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A & P I > APII_Exam 1 > Flashcards

APII_Exam 1 Flashcards

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

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2
Q

what are some waste products the kidneys excrete

A

urea
creatinine
bilirubin
hydrogen

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3
Q

what are some foreign chemicals the kidney excretes

A

drugs
toxins
pesticides
food additives

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4
Q

what are some hormones the kidneys secrete/metabolize/excrete

A

renal erythropoietin factor
vitamin D3
renin

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5
Q

what do kidneys perform gluconeogenesis with

A

amino acids

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6
Q

what does excess BUN indicated

A

kidney disease

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7
Q

what is a normal BUN level

A

20

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8
Q

what is a byproduct of proteins being broken down

A

urea

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9
Q

what is 100% excreted by the kidneys

A

creatinine

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10
Q

what type of metabolism is creatinine metabolized from

A

muscle metabolism

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11
Q

what time of metabolism is urea metabolized from

A

protein metabolism

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12
Q

what type of metabolism is uric acid metabolized from

A

nucleic acid metabolism

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13
Q

what type of metabolism is bilirubin metabolized from

A

hemoglobin metabolism

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14
Q

what is the byproduct of ammonia

A

is all of urea excreted in urine

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15
Q

what is byproduct of RBC breakdown

A

bilirubin

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16
Q

how long does a RBC live for

A

120 days

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17
Q

what is RBC broken down into

A

heme and globin

then into bilirubin

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18
Q

is bilirubin conjugated or nonconjugated when it is first formed

A

non conjugated

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19
Q

where is bilirubin conjugated

A

liver

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20
Q

after bilirubin is conjugated where does it go

A

into bile which then goes into the bowel

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21
Q

what makes urine yellow

A

bilirubin

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22
Q

once liver detoxifies blood, where does part of the waste go

A

kidneys to be excreted

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23
Q

what drug class is commonly excreted through kidney

A

antibiotics

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24
Q

what is a common issue with halothane

A

nephrotoxic and HEPATOtoxic

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25
Q

what hormones are produced in the kidney

A

vitamin D3
renal erythropoetic factor
renin

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26
Q

what hormones are metabolized and excreted in the kidney

A

most peptide hormones such as insulin, angiotensin II

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27
Q

what hormone stimulates RBC production from kidney

A

renal erythropoetic factor

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28
Q

what causes pink puffer COPD

A

polycythemia from low O2 levels in blood which stimulates kidney to make more RBCs

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29
Q

what allows absorption of Ca in digestive tract and puts calcium into bone

A

vitamin D3

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30
Q

how does erythropoietin stimulate RBC production

A

stimulates erythrocyte production in the bone marrow

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31
Q

what ion metabolism is vitamin D3 important in

A

phosphate

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32
Q

what are the only means of excreting non-volatile acids

A

kidneys

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33
Q

how does the kidney regulate the body fluid acidity

A

bicarbonate

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34
Q

what is the carbonic acid formula

A

h2o + co2 <—> H2CO3 <—> HCO3 + H

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35
Q

what is carbonic acid

A

H2CO3

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36
Q

how is most CO2 carried in the blood to the lungs

A

bicarbonate

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37
Q

what actually drives respiration

A

H+ ions around pons in CSF

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38
Q

where does H+ have to be formed to be able to drive respiration

A

CSF from CO2

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39
Q

what does low and high bicarb mean

A

low= metabolic acidosis (high H+)

high= metabolic alkalosis (low H+)

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40
Q

why does high CO2 cause acidosis

A

creates H+ through carbonic acid equation thus a build up of excessive H+ ions

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41
Q

how is CO2 breathed off if carried through body as bicarb

A

combines with H+ to make carbonic acid which gets broken down into CO2 and water

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42
Q

what does the liver use for gluconeogenesis

A

glycogen

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43
Q

what does the kidney use for gluconeogenesis

A

amino acids

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44
Q

how does the kidney regulate arterial pressure

A

raas
prostaglandins (inflammatory)
bradykinin (inflammatory

controls extracellular fluid volume

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45
Q

raas, bradykinin, and prostaglandins are the _________________ function of the kidney

A

endocrine

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46
Q

what electrolytes balance the kidneys

A

Na
K
H+
Ca
Phos
Mg

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47
Q

with increased intake of Na, how many days does it take the kidneys to balance the Na level

A

4-6 dyas

8 days on the graph

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48
Q

what part of the kidney has no glomeruli

A

medulla

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49
Q

what surrounds kidney and provide protection

A

capsule of the kidney

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50
Q

where are nephrons found in the kidney

A

renal pyramids

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51
Q

are nephrons located in teh medulla and the cortex?

A

YES in both

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52
Q

what is the flow of urine

A

nephron (renal pyramid)
papilla
minor calyx
major calyx
renal pelvis
ureter

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53
Q

what is in between the renal pyramids

A

renal columns

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54
Q

where is hydronephrosis found

A

underneath the renal capsule

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55
Q

what surrounds the kidney

A

fat

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56
Q

what is normal GFR per min and per day

A

125 ml/min

180L/day

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57
Q

how many times per day is plasma volume filtered

A

60x

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58
Q

does albumin or other proteins get filtered

A

NO

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59
Q

what is the filtration fraction equation

A

GFR / renal plasma flow= 0.2 (.20 x plasma filtered)

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60
Q

what is role of renal columns

A

extension of renal cortex that gives stability to kidney

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61
Q

what drives renal filtration

A

renal blood supply

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62
Q

what do renal arteries/veins branch out into

A

interlobular arteries and veins

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63
Q

what do interlobular arteries/veins branch into

A

arcuate arteries/veins

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64
Q

when does interlobular turn into arcuate

A

at turn of renal pyramid at the top

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65
Q

what branches off arcuates

A

interlobular

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66
Q

what branches off interlobular

A

afferent arterioles

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67
Q

what do interlobulars form

A

spiralling affect around nephron

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68
Q

how many glomerulus does a nephron have

A

1

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69
Q

what does glomerulus look like

A

bundle of vessels

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70
Q

what encases the glomerulus

A

bowmans capsule

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71
Q

what is the filtration apparatus of the kidney

A

glomerulus

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72
Q

what brings blood to the glomerulus and what artery does it come from

A

afferent arteriole brings it in

branches off interlobular artery

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73
Q

what takes blood away from the glomerulus

A

efferent arteriole

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74
Q

why does the glomerulus coil

A

increases surface area

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75
Q

what attaches to bowman’s capsule carrying filtration content away

A

proximal tubule

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76
Q

what does proximal tubule turn into

A

descending loop of henle

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77
Q

finish the sequence–

proximal tubule-loop of henle–

A

distal tubule

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78
Q

where does collecting duct terminate

A

renal papilla

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79
Q

what does efferent arteries rap around

A

loop of henle

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80
Q

when does efferent arteriole attach to arcuate vein

A

after it wraps around loop of henle

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81
Q

what is ascending loop of henle attached to

A

descending loop and distal tubule

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82
Q

what is descending loop of henle between

A

proximal tubule and ascending loop

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83
Q

what does the distal tubule feed into

A

juxtaglomerular apparatus

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84
Q

what does juxtaglomerular apparatus dump into

A

connecting duct which dumps into collecting duct which dumps into papilla

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85
Q

do nephrons replace themselves

A

no

1.2 million nephrons per kidney

lose 1% per year after 40

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86
Q

what is glomerulus always in and what is loop of henle always in

A

g=cortex
LoH= medulla

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87
Q

which loop of henle has important function with water

A

-juxtamedullary- concentrate urine (pull water into back system)

