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98 Cards in this Set

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hypernatremia
elevated plasma Na+ (>150)
hyponatremia
reduced plasma Na+ (<135)
hyperkalemia
elevated plasma K+ (>5.0)
hypokalemia
reduced plasma K+ (<3.5)
hypercalcemia
elevated plasma Ca2+ (>10)
hypocalcemia
reduced plasma Ca2+ (<8)
acidosis
reduced plasma pH (<7.3)
alkalosis
elevated plasma pH (>7.5)
edema
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
the central physiological role of the kidneys is to control the ____ and ______ of the body fluids
volume
composition
osmolarity
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
what is the average osmolarity of the ECF and ICF?
280-300 mOsm/liter
units for osmolality
mOsm/kg of water
osmosis
the movement of H2O across a semi-permeable membrane d/t differences in osmolarity (an osmotic pressure gradient)
tonicity
the influence of the solution on the volume of a cell
isotonic
solutions which do not change cell volume
hypertonic
solutions that make cells shrink
hypotonic
solutions that make cells swell
osmotic pressure (p)
p = CRT (C-concentration, R-constant, T-temperature)
at 37 degrees, p = 19.3 x osmolarity (mOsm/L)
what is the osmotic pressure of plasma?
5443 mmHg
what is the fundamental unit of the kidney?
the nephron
the nephron is composed of...?``
(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).
what is the initial step in urine formation?
bulk filtration in the glomerulus
two types of nephrons
cortical (superficial-90%)
juxtamedullary (deep-10%)
juxtamedullary nephron structure
long loops of Henle that extend into the inner medulla and also a thin ascending and descending limb
renal blood flow to afferent arterioles
abdominal aorta -> renal arteries -> large segmental arteries -> interlobular arteries -> arcuate arteries -> interlobular arterioles -> afferent arterioles (large resistance to blood flow)
blood flow in superficial cortical nephrons
second major resistance vessel (efferent arteriole) -> second capillary bed (peritubular capillaries) which surround tubular structures in the renal cortex -> venous system
what is the hydrostatic pressure in peritubular capillaries?
20 mmHg
juxtamedullary nephron blood flow
second major resistance vessel (efferent arteriole) -> second capillary bed (vasa recta capillaries) surround tubular structures in the renal MEDULLA -> venous system
what is the function of the postglomerular peritubular capillaries and vasa recta capillaries?
reabsorb fluid to ECF
glomerular capillaries have HIGH or LOW hydrostatic pressure?
high; favors glomerular ultrafiltration
postglomerular capillaries have HIGH or LOW hydrostatic pressure?
low; favors reabsorption
what percentage of the filtered load is reabsorbed?
99%
how much plasma flows into the glomeruli in the kidneys of a normal 70kg man every minute?
700 mL
what are the three layers of the filtration barrier?
(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)
what are two characteristics of the filtration barrier?
size-selective (more permeable to small molecules)
charge-selective (more permeable to positively charged molecules)
what happens to the glomerular filtration barrier in the absence of nephrin?
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
describe the filterability of substances in the glomerulus as they increase in size
filterability declines
compared to neutral compounds, the addition of positive charges _____ the filterability while the addition of negative charges _____ the filterability
increases
decreases
what two factors favor an increased GFR?
(1) increased glomerular capillary filtration coefficient
(2) increased glomerular capillary hydrostatic pressure
what two factors favor a decreased GFR?
(1) increased glomerular capillary colloid osmotic pressure
(2) increased Bowman's capsule hydrostatic pressure
filtration fraction (FF)
(Glomerular Filtration Rate)/ (Renal Plasma Flow)
what is inulin?
a polysaccharide; exogenous substance that is freely filtered at the glomerulus but is not reabsorbed or secreted by the tubules
GFR =
(UF x Uin) / Pin
UF= urine flow
Uin= urine inulin concentration
Pin= plasma inulin concentration
renal clearance definition
the volume of plasma from which a substance has been removed and excreted into the urine per unit time
clearance of substance (Cx) is calculated as:
Cx = (UF x Ux) / Px
why is clearance of creatinine used clinically rather than inulin?
