body fluids
402
what is a normal pk level
6.1- this is when bicarb and co2 are balanced
403
what enzyme is necessary for the carbonic acid equation
carbonic anhydrase
404
what systems closely regulates the bicarbonate buffer system
lungs and kidneys
405
what is the most important buffer in extracellular fluid
bicarbonate buffer system
406
how much co2 is carried in the blood as bicarbonate
70%
407
what happens to alveolar ventilation when there is an increase in hydrogen ions
increases ventilation
408
does increased co2 lead to increased or decreased aciditiy
increased
409
what can reabsorb, produce new, filter, or excrete bicarb
kidney
410
what are some non volatile acid the kidneys eliminate
sulfuric acid, phosphoric acid
411
what does the kidneys conserve or excrete depending on body needs
bicarb
412
if the body is in an alkalotic state, what will the kidney excrete MORE of
bicarb
413
if the body is an acidosis state, what will kidney excrete LESS of
bicarb
414
where is most of bicarbonate reabsorbed in nephron (85%)
proximal convoluted tubule
415
for each bicarbonate reabsorbed, there must be a _________ secreted
hydrogen
416
where is 10% of bicarbonate reabsorbed in
ascending thick portion of loop of henle
417
where is 5% of bicarbonate reabsorbed
late-distal-tubule
418
what is the process for bicarbonate to be reabsorbed into the renal interstitial fluid in the proximal tuble and ascending thick loop of henle
1. sodium from sodium bicarbonate gets taken into tubular cell via sodium-hydrogen exchanger
2. bicarbonate is added with hydrogen from sodium-hydrogen exchanger to make carbonic acid
3. carbonic acid gets broken down in co2 and water
4. co2 is taken into tubular cells
5. co2 and water form carbonic acid in the tubular cell
6. carbonic acid breaks down into bicarbonate and hydrogen
7. bicarbonate goes into renal interstitial fluid with sodium
8. left over hydrogen gets taken out of cell in tubular lumen via sodium-hydrogen exchanger-
- process starts over
419
what is the process for bicarbonate reabsorption and hydrogen secretion in intercalated cells of late distal and collecting tubules
1. co2 from renal interstitial fluid enters the tubular cell
2. co2 and water in cell form carbonic acid
3. carbonic acid breaks down into bicarb and h+
4. bicarbonate is reabsorbed into renal interstitial fluid via bicarbonate-chloride exchanger
5. hydrogen is secreted into lumen via hydrogen atp transporter or hydorgen-potassium exchanger which also uses atp
420
when pco2 is increased, such as in respiratory acidosis, what happens to hydrogen secretion
increases
421
when extracellular hydrogen increases, what happens to h+ secretion
increases
422
when tubular fluid buffers and increased, what happens to H+ secretion
increases
423
what factors increase h+ secretion and hco3 reabsorption
increased: pco2, hydrogen, aldosterone, agiotensin II
decreased: bicarb, extracellular fluid volume, potassium
424
when the body is increasing h+ secretion and hco3 reabsorption, what state is the body in
acidosis
425
how do aldosterone and angiotensin II increase h+ secretion and bicarb rebsorption
increase sodium uptake which increases h+ secretion via sodium-hydrogen exchanger
426
what conditions in body drive angiotensin II and aldosterone release
low bp,
low extracellular fluid
427
how does hypokalemia lead to increase hydrogen secretion
on intercalated cell, there is a hydrogen potassium exchanger, so when there is low potassium, body tries to reabsorb more potassium, so then more hydrogen gets secreted out
428
what factors DECREASE hydrogen secretion and bicarb reabsorption
increased: extracellular fluid volume, potassium, bicarb
decreased: co2,hydrogen, aldosterone, angiotensin II
429
what happens to hydrogen secretion, bicarb reabsorption, and bicarb production during acidosis
H= increased secretion
bicarb= increased reabsorption
bicarb= increase production
430
what happens to hydrogen secretion, bicarb reabsorption, and bicarb in urine during alkalosis
h= decreased secretion
bicarb= decreased reabsorption
bicarb= increased in urine
431
can enough free hydrogen be removed by only secretion/excretion
no- needs buffers
432
what is the minimum urine ph
4.5,
any more acidic will damage tissues
433
t or f- kidney is not limited to amount of free hydrogen that can be excreted
false
434
what is NH3
ammonia
435
what is NH4
ammonium
436
what is made from metabolism of amino acids in the liver
glutamine
437
where is ammonium and bicarb produced and secreted
proximal/distal tubule
thick loop of henle
438
what is the process for making new bicarb from glutamine (ammonium buffer)