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88
Q

what are portions of ascending/descending loop of henle

A

thick and thin

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89
Q

what are two types of nephrons

A

cortical and juxtamedullary

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90
Q

where are all glomeruli vs all loop of henle

A

glomeruli= cortex
loop of henle= medulla

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91
Q

which nephron has shorter loop of henle

A

cortical

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92
Q

which nephron has longer loop of henle

A

juxtamedullary

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93
Q

should there be protein or glucose in the urine

A

NO

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94
Q

what are systems of peripheral nervous system

A

ANS
Somatic

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95
Q

what is the receptor and neurotransmitter of somatic motor

A

Ach
nicotinic

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96
Q

what is the receptor and neurotransmitter of sns

A

epi/norepi- ,
alpha 1,
alpha 2,
beta 1,
beta, 2,
beta 3,

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97
Q

role of alpha and beta receptors

A

alpha 1= constrict
alpha 2= inhibit constriction
beta 1= increases HR
beta 2= inhibit response
beta 3= neutralizer

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98
Q

role of nicotinic vs muscarinic

A

N= muscular

M= organs/glands

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99
Q

how many neurons does a response have to go through

A

2 neurons

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100
Q

what is the receptor and neurotransmitter of pns

A

ach
nicotinic= n1, n2
muscarinic= m1, m2, m3

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101
Q

does sns have long or short pre ganglionic

A

short

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102
Q

does sns have long or short post ganglionic

A

long

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103
Q

does pns have long or short pre ganglionic

A

long

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104
Q

does pns have long or short post ganglionic

A

short

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105
Q

what are muscarinic receptors usually on

A

glands and organs

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106
Q

what is neurotransmitter for preganglionic in pns or sns

A

acetylecholine

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107
Q

by default what are all receptors in 1st synapse in pns or sns

A

nicotinic

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108
Q

what are neurotransmitters and receptors post ganglionic for pns (second synapse)

A

cholinergic (nicotinic/muscarinic)

Ach

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109
Q

what are neurotransmitters and receptors post ganglionic for sns (second synapse)

A

adrenergic receptors (alpha/beta)

epi/norepi

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110
Q

what nicotinic receptor is post ganglionic in somatic nerve

A

N1

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111
Q

what is the bladder muscle

A

detrusor muscle

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112
Q

what are receptor sites on bladder and nerves that synpase with them

A

M3- PNS- Pelvic nerve

Beta 3- SNS- hypogastric

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113
Q

what is the external sphincter in

A

urogenital diaphragm

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114
Q

what separates internal from external sphincter in male

A

prostate

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115
Q

what receptor is on internal sphincter

A

alpha 1 -SNS- Hypogastric

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116
Q

what receptor is on external sphincter

A

somatic- pudenal

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117
Q

what muscle is voluntarily controlled in urethra

A

external sphincter

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118
Q

do women have an internal sphincter

A

Yes, but does not have constricting ability like males do

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119
Q

is male internal sphincter voluntarily controlled

A

NO
females is

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120
Q

what is the sensory nerve attached to the bladder and how does it sense things

A

pelvic- baroreceptors- senses stretch

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121
Q

what regions do nerves come out of that innervate bladder and urethral muscles

A

sacral and thoracic region

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122
Q

how does empty bladder signaling work

A

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

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123
Q

what receptor neutralizes contraction of the bladder

A

Beta 3

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124
Q

full bladder signaling

A

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

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125
Q

what nerve does sensation to urinate come from and where does it go to in the brain

A

pelvic sensory- pons

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126
Q

when does voiding reflex happen

A

after initiation- to completely empty bladder

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127
Q

how does voiding reflex work

A

baroreceptors keep signaling via pelvic nerve to have pelvic motor nerve to to keep detrusor muscle (m3) to constrict

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128
Q

what are the 4 mechanisms of urine formation

A

filtration
reabsorption
secretion
excretion

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129
Q

filtration, reabsorption, excretion of water

A

180
179
1

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130
Q

filtration, reabsorption, excretion of sodium

A

25
560
25
410
150

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131
Q

filtration
reabsoprtion
excretion
of glucose

A

180
180
0

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132
Q

filtration, reabsorption, excretion of creatinine

A

1.8
0
1.8

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133
Q

is any creatinine reabsorbed

A

NO

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134
Q

what is equation for excretion

A

excretion=filteration-reabsorption + secretion

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135
Q

how much renal plasma is filtered

A

20%

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136
Q

what is normal Renal blood flow, GFR and reabsorption

A

RBF= 625 ml/min

GFR= 125ml/min

reabsorption= 124ml/min

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137
Q

how much blood goes to kidney per minute

A

1.1 liter- only 50% is filtered, the rest is for kidney itself

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138
Q

what is gfr in ml/min and l/day

A

125 ml/min and 180/day

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139
Q

should albumin/amino acids/rbc be in urine

A

No should be filtered

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140
Q

who is more likely to develop proteinuria

A

diabetic patients

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141
Q

what are tiny holes inside endothelium of glomerulus that filter

A

fenestrations

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142
Q

what has negatively charged heparin sulfates that repels proteins and amino acids back into circulation

A

basement membrane

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143
Q

what is found in epithelium that has smaller holes than fenestrations

A

split pores

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144
Q

what is a split pore in

A

podocytes

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145
Q

when basement membrane is damaged, what happens

A

proteinuria

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146
Q

what is not a very accurate proteinuria test

A

dipstick

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147
Q

what is the equation for net filtration pressure

A

net filtration pressure = glomerular hydrostatic pressure- bowman’s capsule pressure- glomerular oncotic pressure

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148
Q

what is normal met filtration pressure

A

10
(60-32-18)

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149
Q

what pressure push opposite of glomerular hydrostatic pressure

A

glomerular colloid osmotic and bowman’s capsule pressure

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150
Q

how does glomerular colloid osmotic pressure cause pressure

A

draws water/proteins back into glomerulus against glomerular hydrostatic pressure

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151
Q

how does bowman’s capsule cause pressure

A

funneled to pushes pressure upward

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152
Q

does net filtration rate = GFR

A

NO

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153
Q

what is normal GFR

A

125ml/min

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154
Q

what is kf a measure of

A

measure of surface area and permeability
-more surface area= bigger glomerulus=more filtering

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155
Q

what is kf

A

filtration coefficient

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156
Q

what diseases cause reduced kf and GFR

A

HTN
DM
Obesity
glomerulonephritis

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157
Q

what does cast noted mean in UA

A

tubular necrosis

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158
Q

does bowman’s capsule pressure regulate gfr

A

no- changes because of ghp and gcop

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159
Q

what has most significant/important effect on gfr

A

GHP

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160
Q

what can influence bchp beside gcop and ghp

A

obstruction- stones, bph (urine backs all the up into bowman’s pressure which increases pressure)

