App T3

Front 1

Angiotensin II is famous for?

Back 1

-vasoconstriction

Front 2

what is the primary glucocorticoid?

Back 2

cortisol

Front 3

what is a glucocorticoid that is also secreted and is about 1/3 as active as cortisol?

Back 3

corticosterone

Front 4

-helps a person resist stress

- plays an imp role in carb, prot, and fat metab

-exhibit sig permissive actions for other hormonal activities

Back 4

glucocorticoids (cortisol + corticosterone)

Front 5

mineralocorticoid helps you conserve?

Back 5

electrolytes, specifically Na+

Front 6

Dexamethasone has what kind of activity?

Back 6

glucocorticoid activity

Front 7

major factor for aldosterone release?

Back 7

angiotensin II

Front 8

control of glucocorticoid release?

Back 8

-stress and diurnal rhythyms stim hypo to relase CRH -> AP release ACTH -> adrenal cortex releases glucocorticoids

(negative feedback; glucocorticoids inhibit the hypothalamus and the anterior pituitary gland)

Front 9

clinical point of prolonged treatment w/ glucocorticoids?

Back 9

-anti-inflammatory doses of glucocorticoids inhibit ACTH release

-stopping treatments means pituitary gland can't produce normal ACTH for up to 1 month

- need to taper the withdrawal of glucocorticoids

Front 10

cortisol is bound to ?

Back 10

alpha globulin called transcortin

-only a small amount is free

- the free cortisol is what interacts with tissue

Front 11

what molecule starts cortisol?

Back 11

cholesterol

Front 12

half life of cortisol?

where is cortisol metabolized?

Back 12

60-90 mins

- it is metabolized in the liver

-rate of metabolism is decreased with kidney disease and stress (including surgery)

Front 13

the rate of metabolism of cortisol is decreased with?

Back 13

-kidney disease

-stress (including surgery)

Front 14

mechanism of action for glucocorticoids?

Back 14

steroid-receptor complex acts as TF to turn on seg of dna

-leads to appropriate mRNAs -> enzymes that alter cell function

Front 15

metab effects of glucocorticoids?

Back 15

-stim hep gluconeogenesis, which typically involves conversion of aa into carbs

-helps restore hepatic stores of glycogen

-liver releases stored glucose to help maintain blood glucose levels

-inhibit glucose use by different tissues (except brain)

Front 16

glucocorticoids will increase blood aa levels because?

Back 16

glucocorticoids stimulate protein degradation in tissues, esp muscle

-mobilized AAs are available to GN or to help repair dmg tissue, or synth of new cell structures

Front 17

permissive action of glucocorticoids

Back 17

-small amnts of glucocorticoids must be present for number of metab rxn to occur

-required for : glucagon and catecholamines to exert their calorigenic effects

-important for catecholamines to exert their lipolytic effects

- also small amts for cat to produce pressor responses and bronchodilation

Front 18

person lacking cortisol may go into circulatory shock in a stressful situation that demands immediate widespread vasoconstriction?

Back 18

example of the permissive action of glucocorticoids

; no norep to facilitate vasoconstriction

Front 19

benefits seen from glucocorticoids and why they may aid in resisting stress?

Back 19

increased pool of glucose, AAs, and FAs available

Front 20

long-term high levels of glucocorticoids?

Back 20

Cushing's Syndrome can occur

Front 21

in addition to being antiinflammatory, glucocorticoids are also anti?

Back 21

antiallergic

- they suppress manifestations of allergic disease that are due to release of histamine from tissues

Front 22

prolonged increase in plasma glucocorticoids can occur from?

Back 22

adrenal tumors, prolonged admin of exogenous glucocorticoids(dexamethasone), tumors in the anterior pituitary gland, or even tumors (usually in the lungs) that secrete ACTH

Front 23

symptoms of Cushing's syndrome?

Back 23

fat pads, moon face, red cheeks, pendulous abdomen, striae, bruisability with ecchymoses, thin skin, poor muscle development, and poor wound healing

Front 24

Cushing's syndrome symptoms?

Back 24

-pt. no protein b/c excess protein catabolism

- skin and subcutaneous tissues are therefore thin

- muscles are poorly developed

- wounds heal poorly

-minor injuries can easily cause bruising

-can develop type 2 DM because of resultant hyperglycemia

- can have mineralcorticoid effect (retention of Na+) from glucocorticoids (also contributes to moon face)

-sometimes pts. are also hypertensive

- glucocoritoid excess can lead to bone dissolution and osteaporosis

- may also produce increased appetite, insomnia, and mental symptoms

Front 25

morning vs evening ACTH and cortisol levels?

Back 25

higher in morining, lower in evening

Front 26

circadian rhythm and ACTH?

Back 26

-secreted in irregular bursts throughout the day

-most frequent during early morning

-75% of cortisol production occurs between 4 am and 10 am

-peaks are reversed for persons who work at night and sleep during the day

Front 27

hormones that exert masculinizing effects?

also promote protein anabolism and growth

Back 27

androgens

-testosterone is the most active androgen

Front 28

DHEAS (dehydroepiandrosterone sulfate)

Back 28

androgen that has less than 20% of testosterone activity

Front 29

peak of DHEAS (dehydroepiandrosterone sulfate) is during?

