Block 2 Physiology

Front 1

hypernatremia

Back 1

elevated plasma Na+ (>150)

Front 2

hyponatremia

Back 2

reduced plasma Na+ (<135)

Front 3

hyperkalemia

Back 3

elevated plasma K+ (>5.0)

Front 4

hypokalemia

Back 4

reduced plasma K+ (<3.5)

Front 5

hypercalcemia

Back 5

elevated plasma Ca2+ (>10)

Front 6

hypocalcemia

Back 6

reduced plasma Ca2+ (<8)

Front 7

acidosis

Back 7

reduced plasma pH (<7.3)

Front 8

alkalosis

Back 8

elevated plasma pH (>7.5)

Front 9

edema

Back 9

excess fluid in the tissues; common causes: elevation in capillary hydrostatic pressure (elevated venous pressure, heart failure), drop in capillary oncotic pressure (cirrhosis of liver, nephrotic syndrome), or lymphatic blockade

Front 10

the central physiological role of the kidneys is to control the ____ and ______ of the body fluids

Back 10

volume
composition

Front 11

osmolarity

Back 11

the concentration of osmotically active particles in total solution and is expressed in terms of mOsm/liter of water; for substances that dissolve into two particles (NaCl), the osmolarity with be double or triple the molarity

Front 12

what is the average osmolarity of the ECF and ICF?

Back 12

280-300 mOsm/liter

Front 13

units for osmolality

Back 13

mOsm/kg of water

Front 14

osmosis

Back 14

the movement of H2O across a semi-permeable membrane d/t differences in osmolarity (an osmotic pressure gradient)

Front 15

tonicity

Back 15

the influence of the solution on the volume of a cell

Front 16

isotonic

Back 16

solutions which do not change cell volume

Front 17

hypertonic

Back 17

solutions that make cells shrink

Front 18

hypotonic

Back 18

solutions that make cells swell

Front 19

osmotic pressure (p)

Back 19

p = CRT (C-concentration, R-constant, T-temperature)
at 37 degrees, p = 19.3 x osmolarity (mOsm/L)

Front 20

what is the osmotic pressure of plasma?

Back 20

5443 mmHg

Front 21

what is the fundamental unit of the kidney?

Back 21

the nephron

Front 22

the nephron is composed of...?``

Back 22

(1) Bowman's Capsule (combines with the glomerular capillaries to form the glomerulus); (2) the Proximal Tubule; (3) the Loop of Henle (thin descending limb, thin ascending limb, and thick ascending limb); (4) the distal tubule (early distal tubule); (5) the connecting tubule (late distal tubule); (6) the collecting duct system (cortical, outer medullary, and inner medullary segments).

Front 23

what is the initial step in urine formation?

Back 23

bulk filtration in the glomerulus

Front 24

two types of nephrons

Back 24

cortical (superficial-90%)
juxtamedullary (deep-10%)

Front 25

juxtamedullary nephron structure

Back 25

long loops of Henle that extend into the inner medulla and also a thin ascending and descending limb

Front 26

renal blood flow to afferent arterioles

Back 26

abdominal aorta -> renal arteries -> large segmental arteries -> interlobular arteries -> arcuate arteries -> interlobular arterioles -> afferent arterioles (large resistance to blood flow)

Front 27

blood flow in superficial cortical nephrons

Back 27

second major resistance vessel (efferent arteriole) -> second capillary bed (peritubular capillaries) which surround tubular structures in the renal cortex -> venous system

Front 28

what is the hydrostatic pressure in peritubular capillaries?

Back 28

20 mmHg

Front 29

juxtamedullary nephron blood flow

Back 29

second major resistance vessel (efferent arteriole) -> second capillary bed (vasa recta capillaries) surround tubular structures in the renal MEDULLA -> venous system

Front 30

what is the function of the postglomerular peritubular capillaries and vasa recta capillaries?

Back 30

reabsorb fluid to ECF

Front 31

glomerular capillaries have HIGH or LOW hydrostatic pressure?

Back 31

high; favors glomerular ultrafiltration

Front 32

postglomerular capillaries have HIGH or LOW hydrostatic pressure?

Back 32

low; favors reabsorption

Front 33

what percentage of the filtered load is reabsorbed?

Back 33

99%

Front 34

how much plasma flows into the glomeruli in the kidneys of a normal 70kg man every minute?

Back 34

700 mL

Front 35

what are the three layers of the filtration barrier?

Back 35

(1) capillary wall (fenestrated, freely permeable to small molecules)
(2) basement membrane (porous matrix of extracellular proteins)
(3) podocytes (long finger-like processes with negatively charged proteins)

Front 36

what are two characteristics of the filtration barrier?