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161
Q

what influences glomerular hydrostatic pressure

A

arterial pressure, afferent/efferent arteriole resistance

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162
Q

what does increased afferent arteriole resistance do to ghp

A

decreased ghp thus decreasing gfr
decreased flow

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163
Q

when efferent arteriole resistance is increased what happens

A

fluid backs up, increasing ghp and gfr

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164
Q

where does angiotensin II constrict

A

efferent arteriole- backs up blood so ghp and gfr increase

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165
Q

what does increased ghp cause

A

increased GFR

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166
Q

what does kidney need a lot of oxygen/atp for

A

tubular reabsorption of sodium (active transport)

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167
Q

can you decrease renal blood flow and increase gfr

A

yes- constriction of efferent arterioles by angiotensin II

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168
Q

kidney consumes o2 at _____________ rate of brain but receives ______________ times the blood flow

A

twice

7

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169
Q

how much cardiac output goes to kidney

A

22%

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170
Q

what does sns do to gfr

A

vasoconstriction= increased resistance, decreased renal blood flow so decreased gfr

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171
Q

what does angiotensin II do to arterioles

A

increases efferent arteriole resistance, which backs blood up in glomerulus

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172
Q

overall what does angiotensin II to do gfr

A

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

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173
Q

how do prostaglandins/nitric oxide affect gfr

A

decreases resistance= increased blood flow= increased gfr/renal blood flow

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174
Q

how does ibuprofen affect kidneys

A

blocks prostaglandins- so afferent and efferent arterioles are not as dilate= decreased gfr

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175
Q

what is auto-regulator to stop complete vasoconstriction

A

endothelial derived nitric oxide

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176
Q

nitric oxide

A

vasodilator
makes o2 more soluble

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177
Q

how does endothelin impact gfr

A

decreases it by vasoconstriction (increased resistance)

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178
Q

what are autoregulation control of gfr/renal blood flow

A

myogenic mechanism- increase bp=increase calcium=increased contraction=increased increased resistance= decreased flow/gfr

macula densa feedback=

angiotensin II=

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179
Q

myogenic autoregulation

A

increase bp=increase calcium=increased contraction=increased increased resistance= decreased flow/gfr

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180
Q

where is macula densa

A

juxtaglomerular apparatus

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181
Q

what makes renin

A

juxtaglomerular cells

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182
Q

what cells line distal tubule

A

macula densa- come close to afferent and efferent arterioles

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183
Q

what does macula densa measure

A

sodium and chloride in distal tubule (which is urine)

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184
Q

when sodium chloride is decreased in macula densa, what happens

A

decreases afferent arterial resistance so more blood gets into glomerulus to filter more sodium/chloride out

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185
Q

what does low gfr cause sodium to be in distal tubule, low or high

A

low

more gets absorbed

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186
Q

how does angiotensis II affect GFR

A

decreased gfr= low macula densa nacl= increases renin= angiotensin II= increases efferent arteriole resistance= raises GFR

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187
Q

where does angiotensin II have effect on kidney

A

efferent arterioles

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188
Q

other factors that influence GFR

A

increase= fever, STEROIDS, hyperglycemia, high diet protein

decrease= age, low diet protein

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189
Q

what are the four mechanisms of urine formation

A

filtration
reabsorption
secretion
excretion

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190
Q

what kind of cells do aldosterone antagonists and sodium channel blockers work on

A

principal cells

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191
Q

what location do aldosterone antagonists and sodium channel blockers work

A

collecting duct

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192
Q

what is the equation for excretion

A

filtration - reabsorption + secretion

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193
Q

what is the equation for resborption

A

filtration- excretion

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194
Q

what is the equation for secretion

A

excretion - filtration

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195
Q

what is excretion

A

removing wastes and drugs

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196
Q

what is the process of filtered components going back into body

A

reabsorption

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197
Q

what is the process of stuff coming from body going into lumen to get excreted

A

secretion

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198
Q

is most of water reabsorbed or excreted from body

A

reabsorbed

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199
Q

why is Na so well reabsorbed

A

Na follows H2O

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200
Q

where does stuff that get filtered go to for excretion

A

lumen

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201
Q

where does the lumen lead to

A

collecting duct

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202
Q

what does the lumen connect

A

glomerulus and collecting duct

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203
Q

what is the filtered material in the lumen

A

urine

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204
Q

what are the ways molecules get reabsorbed into the body

A

active transport, passive transport (diffusion), osmosis
paracellular/transcellular paths

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205
Q

what is between the peritbular capillar and lumen

A

tubular cells

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206
Q

what do molecules have to pass through to be reabsorbed in the kidney

A

tubular cells

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207
Q

where do transporter mechanisms occur for reabsorption

A

tubular cells

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208
Q

what ions travel in paracellular path

A

Ca
Mg

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209
Q

what ions travel in the transcellular path

A

Na
K
Cl

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210
Q

what drives diffusion

A

concentration or electrical gradient

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211
Q

how can sodium move against concentration/electrical gradient

A

active transport

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212
Q

what are the 3 methods of transport sodium is reabsorbed in the kidney

A

diffusion
active transport
osmotic pressure

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213
Q

does secondary active transport use ATP

A

NO

gets energy from Na to move molecules

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214
Q

how does secondary active transport work

A

It takes advantage of a gradient that has already provided energy.

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215
Q

what happens to gfr with hyperglycemia and hyperproteinemia

A

increases

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216
Q

how is glucose/amino acids reabsorbed in the kidney

A

secondary active transport

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217
Q

what is it called when a substance reaches its maximum rate of tubular transport in ALL nephrons

A

transport maximum

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218
Q

when the transport maximum is reached for all nephrons, what happens when more substance comes through

A

NOT reabsorbed- excreted

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219
Q

what is it called when transport maximum is exceeded in SOME nephrons

A

threshold

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220
Q

t or f- individual nephrons may have lower transport maximum’s than others

A

True

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221
Q

what are some examples of substances that have a transport maximum

A

glucose
amino acids
phosphate
sulfate

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222
Q

what happens to lumen potential when sodium is reabsorbed

A

negative potential increases (since sodium is positive)

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223
Q

what happens to chloride and urea when sodium and water are reabsorbed in proximal tubule

A

increased concentration–>passive reabsorption due to concentration gradient

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224
Q

how much of all sodium is reabsorbed in proximal tubule

A

65%

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225
Q

what is reabsorbed in proximal tubule

A

sodium
chloride
potassium
bicarb
water
glucose
amino acids

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226
Q

where is most of sodium reabsorbed in kidney

A

proximal tubule

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227
Q

what is excreted out of proximal tubule

A

hydrogen
organic acids
bases

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228
Q

what are the byproducts of metabolism and are most toxic

A

hydrogen
organic acids
bases

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229
Q

what are kidneys key in balancing

A

balance fluid through sodium renetion
acid-base balance through h+ and bicarb

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230
Q

what is the thin descending loop of henle very permeable to

A

water 20%

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231
Q

which nephron is responsible for concentration of urine

A

juxtamedullary nephrons

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232
Q

which nephron absorbs most of water

A

juxtamedullary nephrons

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233
Q

where is 25% of sodium reabsorbed

A

thick ascending loop of henle

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234
Q

what is reabsorbed in the thick ascending loop of henle

A

sodium
chloride
potassium
bicarb
calcium
magnesium

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235
Q

what is the ratio of molecules for the transporter in the thick ascending loop of henle