Back 29

during the early 20s for both sexes

Front 30

secretion of adrenal androgens is controlled by?

Back 30

ACTH,

NOT GONADOTROPINS

Front 31

long term changes of androgens is due to?

Back 31

changes in 17 alpha-hydroxylase, not to changes in ACTH secretion

Front 32

excess adrenal androgens in females?

Back 32

can result in some masculinizing

Front 33

important source of estrogens in men and postmenopausal women?

Back 33

adrenal androgen androstenedione is converted to testosterone and to estrogens in fat and other peripheral tissues

Front 34

steroid hormone formed from vitamin d in the liver and kidneys?

Back 34

1,25-Dihydroxycholecalciferol

-action is to increase calcium absorption in the intestines

Front 35

parathyroid hormone and calcium?

Back 35

parathyroid hormone mobilizes calcium from the bone and increases urinary phosphate excretion

Front 36

calcium-lowering hormone whose role is relatively minor?

Back 36

calcitonin

Front 37

Hydroxyapatite [(Ca3PO4)2]3Ca(OH)2 requires?

Back 37

Ca 2+ and phosphate

-important in bone formation

Front 38

what maintains voltage-gated sodium channels in the closed position?

Back 38

calcium

Front 39

most calcium is where and in what form?

Back 39

99% is in the skele and teeth

it is in a crystalline form

Front 40

what form of calcium is regulated?

Back 40

free calcium in the extra cellular fluid

Front 41

some calcium is where?

Back 41

complexed with phosphate, bound to plasma proteins, and some found intracellularly

Front 42

role of the free, ionized calcium:

Back 42

1. vital 2nd messenger

2. blood coagulation

3. vital for muscle contraction

4. necessary for proper nerve function

Front 43

results of hypocalcemia on nerves?

Back 43

overexcitability of nerves and muscles (problems such as spastic contractions of respiratory muscles)

-lower threshold for depolarization

Front 44

major results of low calcium?

Back 44

hypocalcmic tetany, especially of muscle extremities and the larynx

Front 45

laryngospasms?

Back 45

result of low calcium levels, can be so severe that airway is obstructed and fatal asphyxia is produced

Front 46

what can produce hypocalcemia?

Back 46

alkalosis

Front 47

hyperventilation due to anxiety can result in?

Back 47

alkalosis and therefore hypocalcemia symptoms

Front 48

hypocalcemia can results in what in the fingers, toes and mouth?

Back 48

numbness

Front 49

hypocalcemia can result in what of small muscles such as the hand and wrist?

Back 49

tetany

Front 50

hypercalcemia does what to neuromuscular activity?

Back 50

depresses.

hypercalcemia can cause cardia arrhythmias

makes harder to depolarize

Front 51

hypercalcemia does what to the threshold for membrane depolarization ?

Back 51

it increases it.

Front 52

primary structure of salts in bone?

Back 52

hydroxyapatite

Front 53

bone is?

Back 53

-living tissue that is well vascularized

- bone is able to constantly respond to stress and strains put upon it

- structure includes compact (cortical) bone and trabecular (spongy) bone?

Front 54

what are the two types of bone included in bone structure?

Back 54

compact (cortical) bone

and trabecular (spongy) bone

Front 55

two types of cells that live within the bone?

Back 55

osteoblasts

osteoclasts

Front 56

what cells are responsible for bone formation?

Back 56

osteoblasts

Front 57

what cells are modified fibroblasts?

Back 57

osteblasts

Front 58

which bone cells are responsible for bone resorption?

Back 58

osteoclasts

Front 59

which bone cells are members of the monocyte family?

Back 59

osteoclasts

Front 60

strength of bone comes primarily from inside or outside?

Back 60

outside

Front 61

area sealed off by the cell, acidified by what?, then dissolving what and breakingdown what?

Back 61

osteoclast

acidified by proton pumps

hyroxyapatite and breaking down of collagen

Front 62

calcium turnover in bone in infants vs adults?

Back 62

100% per year in infants vs 18% per year in adults

Front 63

bone formation and reabsorption are equally matches except?

Back 63

during first 20 years and last 20 years

Front 64

osteoporosis is underlying cause of 1.2m fractions/year

1/2m are what kind of fractures?

1/4m are what kind of fractures?

Back 64

1/2m are vertebral fractures

-1/4m are hip fractures

Front 65

what kind of replacement has been one method to help their susceptibility to osteoporosis?

Back 65

estorogen replacement

Front 66

ways to avoid osteoporosis in women?

Back 66

estrogen replacement

- weight bearing exercise

- developing strong bones before menopause with calcium rich diets and adequate exercise

Front 67

where is vit d produced?

Back 67

skin

Front 68

vit d is converted in the liver to ?

Back 68

25-hyrdoxycholecalciferol

Front 69

25-hydroxycholecalciferol is converted in kidney to? which does what to absorption in intestine?