1. glutamine is absorbed into tubular cell from lumen
2. glutamine is broken down into 2 bicarb and 2 ammonium
3. 2 bicarb are reabsorbed into renal interstitial fluid
4. ammonium gets moved to lumen via sodium-ammonium exchanger
5. ammonium combines with chloride in lumen and is excreted as ammonium chloride
439
is ammonium or phosphate buffer system more important
ammoinum
makes more bicarb
440
where is hydrogen buffered by ammonia
collecting tubules
441
is NH3 or NH4 more permeable
NH3
442
explain the buffering of hydrogen by ammonia
1. ammonia goes from tubular cell to lumen since it is permeable
2. co2 enters tubular cell and forms with water to make carbonic acid
3. carbonic acid is broken down into bicarb and hydrogen
4. bicarb (new) is absorbed into renal interstitial fluid
5. hydrogen is put into lumen via atp
6. hydrogen in lumen combines with ammonia to make ammonium
7. ammonium combines with chloride to make ammonium chloride for excretion
443
if bicarb is low causing a ph less than 7.4, what is the cause
metabolic
444
if bicarb is high causing a ph greater than 7.4, what is the cause
metabolic
445
if co2 is low causing a ph greater than 7.4, what is the cause
respiratory
446
if co2 is high causing a ph less than 7.4, what is the cause
respiratory
447
co2 in respiratory acidosis
high
448
bicarb in metabolic acidosis
low
449
CO2 in respiratory alkalosis
low
450
bicarb in metabolic alkalosis
high
451
what is the ph range that is compatible with life
6.8- 7.8
452
what is the goal ratio of hco3 to co2
20 : 1
453
respiratory acidosis
low ph
increased co2
increased renal acid excretion/bicarb reabsorption
454
respiratory alkalosis
high ph
decreased pco2
decreased renal acid secretion, increased bicarb reabsorption
455
metabolic acidosis
low ph
decreased bicarb
hyperventilation to lower co2
456
metabolic alkalosis
high ph
increased bicarb
hypoventilation to increase co2
457
when there is a metabolic acid base imbalance, what responds
lungs
458
when there is a respiratory acid base imbalance, what responds
kidney
459
normal bicarb range
22-26
460
normal PaCO2
35-45
461
how do the kidneys compensate for acidosis
increase: hydrogen excretion, bicarb reabsorption, and produce new bicarb
462
how do kidneys compensate for alkalosis
decrease hydrogen excretion, bicarb reabsorption
excrete bicarb in urine
463
what acid base imbalance does anion gap come into play
metabolic acidosis
464
what is majority of cations
Na
465
what are anions
Cl
bicarb
466
t or f- cations and anions are usually equal in the body
true
467
what are unmeasured anions
proteins
phosphates
sulfate
lactate
468
what are unmeasured cations
K
Mg
Ca
469
normal anion gap
8-16 mEq/L
470
what causes abnormal anion gap
dka
ethylene glycol poisoning
471
what are normal cation and anion levels
142 Cation
132 Anion
472
when there is an increase in anion gap, what is being thrown off
the unmeasurable anions or cation
473
what is called when you lose bicarb but anion gap is normal
hyperchloremic metabolic acidosis
-chloride compensates for decreased bicarb
474
what is it called when unmeasured anions increase and anion gap increases
normochloremic metabolic acidosis
- losing bicarb
475
what are examples of normochlormeic metabolic acidosis
DKA
lactic acidosis
salicylic acidosis
476
what are some causes of resp acidosis
brain damage
pneumonia
emphysema
other lungs problems
477
what are some causes of metabolic alkalosis
increase base intake
vomiting
mineralocorticoid excess
overuse of diuretics- except carbonic anhydrase inhibitors
478
what are preventions of blood loss
-vascular constriction
-Formation of a platelet plug
-Formation of a blood clot
-Healing of vascular damage (clot remodeling/repair)
-fibrinolysis
479
what are the key events in hemostasis
1. severed vessel
2. platelets agglutinate
3. fibrin appears
4. fibrin clot forms
5. clot retraction occurs
480
what causes vascular constriction
Myogenic spasm
Local autocoid factors from damaged tissues and platelets
Nervous reflexes
Smaller vessels: thromboxane A2 released by platelets
481
characteristics of platelets
Released by fragmentation of megakaryocytes
normal level: 150–300,000 per µL
Half-life in blood of 8–12 days
482
what are platelet funtions
Contractile capabilities
-Actin, myosin, thrombosthenin (contractile protein)
Residual ER and Golgi
-Synthesize enzymes, prostaglandins, fibrin-stabilizing factor, PDGF, store Ca++
Mitochondria/enzymes
-Produce ATP, ADP
483
what are the platelet membranes
surface glycoprotein
membrane phospholipids
484
what is the function of surface glycoproteins