A

1 sodium, 2 chloride, 1 potassium

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236
Q

is the proximal tubule isosmotic or hyposmotic

A

isomotic

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237
Q

is the thick ascending loop of henle isosomtic or hyposmotic

A

hyposmotic

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238
Q

what does the thick ascending loop of henle secrete

A

Hydrogen

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239
Q

what is the thick ascending loop of henle NOT premeable to

A

H2O

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240
Q

where is h2o not permealbe to in the kidney

A

thick ascending loop of henle, early distal tubule

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241
Q

where do loop diuretics work

A

thick ascending loop of henle

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242
Q

what are the loop diuretic examples

A

furosemide
bumetanide
ethacrynic acid

243
Q

which transporter does the loop diuretic work on

A

1 na, 2 cl and 1 K transporter
“triple transporter”

244
Q

what do loop diuretics bind up to have effect

A

2 chloride on triple transporter

245
Q

when sodium-hydrogen exchanger in thick ascending loop of henle moves sodium into tubular cells, what does it initiate

A

triple transporter to move into tubular cell

246
Q

what is the pathway of sodium when reabsorbed in the kidney

A

tubular lumen- tubular cell- renal interstitial fluid

247
Q

what does loop diuretic cause excretion of from triple transporter

A

Na
K
Cl

248
Q

are loop diuretics potassium sparing

A

NO. Loop diuretics cause potassium loss into the urine

249
Q

where is 5% of sodium reabsorbed

A

distal convoluted tubule

250
Q

what pump is responsible for sodium being reabsorbed in early distal tubule

A

sodium chloride transporter

251
Q

in the sodium chloride pump on the early distal convoluted tubule, does chloride come into lumen or go into renal interstitial fluid

A

from tubular lumen into tubular cell then into renal interstitial fluid

252
Q

what are the two types of transporters/exchangers on the early distal tubule and where are they located

A

sodium potassium exchanger- between renal interstitial fluid and tubular cells

sodium/chloride transporter- between tubular cells and tubular lumen

253
Q

where do thiazide diuretics work

A

early distal tubule- on sodium chloride transporter

254
Q

what does thiazide diuretic inhibit

A

sodium chloride transporter- so sodium stays in lumen and draws water into lumen for excretion

255
Q

in early distal tubule, where does sodium and chloride travel from and to

A

from tubular lumen to tubular cell and then to renal interstitial fluid

256
Q

what structure has a similar functional to the thick ascending loop of henle

A

early distal tubule

257
Q

is the early distal tubule permeable to water

A

NO

258
Q

where are macula densa located

A

early distal tubule

259
Q

where does active reabsorption of sodium, chloride, calcium, and magnesium occur

A

early distal tubule

260
Q

what is actively reabsorbed in early distal tubule

A

sodium
chloride
potassium
magesium

261
Q

what is called the diluting segment

A

early distal tubule

262
Q

what is the macula densa responsible for

A

Na Cl balancing

263
Q

what part of tubule is not very permeable to urea

A

early and late distal tubule/collecting tubule

264
Q

what does permemability of water in late distal tubule/collecting tubule depend on

A

ADH

265
Q

where are principle cells located

A

late distal tubule/collecting tubule

266
Q

another name for ADH

A

vasopressin

267
Q

where are type a intercalated cells located

A

late distal tubule/collecting tubule

268
Q

what do intercalated cells play a role in

A

acid base balance

269
Q

what is an important role of principal cells

A

what are the types of leaky channels in principal cells

270
Q

in the principal cell, when sodium potassium exchanger puts sodium into renal interstitial fluid (blood), what does that cause

A

sodium leaky channel brings in sodium from tubular lumen

271
Q

what is renal interstitial fluid

A

blood

272
Q

in the principal cell, when sodium potassium exchanger puts potassium from renal interstitial fluid in the cell, what does that cause

A

potassium leaky channel to take potassium from inside cell and put into tubular lumen

273
Q

what does the principal cell work primarily off of

A

sodium potassium transporter
leaky channels- k and na

274
Q

what are some aldosterone antagonists

A

spironolactone, eplerenone

275
Q

what are some sodium channel blockers

A

amiloride, triamterene

276
Q

how do aldosterone antagonists work

A

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
Q

what cell does aldosterone have greatest impact on

A

principal cell

278
Q

what does aldosterone stimulate

A

sodium potassium exchanger- so more sodium is reabsorbed

279
Q

what are the potassium sparing diuretic classes

A

aldosterone antagonists- sprinolactone
sodium channel blockers- amiloride

280
Q

where do sodium channel blockers work

A

blocks leaky channels on principal cells (which are in late distal tubule/collecting tubule)

281
Q

what do the type a intercalated cells help with

A

acidosis- help to decrease h and save bicarb

282
Q

what do the type b intercalated cells help with

A

alkalosis- increase h and decrease bicarb

283
Q

where are the intercalated cells a-b found

A

late distal tubule/collecting tubule

284
Q

where does adh act

A

medullar collecting duct

285
Q

what is reabsorbed in medullary collecting duct

A

sodium
chloride
water
urea
bicarb

286
Q

what is secreted into medullary collecting duct

A

hydrogen

287
Q

what is peritubular capillary reabsorption

A

pressure needed to move from interstitial fluid into capillary

288
Q

when is aldosterone produced

A

low bp, or low extracellular fluid

289
Q

how does aldosterone work

A

acts on sodium potassium exchanger to increase sodium moving from principal cell into interstitial fluid

290
Q

what cell does aldosterone work in

A

principal cell

291
Q

what are the factors that increase aldosterone secretion

A

angiotensin II
increased potassium
adrenocorticotrophic hormone (acth)

292
Q

where is aldosterone secreted from

A

adrenal cortex

293
Q

what are factors that decrease aldosterone secretion

A

atrial natriuretic factor
increased na concentration

294
Q

why does increased potassium increase aldosterone

A

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
Q

what is the permissive role of acth

A

release aldosterone

296
Q

what does high atrial natriuretic factor mean

A

too much fluid

297
Q

what is the opposite of renin

A

atrial natriuretic factor

298
Q

what does angiotensin II stimulate the release of

A

aldosterone

299
Q

where does angiontensin II directly increase sodium reabsorption

A

proximal, loop, distal, and collecting tubules

300
Q

what does angiotensin II do to the efferent arterioles

A

constricts them

301
Q

what happens when angiotensin II constricts efferent arterioles

A

-decreased peritubular capillary hydrostatic pressure
-increases filtration fraction which increases peritubular colloid osmotic pressure

302
Q

what is the important thing to remember with angiotensin II

A

vasoconstriction

303
Q

what are the pumps that angiotensin II affects on tubular cells to increase sodium reabsorption