Back 69

1,25-dihydroxycholecalciferol.

this increases intestine absorption of Ca2+ and PO43-)

Front 70

The active transport of Ca2+ and PO43- from the intestine in increased by a metabolite of Vitamin D.

what is the metabolite?

Back 70

1,25-dihyrdoxycholecalciferol

Front 71

vitamin d is conerted to 25-hydroxycholecalciferol in what organ?

Back 71

liver

Front 72

1,25 dihydroxycholecalciferol is a steroid and binding results in activation of a DNA-binding region -> inc mRNA and these mRNA dictate?

Back 72

formation of calbindin-D proteins

Front 73

what two proteins are correlated with increased Ca2+ transport?

Back 73

calbindin-D9K and calbindin-D28K

1,25 dihydroxycholecalciferol -> mRNA transcription -> calbindin-D proteins

Front 74

regulation of 1,25 dihydroxycholecalciferol?

Back 74

feedback reg by plasma ca2+ and pO4 3-

when these are high, LOW 1,25 dihydroxycholecalciferol is produced in kidneys

Front 75

calcification of bone matrix due to vit d deficiency?

in children?

in adults?

Back 75

in children this is called Rickets

in adults this is called osteomalacia

(result is failure to have adequate amounts of ca2+ and phosphate to sites of mineralization)

Front 76

rickets in children?

Back 76

1. weakness and bowing of weight-bearing bones

2. dental defects

3. hypocalcemia (tetany)

Front 77

parathyroid hormone release is stimulated by?

Back 77

low levels of free calcium in the plasma

Front 78

calcium homeostasis:

low plas ca2+ -> release of parathyroid hormone secretion -> inc plasma parathyroid -> acts on bone to increase Ca resorption -> inc release of calcium into plasma

inc plas parathyroid -> (kidney) inc ca2+ and inc 1,25(oh)2D formation which ultimately?

Back 78

decreases urinary excretion of calcium and also inc plasma 1,25 (oh)2d increases calcium absorption in the intestine

Front 79

the parathyroid glands are located?

Back 79

on the posterior surface of the thyroid gland

Front 80

half-life or parathyroid is approx?

Back 80

10 mins (this hormone has 84 aa residues)

Front 81

where is parathyroid broken down?

Back 81

cleaved by cells in liver and fragments and parathryoid hormone are cleared by the kidneys

Front 82

what hormone acts directly on bone to increase bone resroption and mobilize Ca2+?

Back 82

parathyroid hormone

Front 83

what decreases plas phosphat elevels and increases phophate excretion in urine?

Back 83

parathyroid hormone

Front 84

when ca2+ high?

Back 84

pth inhibited, ca2+ is deposited in the bones

Front 85

tetany from parathyroidectormy?

Back 85

hypocalcemic tetany

Front 86

common metabolic complication of cacner?

Back 86

hypercalcemia

Front 87

hormone that inhibits bone resorption by inhibiting osteoclasts?

Back 87

calcitonin

Front 88

where is calcitonin produced?

Back 88

parafollicular cells in the thyroid glands

Front 89

two function of gonads?

Back 89

1. gametogenesis

2. secretion of sex hormones

Front 90

adrenal cortex produces? which are sometimes converted into what in fat and other tissues?

Back 90

androgens, which are converted to estrogens

Front 91

meiosis vs mitosis

Back 91

meiosis - end up w/ 1/2 chromosome

Front 92

in what week does the embryo have both male and female primordial genital ducts?

Back 92

seventh week of gestation

Front 93

the external genitalia are bipotential until what week?

Back 93

external genitalia are bipotential until the 8th week

Front 94

testosterone (leydig) and mullerian inhibiting substance (sertoli) cause?

Back 94

male development to occur

Front 95

what causes a female system to develop?

Back 95

lack of testosterone (leydig) and MIS (sertoli)

Front 96

during pubery what is activated from the anterior pituitary?

Back 96

gonadotropins are activated from the anterior pituitary to bring about the final maturation of the reproductive system

Front 97

during puberty which gonadotropins increase?

Back 97

FSH + LH both trigger maturation of sex hormones

Front 98

secretion of adrenal androgens, when?

Back 98

near time of puberty.

8-10 in girls

10-12 in boys

Front 99

secretion of adrenal androgens is controlled by what?

Back 99

ACTH

NOT gonadotropins**

Front 100

long term changes of androgens is due to changes in?

Back 100

17 alpha-hydroxylase,

not to changes in ACTH secretion

Front 101

DHT binding vs testosterone?

Back 101

DHT is a more stable receptor-steroid complex

Front 102

where is testosterone produced?

Back 102

in the Leydig cells of the testes

Front 103

abundance of DHT vs testosterone?

Back 103

-there is about 10% as much DHT in the plasma as compared to testosterone

Front 104

what is necessary for sexual maturity at puberty?

Back 104

DHT

Front 105

DHT and effects on action of testosterone?

Back 105

DHT amplifies the action of testosterone in the tissue

Front 106

5 alpha-reducatase catalyzes?