Repels intact endothelium
Adheres to injured endothelium and exposed collagen
485
what is the function of membrane phospholipids on platelets
activate blood clotting
486
what is the process of formation of the platelet plug
-contact with damaged endothelium
-adhere to collagen and vWF
-other platelets accumulate, adhere, and contract, form plug, initiate clotting
487
what does contact with damaged endothelium result in
-assume irregular forms
-endothelium contracts and release granules (ADP and thromboxane A2)
488
what can very low platelets present like
petechiae
bleeding gums
489
in severe vascular trauma, how long for clot formation
15-20 seconds
490
how quickly can an occlusive clot form
within 3-6 min unless very large vascular defect
491
how long does it take for clot retraction
20-60 min
492
what happens within 1-2 weeks of clot formation
-invasion by fibroblasts
-organization into fibrous tissue
493
what are the effector proteins for clotting
prothrombin
fibrinogen
494
characteristics of prothrombin
-α2 globulin,
-15 mg/dL in plasma
-Vitamin K-dependent synthesis in liver
-Cleaved by PT activator to thrombin
495
characteristics of fibrinogen
-100–700 mg/dL in plasma
-Synthesized in the liver (acute phase reactant)
-Usually intravascular; can extravasate with increased vascular permeability
496
what cleaves 4 small peptides from fibrinogen
thrombin
fibrin monomer-> spontaneous polymerization
497
what helps to form clot reticulum
long fibrin fibers
498
characteristics of fibrin stabilizing factor
In plasma and released from platelets
Activated by thrombin
Covalent cross-linking of fibrin monomers and adjacent fibrin fibers
499
what is bound to platelets and trapped in the clot
thrombin
500
what system does thrombin and clot formation work on
positive feedback
501
___ produces more prothrombin activator by acting on other clotting factors
thrombin
502
what is generated at the periphery of the clot
additional fibrin monomers and polymers
503
when does clot retraction begin
within 20-60 min
504
what binds to the damaged vessel wall
fibrin
505
what causes clot contraction
actin, myosin and thrombosthenin
506
describe clot retraction
clot tightens expressing serum and closes the vascular defect
507
what are the two clotting pathways
Extrinsic pathway—Trauma to vessel wall and adjacent tissues
Intrinsic pathway—Trauma to the blood or exposure of the blood to collagen
508
what factor activates the extrinsic pathway
tissue factor
509
what factor activates the intrinsic factor
exposure to factor XII
exposure of platelets to collagen
510
what is the time to clot for extrinsic pathway
<15 sec
511
how long for clotting in intrinsic pathway
1-6min
512
what prevents clotting
-smoothness of endothelial surface
mucopolysaccharide coating (glycocalyx) repels platelets and clotting factors
thrombomodulin
protein C
513
how does mucopolysaccharide coating (glycocalyx) prevent clotting
it repels platelets and clotting factors
514
how does thrombomodulin prevent clotting
Thrombomodulin bound to endothelium binds (competes for) thrombin
515
how does activated protein C prevent clots
Thrombin-thrombomodulin activates Protein C→ inactivates factors V and VIII
516
how does thrombin become localized to the clot
Fibrin fibers bind 85–90% of thrombin and localize it to the clot
517
how does antithrombin III work in the negative feedback system
Antithrombin III combines with the remainder and inactivates it over 12–20 minutes.
518
what is the charge of heparin
highly negative
519
MOA of heparin
Binds anti-thrombin III and increases its effectiveness 100–1000-fold
Heparin-antithrombin III removes free thrombin from the blood almost instantly.
Also removes XIIa, XIa, Xa, and IXa
520
where can heparin be found in the body
Mast cells,
basophils particularly abundant in pericapillary regions of liver and lung
521
what causes clot lysis
Plasminogen is trapped in the clot.
Over several days, injured tissues release tissue plasminogen activator (tPA).
Plasminogen is activated to plasmin, a protease resembling trypsin.
Plasmin digests fibrin fibers and several other clotting factors.
Often results in reopening repaired small blood vessels
522
what are some causes of excessive bleeding
Hepatocellular disease
Vitamin K deficiency
Hemophilia
Low platelet count (thrombocytopenia)
523
what is essential to carboxylate glutamic acid and 5 clotting factors
vitamin K
524
what clotting factors are affected by Vit K deficiency
prothrombin
factor VII
factor IX
factor X
protein C
525
what happens in vitamin K deficiency
In this process vitamin K is oxidized and inactivated.