A

sodium-potassium-exchanger
sodium-hydrogen-exchanger
sodium-bicarb-transporter

304
Q

what do ace inhibitors, arbs and renin inhibitors decrease

A

decreases:
aldosterone
sodium reabsorption
efferent arteriolar resistance

305
Q

what is a renin inhibitor example

A

aliskirin

306
Q

where is ADH secreted from

A

posterior pituitary gland

307
Q

what does adh increase permeability to and where does it do this

A

water- distal and collecting tubules

308
Q

what is an important controller of extracellular fluid osmolarity

A

ADH

309
Q

what hormone allows for differential control of water and solute secretion

A

ADH

310
Q

what is the most important renal action of adh

A

increase water permeability in distal tubule/collecting tubule

311
Q

what does adh attach to on tubular cell

A

V2 receptor

312
Q

when adh binds to v2 receptor, what happens

A

increases formation of cAMP

313
Q

what does camp activate after creation by adh

A

protein kinase

314
Q

what does protein kinase stimulate prodction of

A

protein phosphorylation

315
Q

what does protein phosphorylation stimulate to move to lumen side

A

aquaporin 2

316
Q

where does aquaporin 2 attach to

A

wall of tubular cell on the tubular lumen side

317
Q

where are aquaporin 3 and 4 found

A

tubular cell wall on interstitial fluid side

318
Q

what is the gateway for water to flow from tubular lumen into interstitial fluid

A

aquaporins

319
Q

what does anp increase excretion of

A

Na

320
Q

what are the 3 things anp inhibits

A

sodium reabsorption
renin release
aldosterone formation

321
Q

what impact does anp have on gfr

A

increases

322
Q

what is an example of osmotic diuretic

A

mannitol,
isosorbide,
urea,
glycerin

323
Q

how does diabetes cause diuresis

A

osmosis
water follows glucose

324
Q

does an increase or decrease of unreabsorbed solutes in tubules decrease water reabsorption

A

increase

325
Q

what tests measure plasma concentration of waste products

A

BUN
creatinine

326
Q

what measures urine concentrating ability

A

urine specific gravity (1-2)

327
Q

what measures albumin excretion

A

microalbuminuria

328
Q

what describes rate at which substances are removed from plasma

A

clearance

329
Q

what is the volume of plasma completely cleared of a substance per min by kidney

A

renal clearance

330
Q

clearances of different substances

A

glucose- 0
albumin- 0
sodium- 0.9
urea- 70
inulin- 125
creatinine- 140
pah-600

331
Q

what should renal clearance be equal to

A

GFR

332
Q

what does efferent arteriole turn into

A

vasa recta- which wraps around loop of henle

333
Q

what is between the bowman’s capsule and the descending loop of henle

A

proximal convoluted tubule

334
Q

what is the between the ascending loop of henle and the collecting duct

A

distal convoluted tubule

335
Q

what gets reabsorbed in proximal convoluted tubule

A

sodium
chloride
potassium
glucose
amino acids
urea
water
bicarb

336
Q

where do juxtaglomerular nephrons lie

A

in cortex but near medulla

337
Q

which nephrons concentrate urine

A

juxtamedullary nephrons

338
Q

what is main thing loop of henle reabsorbs

A

water

339
Q

what is reabsorbed at thick ascending loop of henle

A

na, cl, k, bicarb, ca, mag

340
Q

where is the sodium potassium exchanger located in the nephron

A

collecting duct

341
Q

where is the sodium chloride transporter found in nephron

A

distal convoluted tubule

342
Q

how does sodium potassium exchanger work in dct

A

sodium is moved from dct to blood
potassium is moved from blood to dct

343
Q

what is reabsorbed from late distal convoluted tubule

A

sodium
chloride
potassium
bicarb
water (adh)

344
Q

what is reabsorbed from collecting duct

A

sodium
chloride
bicarb
urea
water (adh)

345
Q

what are parts of nephron where things are primarily secreted

A

proximal convoluted tubule

346
Q

how is creatine removed from body

A

urine

347
Q

what is the byproduct of breakdown of muscle and protein

A

creatinine

348
Q

what is secreted into proximal convoluted tubule (lumen)

A

hydrogen, organic acids, bases, creatinine, drugs

349
Q

what is secreted into distal convoluted tubule

A

hydrogen
potassium

350
Q

what are the types of diuretics

A

osmotic
loop
thiazide
potassium sparing
carbonicanhydrase inhibitors

351
Q

where is most (65%) of sodium reabsorbed from in kidney

A

proximal convoluted tubule

352
Q

where is a high concentration of sodium bicarb reabsorbed from

A

proximal convoluted tubule

353
Q

what does the triple transporter transport and where does it do so

A

thick ascending loop of henle
Sodium
2 chloride
potassium

354
Q

where is 25% of sodium reabsorbed from in kidney

A

thick ascending loop of henle

355
Q

what is reabsorbed in the early distal convoluted tubule

A

sodium
chloride
calcium
magesium

356
Q

where is 5% of sodium reabsorbed from

A

distal convoluted tubule

357
Q

in the sodium potassium exchanger in the collecting duct, what is also secreted into collect duct with potassium

A

hydrogen

358
Q

where is 1-2% of sodium reabsorbed from

A

collecting duct

359
Q

t or f- osmotic diuretics last a long time

A

False

360
Q

how do osmotic diuretics work

A

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
Q

where does osmotic diuretics work

A

proximal convoluted tubule

362
Q

what transporter do loop diuretics work on

A

triple transporter

363
Q

what do loop diuretics prevent from being transported

A

2 chlorides
so then sodium and potassium also stay in lumen

364
Q

which diuretic may cause hypokalemia

A

loop diuretics

365
Q

what other ions can loop diuretics have an effect on after a period of time

A

Ca
Mg

366
Q

what ions are transported paracellularly from lumen to blood

A

Ca
Mg

367
Q

what are all of the things loop diuretics can increase excretion of

A

sodium
chloride
potassium
water
calcium
magnesium

368
Q

what can loop diuretics be used to treat

A

pulmonary edema
cirrhosis
acute renal failure

369
Q

what are examples of thiazide diuretics

A

hydrochlorothiazide, chlorothiazide

370
Q

where do thiazide diuretics work

A

distal convoluted tubule

371
Q

what transporter do thiazide diuretics work on

A

sodium chloride transporter-

stops sodium from being reabsorbed

372
Q

what do thiazide diuretics increase reabsorption of

A

Ca
urea

373
Q

what do thiazide diuretics decrease reabsorption of (and therefore increase excretion)

A

mg
Na
Cl

374
Q

what drugs increase reabsorption of urea in distal convoluted tubule

A

thiazide diuretics

375
Q

when are thiazide diuretics contraindicated and why

A

gout

they cause reabsorption of urea in proximal convoluted tubule

376
Q

which diuretics are used to treat hypertension, edema, and renal stones

A

thiazide diuretics

377
Q

why does thiazide diuretics not have a lot of effect on sodium

A

because they act in distal convoluted tubule where only 5% of sodium is reabosrbed

378
Q

where do potassium sparing diuretics work

A

mostly collecting duct

379
Q

why are potassium sparing diuretics often used with other diuretics

A

because they work in areas where only 1% of sodium is reabsorbed, they aren’t as effective as other diuretics

380
Q

which diuretic class potentiates other diuretics

A

K sparing

381
Q

what are the two types of potassium sparing diuretics

A

sodium channel blockers- amiloride
aldosterone antagonists- spironolocatone

382
Q

what channel does sodium channel blocking diuretics block

A

sodium leaky channel- so sodium can’t get out of lumen and into cell

383
Q

what happens to potassium with sodium channel blocking diuretics

A

potassium stays in cell and goes into blood

384
Q

where does aldosterone antagonist have effect and on what transporter

A

collecting duct- on sodium potassium exchanger

385
Q

what does aldosterone increase the number of

A

sodium potassium exchanger- so more sodium gets out of cell into blood

386
Q

how does spironolactone work

A

on sodium potassium exchanger in collecting duct- keeps sodium in lumen and potassium in blood