Back 106

converstion of test -> DHT

Front 107

LH -> testis -> test -> 5alpha-reducatase in target cell -> DHT ->

Back 107

gonadotropin reg

spermatogenesis

sex differentiation (wolffian stim, external virilization)

sex maturation at puberty

Front 108

note these male reproductive system structures:

Back 108

1. testis

2. seminiferous tubules

3. epididymis

4. vas deferens

5. prostate gland

6. seminal vesicle

7. Urethra

Front 109

testes are made up of loops of?

Back 109

seminiferous tubules

Front 110

walls of seminiferous tubules contain?

Back 110

sertoli and primitive germ cells

Front 111

between tubules in testes?

Back 111

insterstitial cells (cells of Leydig)

these secrete test

Front 112

sertoli cells secrete:

Back 112

1. androgen-binding protein (keeps androgen levels high)

2. Inhibin (will inhibit FSH secretion)

3. MIS ( for emb dev)

4. Sertoli cells contains aromatase which converts androgens to estrogens

Front 113

what contains aromatase and what is its function?

Back 113

sertoli cells

aromatase converts andro to estro

Front 114

what matures into primary spermatocytes?

Back 114

spermatogonium

Front 115

primary spermatocytes go through meiosis to become?

Back 115

spermatids, which have the haploid number of 23 chromosomes

Front 116

spermatids associate with what cell to mature into?

Back 116

the spermatids associate with the Sertoli cell to mature to spermatozoa

(which are then released into the lumen of the seminiferous tubules)

Front 117

1 spermatogonium will produce how many spermatids?

Back 117

512

Front 118

temp of the testes is normally ?

Back 118

32 C or 89.6 F

Front 119

what adds fructose and prostaglandins and accoutns for about 60% of the volume of semen?

Back 119

seminal vesicles

Front 120

what adds 20% of the volume and what does it secrete to neutralize acidic vaginal secretion?

Back 120

prostate gland adds 20% of the volume. It secretes and alkaline fluid

Front 121

serine protease that is secreted into the semen?

significance of plasma PSA levels?

Back 121

prostate-specific androgen

-hydrolyzes sperm motility inhibitor

(semenogelin)

-elevated plasma PSA occurs w/ prostate cancer

Front 122

what hormone acts on Leydig cells to reg testosterone secretion?

Back 122

L-L

Luteinizing hormone (LH)

Front 123

FSH acts on what part? and what specific part of that part?

Back 123

seminiferous tubules, specifically Sertoli cells to enhance spermatogenesis

Front 124

LH an FSH are stimulated by ?

Back 124

GnRH from the hypothalamus

Front 125

inhibin B acts where?

Back 125

at the anterior pituitary

Front 126

testosterone positively influences?

Back 126

sertoli cells and spermatogensis

Front 127

test inhibits release of?

Back 127

LH and GnRH

Front 128

inhibin b inhibits?

Back 128

FSH

inhibin secreted by Sertoli

Front 129

primorial follicles formed during?

how many @ time of birth?

Back 129

-formed during fetal dev, no more formed after birth

-normal primordial follicles = 1 million @ time of birth

Front 130

ova undergo first meiotic division and are arrested in what phase until adulthood?

Back 130

prophase

Front 131

# primordial follicles @ puberty?

Back 131

< 300k

Front 132

start of ovarian cycle?

(4)

Back 132

-several primordial follicles enlarge

-cavity forms around each ovum and is filled w/ follicular fluid

-one grows rapidly around day 6

-one wins and the others regress, turning into atretic follicles

Front 133

winning follicle ->

Back 133

theca interna of follicle is primary source of circulating estrogens

- at 14 days distended follicle ruptures and ovum goes into abdominal cavity to be picked up by fimbria

-ovum release is ovulation

Front 134

what picks up the ovum in the abdominal cavity?

Back 134

fimbria

Front 135

follicle ruptures and changes proliferation of granulosa and theca cells occurs forming what?

this initiates ?

now luteal cells

Back 135

-corppus leteum

-luteal phase of menstrual cycle

-secrete estrogens and progesterone

Front 136

purpose of corpus luteum?

Back 136

secrete abundant progest and lesser amounts of estro into blood

Front 137

corpus luteum becomes functional when?

Back 137

4 days after ovulation

Front 138

wall of uterus is called?

Back 138

endometrium

Front 139

where will fertilized egg (blasocyst) implant and form placenta?

Back 139

endometrium

Front 140

when fert has not occured, endometrium goes through cycles of?

Back 140

-menstrual phase

-proliferative phase

-secretory phase

Front 141

proliferative phase and endometrium?

what days?

Back 141

- thickness of endometrium grows

-typically from days 5-14

Front 142

proliferative phase changes to secretory phase (uterine phases) upon?

Back 142

egg implant

Front 143

before ovulation hormone?

after ovulation?

Back 143

-estrogen

-estrogen AND progesterone (in secretory phase of uterine cycle)

Front 144

secretory phase, progest acts on endometrium?