Vitamin K epoxide reductase complex 1 (VKOR c1) reduces vitamin K and reactivates it.
526
where is vitamin K produced
intestines by gut bacteria
527
what can cause fat malabsorption and vitamin K deficiency
lack of bile production
lack of bile delivery
528
what can be done for patients with liver or biliary disease before surgery
In patients with liver or biliary disease, vitamin K can be injected 4–8 hours before surgery.
529
what can also lead to vit K deficiency
malabsorption of fats
vitamin K is fat soluble
530
hemophilia A
Deficiency of factor VIII
85% of hemophilia cases
1/10,000 males
Both genes are on the X chromosome (males only get one copy).
531
hemophilia B
Deficiency of factor IX
15% of cases
532
how does hemophilia effect bleeding
both A and B impair the intrinsic pathway
clinically present: bleeding after minor trauma
533
what factor deficiency cause hemophilia A
factor VIII
Deficiency of the small component causes hemophilia A.
→ Treat bleeding with factor VIII replacement.
534
what factor deficiency causes vWF disease
factor VIII large component
Deficiency of the large component causes von Willebrand disease (resembles decreased platelet function).
535
what are the two components of factor VIII deficiency
Large: MW >106
Small: MW ~230,000
536
characteristics of thrombocytopenia
Low numbers of platelets
Bleeding from small venules or capillaries
Petechaiae, thrombocytopenic purpura
Often idiopathic
< 50,000 platelets/µL—usually modest bleeding
< 10,000 platelets/µL—life-threatening
537
how do you treat thrombocytopenia
platelet infusion
infusion is effective for 1-4 days each time
538
what is a thrombus
an abnormal clot
539
what is an embolus
a thrombus that floats/gets dislodged
540
what can cause emboli/thrombi
Endothelial roughening (e.g., atherosclerosis)
Slow flow (e.g., prolonged air travel)
541
what is the treatment for thrombus/embolus
tPA
embolectomy
542
where does pulmonary embolus usually originate from
deep leg veins
543
what is DIC
disseminated intravascular coagulation
Occurs in the setting of massive tissue damage or sepsis
Wide-spread coagulation in small vessels
Manifested as bleeding from multiple sites because of depletion of clotting factors
544
what are some anticoagulants
heparin
coumarins
545
how does heparin work
Binds, potentiates antithrombin III
Works rapidly, generally used acutely
546
how do coumarins work
Inhibit VKOR c1
Deplete active vitamin K → deplete active prothrombin, factors VII, IX, X
Slower acting (days); used chronically
547
how do you treat over anticoagulation of coumarins
treat with FFP and vitamin K
548
what are calcium chelators and what are they used in
citrate, EDTA
used in blood collection and blood storage
549
bleeding time coag test
normal 1-6 min
reflects platelet function
550
clotting time coag test
-invert tube every 30 sec
normal 6-10 min
not reproducible, not generally used
551
Prothrombin time coag test
normal 12 sec
assess extrinsic and common pathways
Add excess calcium and tissue factor to oxylated blood, measure time to clot
tissue factor batches have to be standardized (activity expressed as "international sensitivity index" (ISI)
552
INR coag test
"international normalized ratio"
Normal: 0.9 - 1.3
therapeutic range 2.0-3.0
INR= PT test / PT normal
553
how do you test for other clotting factors
Mix the patient’s plasma with a large excess of all needed components except the factor being tested.
Compare time to coagulation with that for pooled plasma of healthy volunteers.
554
how is hemostasis acheived
(1) vascular constriction,
(2) formation of a platelet plug,
(3) formation of a blood clot as a result of blood coagulation,
(4) eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.
555
what does trauma to vessel cause
smooth muscle contract in vessel
results from
(1) local myogenic spasm,
(2) local autacoid factors from the traumatized tissues
and blood platelets,
(3) nervous reflexes
556
how is the nervous reflex initiated in the vessel contraction
initiated by pain nerve impulses or other sensory impulses that originate from the traumatized vessel or nearby tissues
557
myogenic contraction of the vessel
initiated by direct damage to the vascular wall.
the smaller vessels, the platelets are responsible for much of the vasoconstriction
by releasing a vasoconstrictor substance, thromboxane A2.