Back 36

size-selective (more permeable to small molecules)
charge-selective (more permeable to positively charged molecules)

Front 37

what happens to the glomerular filtration barrier in the absence of nephrin?

Back 37

the slit pore diaphragm is disrupted and the molecular lattice bridging the slit pore is altered -> excess albumin and protein are filtered -> albuminuria and proteinuria

Front 38

describe the filterability of substances in the glomerulus as they increase in size

Back 38

filterability declines

Front 39

compared to neutral compounds, the addition of positive charges _____ the filterability while the addition of negative charges _____ the filterability

Back 39

increases
decreases

Front 40

what two factors favor an increased GFR?

Back 40

(1) increased glomerular capillary filtration coefficient
(2) increased glomerular capillary hydrostatic pressure

Front 41

what two factors favor a decreased GFR?

Back 41

(1) increased glomerular capillary colloid osmotic pressure
(2) increased Bowman's capsule hydrostatic pressure

Front 42

filtration fraction (FF)

Back 42

(Glomerular Filtration Rate)/ (Renal Plasma Flow)

Front 43

what is inulin?

Back 43

a polysaccharide; exogenous substance that is freely filtered at the glomerulus but is not reabsorbed or secreted by the tubules

Front 44

GFR =

Back 44

(UF x Uin) / Pin
UF= urine flow
Uin= urine inulin concentration
Pin= plasma inulin concentration

Front 45

renal clearance definition

Back 45

the volume of plasma from which a substance has been removed and excreted into the urine per unit time

Front 46

clearance of substance (Cx) is calculated as:

Back 46

Cx = (UF x Ux) / Px

Front 47

why is clearance of creatinine used clinically rather than inulin?

Back 47

inulin must be administered intravenously until a steady plasma concentration is achieved; creatinine is a product of protein catabolism and is assumed to be produced at a constant rate

Front 48

when GFR is reduced by 50%, what happens to the excretion of creatinine and the plasma concentration of creatinine?

Back 48

excretion is reduced by 50%
plasma concentration doubles

Front 49

how effectively are creatinine and urea regulated as GFR is decreased?

Back 49

very poorly

Front 50

how effectively are bicarbonate, calcium and phosphate regulated when GFR is decreased?

Back 50

poorly

Front 51

how effectively are Na, K and H2O regulated as GFR is decreased?

Back 51

well-regulated

Front 52

renal clearance of PAH is an index of ____?

Back 52

renal plasma flow (filtered and secreted but not reabsorbed)

Front 53

Renal Blood Flow (RBF) =

Back 53

RPF / (1-Hct)

Front 54

what is normal renal plasma flow?

Back 54

650 ml/min

Front 55

what are the two mechanisms of autoregulation of GFR and RBF?

Back 55

(1) myogenic mechanisms
(2) tubuloglomerular feedback

Front 56

myogenic mechanisms

Back 56

stretch of vascular smooth muscle (increase in arterial pressure) elicits contraction which elevates vascular resistance and maintains GFR constant

Front 57

tubuloglomerular feedback

Back 57

elevation of perfusion pressure -> increased delivery of NaCl to the macula densa (adjacent to the afferent and efferent arterioles) -> increase in vascular resistance

Front 58

when are GFR and RBF elevated?

Back 58

when the body needs to excrete large amounts of fluid and solute

Front 59

when are GFR and RBF decreased?

Back 59

when the body needs to retain fluid and solute

Front 60

what hormones/autacoids increase GFR?

Back 60

endothelial-derived nitric oxide
prostaglandins (bradykinin)

Front 61

what hormones/autacoids decrease GFR?

Back 61

norepninephrine
epinephrine
endothelin

Front 62

how much of the filtered load is reabsorbed?

Back 62

99%

Front 63

what are the two pathways for filtered substances to be reabsorbed in the lumen?

Back 63

(1) paracellular (across tight junctions)
(2) transcellular (across the cells)

Front 64

on which side of the epithelial membrane is Na/K ATPase found?

Back 64

basolateral

Front 65

what substances are reabsorbed in the PT?

Back 65

67% H2O, Na+, K+
50% urea
85% bicarbonate
100% glucose, amino acids & proteins

Front 66

what are the three mechanisms for Na+ reabsorption in the PT?

Back 66

(1) Na/H+ exchanger
(2) co-transport with glucose or amino acids
(3) Na+/H+ exchanger coupled to an anion/Cl- exchanger (anion=formate, hydroxide, oxalate, sulfate)

Front 67

the TF/P ratio is decreased to the greatest extent for which two substances?