Back 144

thickened, estrogen-primed endometrium conversion to richly vascularized, glycogen-filled tissue

Front 145

secretory phase occurs from days?

Back 145

14-28

Front 146

corpus luteum regress hormonal support for endometrium is withdrawn and what happens?

Back 146

-endometrium becomes thinner and the endometrium will shed (menstrual phase)

Front 147

usually duration of menstrual flow?

Back 147

3-5 days

Front 148

ovarian cycle:

Back 148

1. dev of follicle

2. release of estrogen by theca interna and granulosa cells of follicle

3. ovulation (day14)

4. formation of corpus luteum

5. release of estrogen and progesterone

Front 149

the uterus is lined by a cell layer called?

Back 149

the endometrium (where blastocyst (egg) ) implants and forms the placenta

Front 150

shift from proliferative to secretory phase in uterine cycle?

Back 150

day 14 (ovulation)

Front 151

time between fertilization and implantation:

Back 151

7 days: so about day 22 in secretory phase is when implantation can occur

Front 152

during secretory phase of the uterine cycle, what is the function of progesterone?

Back 152

converts thickened, estrogen-primed endometrium into a richly vascularized, glycogen-filled tissue

Front 153

secretory phase occurs from what days?

Back 153

14-28 days (relatively constant in length)

Front 154

secretory phase of uterine cycle is what part of the ovarian phase?

Back 154

secretory phase of uterine = luteal phase of ovarian cycle

Front 155

what triggers LH surge @ day 9?

Back 155

constant increase in estrogen

Front 156

what does the LH surge cause?

Back 156

ovulation

Front 157

what inhibits LH and FSH?

Back 157

progesterone from the corpus lutuem

Front 158

why corpus luteum has a limited life span?

Back 158

no LH bc it inhibits it via progesterone

Front 159

what triggers the beginning of the cycyle?

Back 159

increase of LH and FSH

Front 160

what stimulates proliferation of the granulosa cells of the follicle?

Back 160

FSH and estrogen

Front 161

LH acts on the theca interna cells to?

Back 161

produce androgens, then FSH acts on granulosa cells to convert androgens to estrogen

Front 162

what are the three naturally occurring estrogens?

Back 162

1. 17 beta-estradiol

2. estrone

3. estriol

Front 163

LH stims theca interna to produce?

Back 163

androgens

Front 164

FSH stims granulosa cells to convert androgens from where into what?

Back 164

from LH-stim'd theca interna cells

converts those androgens into estrogens

Front 165

LH receptors in ?

Back 165

theca interna cell

granulosa cells (also has FSH receptors)

Front 166

what has LH AND FSH receptors?

Back 166

granulosa cells

Front 167

what produces inhibin B?

Back 167

granulosa cells

this inhibits FSH

Front 168

inhibitor of FSH?

Back 168

inhibin B from granulos cells

Front 169

estrogen inhibits?

Back 169

LH and GnRH

Front 170

what stims both LH and FSH?

Back 170

GnRH

Front 171

how early can hCG be detected in the blood?

Back 171

as early as 6 days after conception

Front 172

how early can hCG be detected in the urine?

Back 172

as early as 14 days after conception

Front 173

how much cardiac output does the kidney receive?

Back 173

about 20-25% of the cardiac output

it is only 0.5% of the total body mass

Front 174

what hormone control Na reabsorption in the body?

Back 174

aldosterone

Front 175

where is aldosterone formed?

Back 175

adrenal cortex

Front 176

how much urine is voided per day?

Back 176

about 1 L of urine is voided per day

Front 177

how much fluid gets filtered across the glomeruli per day?

Back 177

180 L of fluid

Front 178

how many mmol of glucose is filtered?

how many mmol of glucose is excreted?

Back 178

800 mmol of glucose filtered/day

0 mmol of glucose excreted/day

Front 179

meq Na filtered into renal tubules each day?

excreted?

Back 179

26000 meq Na+ filtered in to renal tubules each day

only 150 meq goes out in urine each day

Front 180

-formation of a plasma filtrate, free of protein, which enters the proximal tubule

Back 180

glomerular filtration

Front 181

t-transfer of desirable water and solutes from the tubular fluid to the renal tubule cells ( and hence back into the blood stream )

Back 181

tubular reabsorption

Front 182

-secretion of solutes from the renal tubules into the tubular fluid

Back 182

tubular secretion

Front 183

first part of proximal tubule vs latter portion of proximal tubule?

Back 183

first part: sodium reabsorbed mostly by co-transport w/ glucose and amino acids

latter part: sodium is reabsorbed mostly by diffusion through sodium channels

Front 184

sodium is co-transported w/ K+ and Cl- where?

Back 184

in the ascending loop of Henle

Front 185

why does a diabetic have higher urine output than normal?

Back 185

osmotic pressure from glucose pulls water into the urine

Front 186

PAH (para-aminohippuric acid) ?

Back 186

tubular secretion is demonstrated by PAH

Front 187

the secretion of K+ is regulated by?

Back 187

aldosterone; takes sodium out of tubule, and helps set it up so potassium goes into the tubule

Front 188

what is secreted into the proximal tubule, distal tubule, and collecting duct ?