387
Q

what are the uses of potassium sparing diuretics

A

primary and secondary aldosteronism
resistant hypertension
heart failure
hypertension (na channel blockers)

388
Q

what is ph range for hydrogen

A

7.2-7.4

389
Q

what are the body fluid chemical buffers that play a role in hydrogen ion regulation

A

bicarb
ammonia
phosphate
proteins

390
Q

how do lungs play a role in hydrogen regulation

A

increased hydrogen= increased ventilation to increase co2 exhalation

391
Q

how do kidneys regulate hydrogen ions

A

secrete H
reabsorb bicarb
generates new bicarb

392
Q

what is the most important extracellular fluid buffer

A

bicarb

393
Q

what kind of buffers are phsophate and ammonia

A

renal tubular buffers

394
Q

what is the intracellular buffer

A

proteins (Hgb)

395
Q

what does phosphate and hydrogen form

A

phosphuric acid

396
Q

what does ammonia and hydrogen form

A

ammonium

397
Q

what does proteins and hydrogen form

A

hydrogen-hemoglobin

398
Q

why does hydrogen have to be buffered instead of excreted

A

fixed amount of hydrogen that can be directly excreted from kidneys

399
Q

what is the most important kidney hydrogen buffer system

A

bicarb

400
Q

what is pk

A

concentration of hydrogen at a certain ph

401
Q

what does the effectiveness of the bicarbonate buffer system depend on

A

concentration of reactants
pk of system
ph of body fluids

402
Q

what is a normal pk level

A

6.1- this is when bicarb and co2 are balanced

403
Q

what enzyme is necessary for the carbonic acid equation

A

carbonic anhydrase

404
Q

what systems closely regulates the bicarbonate buffer system

A

lungs and kidneys

405
Q

what is the most important buffer in extracellular fluid

A

bicarbonate buffer system

406
Q

how much co2 is carried in the blood as bicarbonate

A

70%

407
Q

what happens to alveolar ventilation when there is an increase in hydrogen ions

A

increases ventilation

408
Q

does increased co2 lead to increased or decreased aciditiy

A

increased

409
Q

what can reabsorb, produce new, filter, or excrete bicarb

A

kidney

410
Q

what are some non volatile acid the kidneys eliminate

A

sulfuric acid, phosphoric acid

411
Q

what does the kidneys conserve or excrete depending on body needs

A

bicarb

412
Q

if the body is in an alkalotic state, what will the kidney excrete MORE of

A

bicarb

413
Q

if the body is an acidosis state, what will kidney excrete LESS of

A

bicarb

414
Q

where is most of bicarbonate reabsorbed in nephron (85%)

A

proximal convoluted tubule

415
Q

for each bicarbonate reabsorbed, there must be a _________ secreted

A

hydrogen

416
Q

where is 10% of bicarbonate reabsorbed in

A

ascending thick portion of loop of henle

417
Q

where is 5% of bicarbonate reabsorbed

A

late-distal-tubule

418
Q

what is the process for bicarbonate to be reabsorbed into the renal interstitial fluid in the proximal tuble and ascending thick loop of henle

A
  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
Q

what is the process for bicarbonate reabsorption and hydrogen secretion in intercalated cells of late distal and collecting tubules

A
  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
Q

when pco2 is increased, such as in respiratory acidosis, what happens to hydrogen secretion

A

increases

421
Q

when extracellular hydrogen increases, what happens to h+ secretion

A

increases

422
Q

when tubular fluid buffers and increased, what happens to H+ secretion

A

increases

423
Q

what factors increase h+ secretion and hco3 reabsorption

A

increased: pco2, hydrogen, aldosterone, agiotensin II

decreased: bicarb, extracellular fluid volume, potassium

424
Q

when the body is increasing h+ secretion and hco3 reabsorption, what state is the body in

A

acidosis

425
Q

how do aldosterone and angiotensin II increase h+ secretion and bicarb rebsorption

A

increase sodium uptake which increases h+ secretion via sodium-hydrogen exchanger

426
Q

what conditions in body drive angiotensin II and aldosterone release

A

low bp,
low extracellular fluid

427
Q

how does hypokalemia lead to increase hydrogen secretion

A

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
Q

what factors DECREASE hydrogen secretion and bicarb reabsorption

A

increased: extracellular fluid volume, potassium, bicarb

decreased: co2,hydrogen, aldosterone, angiotensin II

429
Q

what happens to hydrogen secretion, bicarb reabsorption, and bicarb production during acidosis

A

H= increased secretion
bicarb= increased reabsorption
bicarb= increase production

430
Q

what happens to hydrogen secretion, bicarb reabsorption, and bicarb in urine during alkalosis

A

h= decreased secretion
bicarb= decreased reabsorption
bicarb= increased in urine

431
Q

can enough free hydrogen be removed by only secretion/excretion

A

no- needs buffers

432
Q

what is the minimum urine ph

A

4.5,

any more acidic will damage tissues

433
Q

t or f- kidney is not limited to amount of free hydrogen that can be excreted

A

false

434
Q

what is NH3

A

ammonia

435
Q

what is NH4

A

ammonium

436
Q

what is made from metabolism of amino acids in the liver

A

glutamine

437
Q

where is ammonium and bicarb produced and secreted

A

proximal/distal tubule
thick loop of henle

438
Q

what is the process for making new bicarb from glutamine (ammonium buffer)

A
  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
Q

is ammonium or phosphate buffer system more important

A

ammoinum

makes more bicarb

440
Q

where is hydrogen buffered by ammonia

A

collecting tubules

441
Q

is NH3 or NH4 more permeable

A

NH3

442
Q

explain the buffering of hydrogen by ammonia

A
  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
Q

if bicarb is low causing a ph less than 7.4, what is the cause

A

metabolic

444
Q

if bicarb is high causing a ph greater than 7.4, what is the cause

A

metabolic

445
Q

if co2 is low causing a ph greater than 7.4, what is the cause

A

respiratory

446
Q

if co2 is high causing a ph less than 7.4, what is the cause

A

respiratory

447
Q

co2 in respiratory acidosis

A

high

448
Q

bicarb in metabolic acidosis

A

low

449
Q

CO2 in respiratory alkalosis

A

low

450
Q

bicarb in metabolic alkalosis

A

high

451
Q

what is the ph range that is compatible with life

A

6.8- 7.8

452
Q

what is the goal ratio of hco3 to co2

A

20 : 1

453
Q

respiratory acidosis

A

low ph
increased co2
increased renal acid excretion/bicarb reabsorption

454
Q

respiratory alkalosis

A

high ph
decreased pco2
decreased renal acid secretion, increased bicarb reabsorption