Back 67

glucose
amino acids
(almost 100% reabsorbed)

Front 68

at what point does glucose spill into the urine and why?

Back 68

at the transport maximum (when the filtered load exceeds the reabsorptive rate for glucose); the Na/glucose co-transporter is saturable

Front 69

what is secretion?

Back 69

the movement of solute from the interstitium into the tubular lumen

Front 70

what substances are permeable in the thin descending loop of Henle?

Back 70

H2O
limited permeability to solutes

Front 71

hemostasis

Back 71

physiological, healthy mechanism to stop blood loss and keep blood "liquid"

Front 72

thrombosis

Back 72

pathological formation of blood clots

Front 73

hemorrhage

Back 73

pathological bleeding, inability to form clots

Front 74

primary hemostasis

Back 74

initiated upon structural or functional damage to the vascular endothelium; primary response occurs within seconds, mediated by rapid adhesion, activation, and aggregation of blood platelets to the site of injury; does NOT involve enzymatic reactions

Front 75

secondary hemostasis

Back 75

a series of enzymatic processes in the blood, leading to conversion of soluble fibrinogen molecules into an insoluble, sticky fibrin "glue" stabilizing the platelet clot

Front 76

fibrinolysis

Back 76

the enzymatic degradation of fibrin; mediates the dissolution of fibrin-platelet clots

Front 77

what is the key enzyme of the fibrinolytic system and what does it cleave?

Back 77

the protease plasmin; cleaves insoluble fibrin fibrils into soluble fibrin degradation products

Front 78

where are platelets produced?

Back 78

bone marrow and spleen

Front 79

Glanzmann thrombasthenia

Back 79

defect in fibrinogen receptor GPIIb-IIIa complex (no aggregation of platelets with fibrinogen)

Front 80

von Willebrand disease

Back 80

defect in vWF

Front 81

Bernard-Soulier Syndrome

Back 81

defect in GP1b alpha (no binding of proteins to vWF)

Front 82

how is platelet function tested?

Back 82

aggregation test (platelets are incubated with agonists in a cuvette, and the ensuing shape change and aggregation alter the absorption pattern and scattering of a light beam directed through the cuvette)

Front 83

where are enzymatic coagulation factors secreted from?

Back 83

the liver

Front 84

how are enzymatic coagulation factors activated?

Back 84

produced as inactive precursors ("zymogens") and activation occurs by proteolytic cleavage

Front 85

what is the significance of vit K for clotting?

Back 85

it is a fat-soluble vitamin necessary for the gamma-carboxylation of specific clotting factors (factors II, VII, IX, X); they need to be gamma-carboxylated in order to bind calcium and assimilate

Front 86

warfarin (Coumadin)

Back 86

blocks vitamin K-epoxide reductase, the enzyme that regenerates the active form of vitamin K; results in less gamma-carboxylation (less formation of fibrin clots and longer bleeding time)

Front 87

what does factor VIII do?

Back 87

cross-links fibrin to form a stable clot

Front 88

what are the three stages of coagulation?

Back 88

initiation
amplification
termination

Front 89

initiation of coagulation

Back 89

contact of the membrane-anchored tissue factor molecule with coagulation factor VII circulating in the blood; TF-VII complex activates other factors that assemble on the surface of platelets into two enzyme complexes converting factor X to Xa and prothrombin to thrombin

Front 90

amplification

Back 90

thrombin can activate all the factors required for the assembly of the Xase and prothrombinase complexes

Front 91

termination (3 anticoagulant pathways)

Back 91

(1) antithrombin
(2) tissue factor pathway inhibitor (TFPI)
(3) protein C anticoagulant pathway

Front 92

antithrombin

Back 92

binds and inhibits factors II (thrombin) and X; activity is enhanced by heparin

Front 93

tissue factor pathway inhibitor

Back 93

inhibits formation of factor VII/tissue factor complex, as well as factor X

Front 94

protein c anticoagulant pathway

Back 94

thrombomodulin on endothelial cells change thrombin so that it only activates protein C, not fibrinogen; activated protein C inhibits factors V and VIII

Front 95

the fV Leiden mutation

Back 95

mutation in coagulation factor V that is the most common cause of a genetic predisposition for venous thrombosis in Caucasians

Front 96

hemophilia A

Back 96

deficiency in factor VIII

Front 97

hemophilia B

Back 97

deficiency in factor IX

Front 98

what are some ways edema can develop?

Back 98

(1) elevated vascular pressure (congestive heart failure)
(2) decreased plasma protein (nephrotic disease - lost in urine, liver disease - not enough albumin made)
(3) lymphatic block