Back 188

hydrogen ions

-this is an important mechanism in the acid-base balance

Front 189

what monitors the Na+ and Cl- levels in the tubular fluid?

Back 189

juxtaglomerular apparatus

-thus GFR can be controlled through autoregulation

-feedback mechanism can occur within a few seconds

Front 190

distal proximal tubule goes through what ?

Back 190

the juxtaglomerular apparatus

Front 191

macula densa cells:

Back 191

senses what goes on inside renal tubule (Na)

Front 192

GFR and fluid velocity?

Back 192

more glomerular filtration rate = more fluid velocity

(thus less time to pull out sodium from tubular fluid)

Front 193

more sodium absorbed by macula densa cells?

Back 193

inc na/k pump activity, more adenosine forms, more adenosine increases calcium released by macular densa cells and smooth muscle contraction occurs in afferent arterioles -> decrease GFR

Front 194

proximal convuluted tubule and water?

Back 194

permeable to water

water reabsorption is automatic

watter passively follows osmotic gradient set up by active transport of sodium

Front 195

in proximal tubule, how much water is reabsorbed?

Back 195

65% of water is already absorbed

Front 196

descending loop of henle and water?

Back 196

permeable to water, but no sodium reabsorb

Front 197

ascending loop and water?

Back 197

impermeable to water, but Na reabsorb

Front 198

sodium level in plasma?

Back 198

300 mosm/kg

Front 199

in Henle how much water is removed?

Back 199

about 15% of total water

Front 200

osmolality at bottom of loop of henle?

Back 200

1200

Front 201

adh (vasopressin) and collecting duct?

Back 201

more aquaporins -> more water reabsorption

Front 202

loop of Henle establishes a concentration gradient

Back 202

important for collecting duct

Front 203

Primary site for regulation of the amount of water and sodium that go out in the urine.

Back 203

collecting ducts

Front 204

Distal convoluted tubule:

Back 204

impermeable to water, also reabsorbs sodium (5% water absorbed here)

Front 205

aldoesterone turns on pumps AND?

Back 205

it activated na/k pumps, but it also opens up new sodium channels

Front 206

dilute urine and vasopressin levels?

Back 206

low vasopressin leads to higher urine volume (dilute urine)

Front 207

what inhibits the release of vasopressin

Back 207

alcohol

Front 208

factors that influence vasopressin secretion

Back 208

1. increased osmotic pressure of plasma

2. decreased ecf volume

3. pain, emotion, "stress", exercise

4. nausea and vomiting

5. standing

6. clofibrate, carbamazepine

7. angiotensin II

Front 209

vasopressin secretion decreased

Back 209

1. decreased effective osmotic pressure of plasma

2. increased ECF volume

3. alcohol

Front 210

two drugs that increase vasopressin secretion?

Back 210

clofibrate and carbamazepine

Front 211

normal gfr?

Back 211

125 ml/min

Front 212

what catalyzes carbonic acid formation?

Back 212

carbonic acid formation is catalyzed by carbonic anhydrase

Front 213

what has the ability to acidify the urine?

Back 213

the kidneys have the ability to acidify the urine

Front 214

hyperventilation =

Back 214

less co2 and shifts the equilibrium towards carbonic acid, thus acidifying the blood in the process

Front 215

reabsorption of bicarbonate ion: 1 of 3 principle mechanisms for acidification of the urine

Back 215

-occurs primarily in proximal tubule

-

Front 216

formation of monobasic phosphate happens mostly in?

Back 216

distal tubule and collecting ducts

Front 217

what is formed in the cells of the proximal and distal convoluted tubules?

Back 217

ammonia

glutamine to glutamine is the principle reaction forming ammonium (NH4)

Front 218

two enzymes that convert glutamine into product and NH4+

Back 218

glutaminase and glutamic dehydrogenase

Front 219

regulation of sodium primarily occurs?

Back 219

in the collecting ducts via aldosterone

Front 220

what is amiloride?

Back 220

a diuretic, it functions by inhibiting the epithelial sodium channel

Front 221

Ouabain function?

Back 221

inhibits sodium/potassium pump, which means sodium stays in renal tubule fluid

Front 222

stimuli for aldosterone:

Back 222

1. low Na+ (turn on renin-angiotensin-aldosterone system)

(renin comes out of juxtaglomerular apparatus)

2. increased plasma K+ levels directly stimulate aldosterone (from adrenal cortex) which simulates aldosterone

3. ACTH (adrenocorticotropoic hormone) acutely increases aldosterone production

Front 223

atrial natriuretic peptide

Back 223

1. released by cells in atria in response to increased volume

2. inhibits renin and therefore aldosterone

3. which therefore inhibits sodium channels in the collecting duct

4. end result is more sodium excreted in urine

Front 224

K extra cellular = 5.5 mmol/l and intracellular =?

Back 224

150mmol/l

Front 225

hyperkalemia ->

Back 225

arrhythmias and low levels cna produce muscle weakness, decreased glucose tolerance and arrhythmias

Front 226

where is K+ reabsorbed?