455
Q

metabolic acidosis

A

low ph
decreased bicarb
hyperventilation to lower co2

456
Q

metabolic alkalosis

A

high ph
increased bicarb
hypoventilation to increase co2

457
Q

when there is a metabolic acid base imbalance, what responds

A

lungs

458
Q

when there is a respiratory acid base imbalance, what responds

A

kidney

459
Q

normal bicarb range

A

22-26

460
Q

normal PaCO2

A

35-45

461
Q

how do the kidneys compensate for acidosis

A

increase: hydrogen excretion, bicarb reabsorption, and produce new bicarb

462
Q

how do kidneys compensate for alkalosis

A

decrease hydrogen excretion, bicarb reabsorption
excrete bicarb in urine

463
Q

what acid base imbalance does anion gap come into play

A

metabolic acidosis

464
Q

what is majority of cations

A

Na

465
Q

what are anions

A

Cl
bicarb

466
Q

t or f- cations and anions are usually equal in the body

A

true

467
Q

what are unmeasured anions

A

proteins
phosphates
sulfate
lactate

468
Q

what are unmeasured cations

A

K
Mg
Ca

469
Q

normal anion gap

A

8-16 mEq/L

470
Q

what causes abnormal anion gap

A

dka
ethylene glycol poisoning

471
Q

what are normal cation and anion levels

A

142 Cation
132 Anion

472
Q

when there is an increase in anion gap, what is being thrown off

A

the unmeasurable anions or cation

473
Q

what is called when you lose bicarb but anion gap is normal

A

hyperchloremic metabolic acidosis
-chloride compensates for decreased bicarb

474
Q

what is it called when unmeasured anions increase and anion gap increases

A

normochloremic metabolic acidosis
- losing bicarb

475
Q

what are examples of normochlormeic metabolic acidosis

A

DKA
lactic acidosis
salicylic acidosis

476
Q

what are some causes of resp acidosis

A

brain damage
pneumonia
emphysema
other lungs problems

477
Q

what are some causes of metabolic alkalosis

A

increase base intake
vomiting
mineralocorticoid excess
overuse of diuretics- except carbonic anhydrase inhibitors

478
Q

what are preventions of blood loss

A

-vascular constriction
-Formation of a platelet plug
-Formation of a blood clot
-Healing of vascular damage (clot remodeling/repair)
-fibrinolysis

479
Q

what are the key events in hemostasis

A
  1. severed vessel
  2. platelets agglutinate
  3. fibrin appears
  4. fibrin clot forms
  5. clot retraction occurs
480
Q

what causes vascular constriction

A

Myogenic spasm

Local autocoid factors from damaged tissues and platelets

Nervous reflexes

Smaller vessels: thromboxane A2 released by platelets

481
Q

characteristics of platelets

A

Released by fragmentation of megakaryocytes

normal level: 150–300,000 per µL

Half-life in blood of 8–12 days

482
Q

what are platelet funtions

A

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
Q

what are the platelet membranes

A

surface glycoprotein
membrane phospholipids

484
Q

what is the function of surface glycoproteins

A

Repels intact endothelium

Adheres to injured endothelium and exposed collagen

485
Q

what is the function of membrane phospholipids on platelets

A

activate blood clotting

486
Q

what is the process of formation of the platelet plug

A

-contact with damaged endothelium

-adhere to collagen and vWF

-other platelets accumulate, adhere, and contract, form plug, initiate clotting

487
Q

what does contact with damaged endothelium result in

A

-assume irregular forms

-endothelium contracts and release granules (ADP and thromboxane A2)

488
Q

what can very low platelets present like

A

petechiae
bleeding gums

489
Q

in severe vascular trauma, how long for clot formation

A

15-20 seconds

490
Q

how quickly can an occlusive clot form

A

within 3-6 min unless very large vascular defect

491
Q

how long does it take for clot retraction

A

20-60 min

492
Q

what happens within 1-2 weeks of clot formation

A

-invasion by fibroblasts
-organization into fibrous tissue

493
Q

what are the effector proteins for clotting

A

prothrombin
fibrinogen

494
Q

characteristics of prothrombin

A

-α2 globulin,
-15 mg/dL in plasma
-Vitamin K-dependent synthesis in liver
-Cleaved by PT activator to thrombin

495
Q

characteristics of fibrinogen

A

-100–700 mg/dL in plasma

-Synthesized in the liver (acute phase reactant)

-Usually intravascular; can extravasate with increased vascular permeability

496
Q

what cleaves 4 small peptides from fibrinogen

A

thrombin

fibrin monomer-> spontaneous polymerization

497
Q

what helps to form clot reticulum

A

long fibrin fibers

498
Q

characteristics of fibrin stabilizing factor

A

In plasma and released from platelets

Activated by thrombin

Covalent cross-linking of fibrin monomers and adjacent fibrin fibers

499
Q

what is bound to platelets and trapped in the clot

A

thrombin

500
Q

what system does thrombin and clot formation work on

A

positive feedback

501
Q

___ produces more prothrombin activator by acting on other clotting factors

A

thrombin

502
Q

what is generated at the periphery of the clot

A

additional fibrin monomers and polymers

503
Q

when does clot retraction begin

A

within 20-60 min

504
Q

what binds to the damaged vessel wall

A

fibrin

505
Q

what causes clot contraction

A

actin, myosin and thrombosthenin

506
Q

describe clot retraction

A

clot tightens expressing serum and closes the vascular defect

507
Q

what are the two clotting pathways

A

Extrinsic pathway—Trauma to vessel wall and adjacent tissues

Intrinsic pathway—Trauma to the blood or exposure of the blood to collagen

508
Q

what factor activates the extrinsic pathway

A

tissue factor

509
Q

what factor activates the intrinsic factor

A

exposure to factor XII
exposure of platelets to collagen

510
Q

what is the time to clot for extrinsic pathway

A

<15 sec

511
Q

how long for clotting in intrinsic pathway

A

1-6min

512
Q

what prevents clotting

A

-smoothness of endothelial surface

mucopolysaccharide coating (glycocalyx) repels platelets and clotting factors

thrombomodulin

protein C

513
Q

how does mucopolysaccharide coating (glycocalyx) prevent clotting

A

it repels platelets and clotting factors

514
Q

how does thrombomodulin prevent clotting

A

Thrombomodulin bound to endothelium binds (competes for) thrombin

515
Q

how does activated protein C prevent clots

A

Thrombin-thrombomodulin activates Protein C→ inactivates factors V and VIII

516
Q

how does thrombin become localized to the clot

A

Fibrin fibers bind 85–90% of thrombin and localize it to the clot

517
Q

how does antithrombin III work in the negative feedback system

A

Antithrombin III combines with the remainder and inactivates it over 12–20 minutes.

518
Q

what is the charge of heparin

A

highly negative

519
Q

MOA of heparin

A

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
Q

where can heparin be found in the body

A

Mast cells,

basophils particularly abundant in pericapillary regions of liver and lung

521
Q

what causes clot lysis

A

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
Q

what are some causes of excessive bleeding

A

Hepatocellular disease

Vitamin K deficiency

Hemophilia

Low platelet count (thrombocytopenia)

523
Q

what is essential to carboxylate glutamic acid and 5 clotting factors

A

vitamin K

524
Q

what clotting factors are affected by Vit K deficiency

A

prothrombin
factor VII
factor IX
factor X
protein C

525
Q

what happens in vitamin K deficiency

A

In this process vitamin K is oxidized and inactivated.

Vitamin K epoxide reductase complex 1 (VKOR c1) reduces vitamin K and reactivates it.

526
Q

where is vitamin K produced

A

intestines by gut bacteria

527
Q

what can cause fat malabsorption and vitamin K deficiency

A

lack of bile production
lack of bile delivery

528
Q

what can be done for patients with liver or biliary disease before surgery

A

In patients with liver or biliary disease, vitamin K can be injected 4–8 hours before surgery.