558
The more severely a vessel is traumatized, the greater the ______
the degree of vascular spasm
559
where are platelets formed
bone marrow from megakaryocytes
560
factor I
fibrinogen
561
factor II
prothrombin
562
factor 3
tissue factor
563
factor 4
calcium
564
factor 5
proaccelerin
"labile factor"
565
factor VII
serum prothrombin conversion accelerator (SPCA)
proconvertin
stable factor
566
factor VIII
antihemophilic factor (AHF)
antihemophilic globulin (AHG)
antihemophilic factor A
567
Factor IX
plasma thromboplastin component (PTC)
Christmas factor
antihemolitic factor B
568
Factor X
stuart prower factor
569
factor XI
plasma thromboplastin antecedent (PTA)
antihemolitic factor C
570
Factor XII
Hageman Factor
571
Factor XIII
fibrin stabilizing factor
572
prekallikrein
fletcher factor
573
High molecular weight kininogen
Fitzgerald factor
HMWK
574
3 essential steps of clotting
1. In response to rupture of the vessel or damage to the blood itself, a complex cascade of chemical reactions occurs in the blood involving more than a dozen blood coagulation factors. The net result is formation of a complex of activated substances collectively called prothrombin activator.
2. The prothrombin activator catalyzes conversion of prothrombin into thrombin.
3. The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that enmesh platelets, blood cells, and plasma to form the clot.
575
Describe conversion of prothrombin to thrombin
1) prothrombin activator is formed from ruptured vessels
2) prothrombin activator, in the presence of Ca, converts prothrombin to thrombin
3) thrombin causes polymerization of fibrinogen molecules into fibrin fibers within 10-15 seconds
576
What is required by the liver for normal activation of prothrombin and many other clotting factors
Vitamin K
577
Where is fibrinogen formed
In the liver
578
What is the reticulum of the clot
Many fibrin monomer molecules that polymerize within seconds into long fibrin fibers make up the reticulum of the blood clor
579
What does plasmin digest
Fibrin fibers
Fibrinogen
Factor V
Factor VIII
Factor XII
580
Vitamin K adds a ___ to _____ on which 5 clotting factors
Carboxylic group to glutamic acid
Prothrombin
Factor VII
Factor 9
Factor X
Protein C
581
name the surface glycoproteins on platelets
glycoprotein Ia
glycoprotein IIb/ IIIa
582
what in in the granules released when platelets come into contact with damaged endothelium
ADP
Serotonin
thromboxane A2
583
where is vWF produced
endothelium
584
ADP + thromboxane A2 does what
activates glycoproteins so that platelets stick together
585
what is PDGF
platelet derived growth factor
aids in the repair of muscle and connective tissue during clot retraction
586
what is VEGF
vascular endothelial growth factor
aids in repair of vessels and endothelium during clot retraction
587
what initiates/activates factor 12
negative charge on the platelet plug
588
what does protein C do
binds to and inactivates factor 5 and 8
589
what does Nitric oxide do
nitric oxide binds with PGI2 to inactivate glycoproteins on platelets
590
what factors are affected by heparin
XIIa,
XIa
Xa
IXa
IIa
591
what does tpa do
converts plasminogen to plasmin which "eats" up fibrin
592
what is byproduct of plasmin destroying fibrin
fibrinogen
d dimer
593
what are the three steps to Na Reabsorption?
1. diffuses because on concentration and electrical from lumen into tubular cells
2. Na transported against electrical gradient by ATP
3. Na and H2O move from ICF to capillaries by osmotic pressure
594
Na K atpase pump ratio
2 K in
3 Na out
595
what symporter does loop diuretics work on
tri sympoter in thick ascending loop of henle
1 Na, 2 Cl, 1 K
596
what symporter does thiazide work on
Na Cl symporter in early distal tubule
597
important points on early distal tubule
-not permeable to water
-active reabsorption of Na, Cl, K, Mg
-contains macula densa
-5% of filtered load NaCl reabsorbed
598
trace starting from thick ascending LOH
early distal tubule
late distal tubule
connecting tubule
collecting tubule
collecting duct
599
where does ADH work
late/distal tubule and collecting tubule
600
what do aldosterone antagonists work on
Na K atpase pump in late distal and cortical collecting tubules
601
Na Channel blockers work on what
leaky Na channels in late distal/collecting tubules
602
what pumps does angiotensin II work on
ATPase pump
Na Bicarb pump
Na hydrogen ion pump
603
MOH of ADH in distal and collecting tubules
604
how does parathyroid hormone increase Ca reabsorption
-increases Ca reabsorption in kidneys
-increases Ca reabsorption in gut
-decreases phosphate reabsorption
-increases intracellular Ca