Back 226

proximal tuble and in henle

Front 227

where is potassium secreted?

Back 227

in distal tubule and in collecting duct

Front 228

aldosterone controls amount of what secreted in the colelcting duct?

Back 228

K+ ; via activity of the sodium/potassium pumps in the colelcting duct, and this increases the number of epithelial sodium channels

Front 229

turning on renin-angiotensin aldosterone system?

Back 229

1. conserve water

2. increase wate retention/volume

3. increase blood pressure

Front 230

increase in blood pressure then renin?

Back 230

decreases, so no reabsorption of sodium

Front 231

what triggers the activation of renin?

Back 231

low sodium

-renin helps to release aldosterone (which attempts to save sodium)

Front 232

low gfr

Back 232

low blood volume or low blood pressure

Front 233

how anp reduce blood volume?

Back 233

inhibits release of renin

Front 234

renal failure

Back 234

metabolic acidosis- results in altered enzyme activity bc too much aicd

will depress cns (interfereing with neuronal excitability)

potassium retention (hyperkalemia)

-altered cardia and neural activity because of changing resting membrane potential

uremic toxicity

Front 235

ramifications of sodium imbalance

Back 235

-high sodium -> elevated bp, generalized edema, congestive heart disease if too much sodium

-hypotension and possible circulatory shock if too little sodium is consumed

Front 236

ramifications of loss of plasma proteins because of leakiness ofglomeruli

Back 236

-edema caused by a reduction in plasma-colloid osmotic pressure

Front 237

-refers to acute decline in GFR

-includes increasei n bloodurea nitrogen and serum creatinine

-frequent complication of hypotensive shock

Back 237

acute renal failure

Front 238

-refers to end-stage renal disease

- characterized by servere and chorinically elevated levels of BUN

-characterized by marked sclerosis of both glomeruli and intersitium and by tubular atrophy

Back 238

chronic renal failure

Front 239

one of the most common causes of chronic renal failure

Back 239

chronic glomerulonephritis

Front 240

disease which have secondary effects on glomerulus?

Back 240

1. diabetes mellitus

2. systemic lupus erythematosus

3. hypertension

4. amyloidosis

Front 241

noninflammatory glomerulupathies?

Back 241

nephrosis (nephrotic syndrome)

Front 242

inflammatory glomerular diseases?

Back 242

nephritic (nephritis)

Front 243

major chars of nephrosis (noninflammatory glomerulupathies)

Back 243

1. heavy proteinuria

2. hypoproteinemis (esp. hypoalbuminemia)

3. peripheral edema

4. hyperlipidemia and lipiduria

Front 244

initial event in nephrosis?

Back 244

derangement in glomerular capillary walls resulting in increased permeability to plasma protein

massive proteinuria results

largest proportion of protein lost in he urine is albumin

fluid escapes into tissue because of decreased plasma oncotic pressure

Front 245

major causes of syndrome in adults?

Back 245

1. membranous nephropathy (30%)

2. glomerulopatheis associated with systemic diseases

Front 246

major causes of nephrotic syndrome in children

Back 246

1. epithelial cell (minimal change) disease (70%)

Front 247

characterized by diffuse thickening of the glomerular capillary wall and accumulation of immunoglobulin-containing deposits along basement membrane

form of chronic immun complex-mediated disease

Back 247

membranous nephropathy

Front 248

major nephrotic syndrome:`

Back 248

association w/ other systemic disease of with various drugs

(drugs including penicillamine, captopril, gold, nonsteroidal anti-inflammatory drugs

underlying malignant tumars

and lupus

Front 249

diabetic microangiopathy involves hyaline arteriolosclerosis (hyaline thickening of the vessel walls narrowing the lumun) of both the afferent and efferent arterioles?

Back 249

diabetic glomerulusclerosis

-leading cuase of end-stage renal disease in the US

Front 250

epithelial cell disease

Back 250

* largely a disorder in children

* alteration in podocytes (forms slits in glomerulus)

* responds well to corticosteroids and the changes are reversible during remission

Front 251

nephritis (inflammatory glomerular diseases) are characterized by:

Back 251

-hematuria

-proteinuria

-oliguria

-dereased GFR (elevated BUN and serum creatinine )

Front 252

circulating immune complex nephritis:

Back 252

*glomerular trapping of circulating antigen/antibody complexes

* aggregates of these can penetrate glomerulus and become trapped in subepithelial location

*htne neutrophils attracted

Front 253

acute postinfectious glomerulonephritis

Back 253

-sudden onset of nephritic syndrome

- sequel to infection (commonly from streptococci)

- most commonly affect children

(streptococci can affect the valves of the heart)

Front 254

primary infection in acute postinfectious glomerulonephritis?