529
Q

what can also lead to vit K deficiency

A

malabsorption of fats

vitamin K is fat soluble

530
Q

hemophilia A

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
Q

hemophilia B

A

Deficiency of factor IX

15% of cases

532
Q

how does hemophilia effect bleeding

A

both A and B impair the intrinsic pathway

clinically present: bleeding after minor trauma

533
Q

what factor deficiency cause hemophilia A

A

factor VIII

Deficiency of the small component causes hemophilia A.
→ Treat bleeding with factor VIII replacement.

534
Q

what factor deficiency causes vWF disease

A

factor VIII large component

Deficiency of the large component causes von Willebrand disease (resembles decreased platelet function).

535
Q

what are the two components of factor VIII deficiency

A

Large: MW >106

Small: MW ~230,000

536
Q

characteristics of thrombocytopenia

A

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
Q

how do you treat thrombocytopenia

A

platelet infusion

infusion is effective for 1-4 days each time

538
Q

what is a thrombus

A

an abnormal clot

539
Q

what is an embolus

A

a thrombus that floats/gets dislodged

540
Q

what can cause emboli/thrombi

A

Endothelial roughening (e.g., atherosclerosis)

Slow flow (e.g., prolonged air travel)

541
Q

what is the treatment for thrombus/embolus

A

tPA
embolectomy

542
Q

where does pulmonary embolus usually originate from

A

deep leg veins

543
Q

what is DIC

A

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
Q

what are some anticoagulants

A

heparin
coumarins

545
Q

how does heparin work

A

Binds, potentiates antithrombin III

Works rapidly, generally used acutely

546
Q

how do coumarins work

A

Inhibit VKOR c1

Deplete active vitamin K → deplete active prothrombin, factors VII, IX, X

Slower acting (days); used chronically

547
Q

how do you treat over anticoagulation of coumarins

A

treat with FFP and vitamin K

548
Q

what are calcium chelators and what are they used in

A

citrate, EDTA

used in blood collection and blood storage

549
Q

bleeding time coag test

A

normal 1-6 min

reflects platelet function

550
Q

clotting time coag test

A

-invert tube every 30 sec

normal 6-10 min

not reproducible, not generally used

551
Q

Prothrombin time coag test

A

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
Q

INR coag test

A

“international normalized ratio”

Normal: 0.9 - 1.3

therapeutic range 2.0-3.0

INR= PT test / PT normal

553
Q

how do you test for other clotting factors

A

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
Q

how is hemostasis acheived

A

(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
Q

what does trauma to vessel cause

A

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
Q

how is the nervous reflex initiated in the vessel contraction

A

initiated by pain nerve impulses or other sensory impulses that originate from the traumatized vessel or nearby tissues

557
Q

myogenic contraction of the vessel

A

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
Q

The more severely a vessel is traumatized, the greater the ______

A

the degree of vascular spasm

559
Q

where are platelets formed

A

bone marrow from megakaryocytes

560
Q

factor I

A

fibrinogen

561
Q

factor II

A

prothrombin

562
Q

factor 3

A

tissue factor

563
Q

factor 4

A

calcium

564
Q

factor 5

A

proaccelerin

“labile factor”

565
Q

factor VII

A

serum prothrombin conversion accelerator (SPCA)

proconvertin

stable factor

566
Q

factor VIII

A

antihemophilic factor (AHF)

antihemophilic globulin (AHG)

antihemophilic factor A

567
Q

Factor IX

A

plasma thromboplastin component (PTC)

Christmas factor

antihemolitic factor B

568
Q

Factor X

A

stuart prower factor

569
Q

factor XI

A

plasma thromboplastin antecedent (PTA)

antihemolitic factor C

570
Q

Factor XII

A

Hageman Factor

571
Q

Factor XIII

A

fibrin stabilizing factor

572
Q

prekallikrein

A

fletcher factor

573
Q

High molecular weight kininogen

A

Fitzgerald factor
HMWK

574
Q

3 essential steps of clotting

A
  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
Q

Describe conversion of prothrombin to thrombin

A

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
Q

What is required by the liver for normal activation of prothrombin and many other clotting factors

A

Vitamin K

577
Q

Where is fibrinogen formed

A

In the liver

578
Q

What is the reticulum of the clot

A

Many fibrin monomer molecules that polymerize within seconds into long fibrin fibers make up the reticulum of the blood clor

579
Q

What does plasmin digest

A

Fibrin fibers
Fibrinogen
Factor V
Factor VIII
Factor XII

580
Q

Vitamin K adds a ___ to _____ on which 5 clotting factors

A

Carboxylic group to glutamic acid

Prothrombin
Factor VII
Factor 9
Factor X
Protein C

581
Q

name the surface glycoproteins on platelets

A

glycoprotein Ia
glycoprotein IIb/ IIIa

582
Q

what in in the granules released when platelets come into contact with damaged endothelium

A

ADP
Serotonin
thromboxane A2

583
Q

where is vWF produced

A

endothelium

584
Q

ADP + thromboxane A2 does what

A

activates glycoproteins so that platelets stick together

585
Q

what is PDGF

A

platelet derived growth factor

aids in the repair of muscle and connective tissue during clot retraction

586
Q

what is VEGF

A

vascular endothelial growth factor

aids in repair of vessels and endothelium during clot retraction

587
Q

what initiates/activates factor 12

A

negative charge on the platelet plug

588
Q

what does protein C do

A

binds to and inactivates factor 5 and 8

589
Q

what does Nitric oxide do

A

nitric oxide binds with PGI2 to inactivate glycoproteins on platelets

590
Q

what factors are affected by heparin

A

XIIa,
XIa
Xa
IXa
IIa

591
Q

what does tpa do

A

converts plasminogen to plasmin which “eats” up fibrin

592
Q

what is byproduct of plasmin destroying fibrin

A

fibrinogen
d dimer

593
Q

what are the three steps to Na Reabsorption?

A
  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
Q

Na K atpase pump ratio

A

2 K in
3 Na out

595
Q

what symporter does loop diuretics work on

A

tri sympoter in thick ascending loop of henle
1 Na, 2 Cl, 1 K

596
Q

what symporter does thiazide work on

A

Na Cl symporter in early distal tubule

597
Q

important points on early distal tubule

A

-not permeable to water
-active reabsorption of Na, Cl, K, Mg
-contains macula densa
-5% of filtered load NaCl reabsorbed

598
Q

trace starting from thick ascending LOH

A

early distal tubule
late distal tubule
connecting tubule
collecting tubule
collecting duct

599
Q

where does ADH work

A

late/distal tubule and collecting tubule

600
Q

what do aldosterone antagonists work on

A

Na K atpase pump in late distal and cortical collecting tubules

601
Q

Na Channel blockers work on what

A

leaky Na channels in late distal/collecting tubules

602
Q

what pumps does angiotensin II work on

A

ATPase pump
Na Bicarb pump
Na hydrogen ion pump

603
Q

MOH of ADH in distal and collecting tubules

A
604
Q

how does parathyroid hormone increase Ca reabsorption

A

-increases Ca reabsorption in kidneys
-increases Ca reabsorption in gut
-decreases phosphate reabsorption
-increases intracellular Ca

A & P I (4 decks)

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