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
when GFR is reduced by 50%, what happens to the excretion of creatinine and the plasma concentration of creatinine?
excretion is reduced by 50%
plasma concentration doubles
how effectively are creatinine and urea regulated as GFR is decreased?
very poorly
how effectively are bicarbonate, calcium and phosphate regulated when GFR is decreased?
poorly
how effectively are Na, K and H2O regulated as GFR is decreased?
well-regulated
renal clearance of PAH is an index of ____?
renal plasma flow (filtered and secreted but not reabsorbed)
Renal Blood Flow (RBF) =
RPF / (1-Hct)
what is normal renal plasma flow?
650 ml/min
what are the two mechanisms of autoregulation of GFR and RBF?
(1) myogenic mechanisms
(2) tubuloglomerular feedback
myogenic mechanisms
stretch of vascular smooth muscle (increase in arterial pressure) elicits contraction which elevates vascular resistance and maintains GFR constant
tubuloglomerular feedback
elevation of perfusion pressure -> increased delivery of NaCl to the macula densa (adjacent to the afferent and efferent arterioles) -> increase in vascular resistance
when are GFR and RBF elevated?
when the body needs to excrete large amounts of fluid and solute
when are GFR and RBF decreased?
when the body needs to retain fluid and solute
what hormones/autacoids increase GFR?
endothelial-derived nitric oxide
prostaglandins (bradykinin)
what hormones/autacoids decrease GFR?
norepninephrine
epinephrine
endothelin
how much of the filtered load is reabsorbed?
99%
what are the two pathways for filtered substances to be reabsorbed in the lumen?
(1) paracellular (across tight junctions)
(2) transcellular (across the cells)
on which side of the epithelial membrane is Na/K ATPase found?
basolateral
what substances are reabsorbed in the PT?
67% H2O, Na+, K+
50% urea
85% bicarbonate
100% glucose, amino acids & proteins
what are the three mechanisms for Na+ reabsorption in the PT?
(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)
the TF/P ratio is decreased to the greatest extent for which two substances?
glucose
amino acids
(almost 100% reabsorbed)
at what point does glucose spill into the urine and why?
at the transport maximum (when the filtered load exceeds the reabsorptive rate for glucose); the Na/glucose co-transporter is saturable
what is secretion?
the movement of solute from the interstitium into the tubular lumen
what substances are permeable in the thin descending loop of Henle?
H2O
limited permeability to solutes
hemostasis
physiological, healthy mechanism to stop blood loss and keep blood "liquid"
thrombosis
pathological formation of blood clots
hemorrhage
pathological bleeding, inability to form clots
primary hemostasis
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
secondary hemostasis
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
fibrinolysis
the enzymatic degradation of fibrin; mediates the dissolution of fibrin-platelet clots
what is the key enzyme of the fibrinolytic system and what does it cleave?
the protease plasmin; cleaves insoluble fibrin fibrils into soluble fibrin degradation products
where are platelets produced?
bone marrow and spleen
Glanzmann thrombasthenia
defect in fibrinogen receptor GPIIb-IIIa complex (no aggregation of platelets with fibrinogen)
von Willebrand disease
defect in vWF
Bernard-Soulier Syndrome
defect in GP1b alpha (no binding of proteins to vWF)
how is platelet function tested?
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)
where are enzymatic coagulation factors secreted from?
the liver
how are enzymatic coagulation factors activated?
produced as inactive precursors ("zymogens") and activation occurs by proteolytic cleavage
what is the significance of vit K for clotting?
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
warfarin (Coumadin)
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)
what does factor VIII do?
cross-links fibrin to form a stable clot
what are the three stages of coagulation?
initiation
amplification
termination
initiation of coagulation
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
amplification
thrombin can activate all the factors required for the assembly of the Xase and prothrombinase complexes
termination (3 anticoagulant pathways)
(1) antithrombin
(2) tissue factor pathway inhibitor (TFPI)
(3) protein C anticoagulant pathway
antithrombin
binds and inhibits factors II (thrombin) and X; activity is enhanced by heparin
tissue factor pathway inhibitor
inhibits formation of factor VII/tissue factor complex, as well as factor X
protein c anticoagulant pathway
thrombomodulin on endothelial cells change thrombin so that it only activates protein C, not fibrinogen; activated protein C inhibits factors V and VIII
the fV Leiden mutation
mutation in coagulation factor V that is the most common cause of a genetic predisposition for venous thrombosis in Caucasians
hemophilia A
deficiency in factor VIII
hemophilia B
deficiency in factor IX
what are some ways edema can develop?
(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