Back 254

in pharynx

begins w/ oliguria, hematuria, facial edema, and hypertension

Front 255

systemic lupus erythematosus

Back 255

70 percent of patients w/ SLE will develop clinically significant renal disease

about 15% develop membranous glomerulopathy

trapping of immune complexes -> renal damage

renal failure = cause of death in 1/3 of patients

Front 256

percent water of :

plasma

soft tissues (muscle, skin, organs)

bone

fat

Back 256

plasma is more than 90% water

soft tissues are 70-80% water

bone is 22% water

Fat is only 10 % water

Front 257

only body fluid which can be directly altered or regulated?

how is it altered?

Back 257

plasma (20% of 1/3) is filtered by the kidney

Front 258

what is controling factor for fluid shifts between interstitial fluid and intracellular ?

Back 258

sodium/potassium pump

cell would not be able to export sodium if na/k pump stopped working?

Front 259

alkalosis?

Back 259

causes convulsions and overexcitability of CNS (may seem like extreme nervousness)

Front 260

hypoventilation results in?

Back 260

acidosis

Front 261

hyperventilation results in?

Back 261

respiratory alkalosis

Front 262

carbonic anhydrase

Back 262

-high levels found in renal cells

-converts co2 and h2o to h2co3

Front 263

lymphatic circulation route?

Back 263

capillaries/ecf/lyphatic vessels/thoracic duct/ veins

Front 264

lyphatic system starts where?

Back 264

in the capillary bed

they run parallel to the blood vessels

Front 265

thoracic duct of lymph system empties into?

Back 265

the subclavian vein

Front 266

blood volume is what percent of body wt?

what percent of that blood volume is plasma?

Back 266

blood volume is about 8% of body weight

plasma is 55% of blood volume (other part is cellular elements )

Front 267

active in production of cells

in almost all bones in children (also in extramedullar sites)

adults: usually in vertebrae, sternum, and some long bones

has pluripotent stem cells and progenitor cells

Back 267

red marrow

Front 268

inactive form of marrow

color due to lipid storage

can be reactivated if needed for cell production

Back 268

yellow marrow

Front 269

three types of granulocytes?

Back 269

Basophils - resemble mast cells; contain heparin/hestiamin; allergic rxns

Neutrophils - nonspecific phagocytes

Eosinophils - not esp phago, involved in allergies/parasitic disease

Front 270

most abundant granulocyte?

Back 270

neutrophils -nonspecific phagocytes

Front 271

types of agranulocytes:

Back 271

lymphocytes (B+T)

monocytes - differentiate into macrophages

Front 272

what cells contain heparin/histamine?

Back 272

basophil (type of granulocyte, which is a type of wbc)

resemble mast cells and involved in allergic rxns

also eosinophils are involved in allergies/parasitic disease

Front 273

most abundant type of agranulocyte:

Back 273

lymphocytes (B+T)

Front 274

megakaryocyte will form?

Back 274

platelets

Front 275

half life of this granulocyte is 6 hours

100 billion per da

enter tissues when triggered by infection of inflammatory cytokines

non-specific phagocytes

Back 275

neutrophils

Front 276

how do neutrophils cain access to pint of inflammation in either superficial tissue or deeper tissue?

Back 276

chemotaxis and diapedesis

Front 277

after neutrophil phagocytosis then?

Back 277

degranulation and respiratory burst

Front 278

neutrophils discharge this enzyme that catalyzes the conversion of cl-,br-,i-, and scn- to acids.

Back 278

myeloperoxidase

Front 279

associated w/ sharp increase in O2 uptake and metabolism in neutrophil (respiratory burst) and generation of O2-

Back 279

NADPH oxidase

Front 280

O2- + 2H+ -> h2o2 catalyzed by?

Back 280

cytoplasmic form of SOD-1

cytoplasmic form of superoxide dismutase

Front 281

kiling zone in neutrophils formed from?

Back 281

elastase, o2-, h2o2, and hocl

neutrophils contain elastase and metalloproteinases

Front 282

enter blood from bonemarrow, circulate for 72 hours then enter tissue where they live for 3 months. they then differentiate into?

Back 282

monocytes differentiate into macrophages.

Front 283

wandering cells found esp. in connective tissue and underlying epithelial surfaces

contain histamin, heparin and proteases

participate in allergic rxns and parasite rxns

Back 283

mast cells

Front 284

rbc is regulated by?

Back 284

erythropoietin (kidney + Kupffer cells of liver)

Front 285

secreted hormonal factor (from wbcs) if aa sequence is known

Back 285

interleukins (IL)

Front 286

secreted hormonal factor (from wbcs) if aa sequence is unknown

Back 286

cytokines or lymphokines

Front 287

develop from population in thymus

Back 287

lymphocytes

Front 288

large lymphocytes

imp in cancer and viral infections (these and monocytes are responsible for innate immunity

Back 288

natural killer cells (NK)

1 of 3 population of lymphocyte

Front 289

consists of a series of proenzymes circulating in plasma. Activation of the system ("fixing complement") leads to several effects, including lysis of lipid membranes, release of histamine, chemotaxis, opsonization.

Back 289

the complement system

Front 290

active/acquired immunity mechanisms are mediated by?

Back 290

B+T lymphocytes

divided into 2 systems: humoral and cellular; specific antibodies and cytokine directed (cell-on-cell)