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195 Cards in this Set
- Front
- Back
what is the most likely cause of death in a blocked cat? |
hyperkalemia |
|
6 functions of the kidney |
1. excretion of waste 2. regulation of water & electrolyte balance 3. regulation of arterial blood pressure 4. regulation of red blood cell production 5. regulation of acid-base balance 6. production/secretion of hormones & vitamin D |
|
what percent of cardiac output goes to the kidneys? |
25% |
|
what % if total body weight is the kidney? |
1% |
|
what % of O2 consumption goes to the kidney? |
8% |
|
3 distinct regions of the kidney |
cortex, medulla, pelvis |
|
what are the 2 types of nephrons and where are they located? |
1. cortical nephrons - completely within cortex (85%)
2. juxtamedullary nephrons - both in cortex & medulla |
|
5 parts of the nephron |
1. glomerulus (renal capsule) 2. proximal convoluted tubules 3. loop of henle (descending/ascending) 4. distal convoluted tubules 5. collecting duct |
|
the average human kidney has how many nephrons? |
1 million |
|
describe blood flow through kidney |
renal a - interlobar a - arcuate a - interlobular a - afferent arteriole - glomerulus cap bed - efferent arteriole - peritubular capillaries - vasa recta - interlobular v....renal v |
|
where does perfusion happen in the blood flow in kidney? |
peritubular capillaries |
|
which is larger: afferent or efferent arteriole? |
afferent |
|
what is the juxtaglomerular apparatus? |
- thick ascending loop of henle into early distal convoluted tubule as it runs adjacent to afferent and efferent arterioles of its own glomerulus |
|
what is the juxtaglomerular apparatus composed of? |
1) granular cells (in afferent arteriole)
2. macula densa (cells from ascending limb)
3. lacis cells (periglomerular) |
|
what is the function of the juxtaglomerular apparatus? |
detects changes in blood pressure and plasma osmolarity
- allows for autoregulation |
|
is the kidney primarily sympathetic or parasympathetic? |
sympathetic |
|
what term is used universally to tell you "how many of something you have?" |
mole |
|
"amount of substance relative to its molecular weight per unit of volume" |
molarity |
|
"amount of substance in moles relative to its charge" |
equivalence |
|
"weight of a volume of solution divided by the weight of equal volume of distilled water" |
specific gravity |
|
increase in specific gravity indicates that urine is (less/more) concentrated |
more |
|
"specific gravity less than plasma" |
hyposthenuria |
|
"specific gravity the same as plasma" |
isothenuria |
|
"specific gravity greater than plasma" |
hypersthenuria |
|
can specific gravity be used to evaluate a patient by itself? |
no - have to look at water consumption |
|
"process by which water moves across semi-permeable membrane due to concentration gradients" |
osmosis |
|
T/F - Urea is an effective osomole, while glucose is a non-effective osmole. |
false - other way around |
|
"number of osmoles per kg of solvent" |
osmolality |
|
"number of osmoles per liter of solvent" |
osmolarity |
|
1 L of water = ? kg |
1 |
|
what is the normal plasma osmolality? |
300 mOsm/L |
|
what is an osmole gap? what does it mean? |
- calculated osmolality does not equal measured osmolality
- addition of osmotically active molecules not normally present in plasma |
|
"pressure required to prevent mvmt of water across the semi-permeable membrane" |
osmotic pressure |
|
does osmotic pressure equal oncotic pressure |
nope! |
|
what is colloid osmotic pressure? |
oncotic pressure |
|
"effective osmolality of solution relative to a semi-permeable cell membrane" |
tonicity |
|
"same tonicity of cell" |
isotonic |
|
"lower tonicity than cell"
effect? |
hypotonic
causes cell to swell |
|
"higher tonicity than cell"
effect? |
hypertonic
causes cell to shrink |
|
in adult mammals, what % of body weight is water? |
60% |
|
where is MOST of the fluid located in your body?
what %? |
intracellular
40% *2/3 of fluid in body |
|
what % of body weight is extracellular fluid?
how much of total body fluid? |
20%
1/3 |
|
what are the 3 types of extracellular fluid and what fraction of ECF are they? |
1. interstitial fluid (3/4)
2. intravascular fluid (1/4)
3. transcellular fluid (only about 1% of total body weight) |
|
which type of fluid (location) is most readily accessible for testing and clinical replacement of fluid loss? |
intravascular |
|
which type of fluid (location) is the only one that is not a usable source of body water? |
transcellular |
|
T/F - there is no direct way to measure the intravascular fluid volume |
true - indirectlya ssessed via blood pressure, HR, PCV/TS and central venous pressure |
|
how do we measure interstitial fluid volume? |
indirectly - skin turgor & eye position |
|
what causes the movement of water from intvascular to interstitial space? |
osmolality gradient |
|
across a cell wall, mvmt of fluid is primarily due to differences in ____________, while across a capillary wall it is due to differences in __________ |
osmotic pressure
oncotic & hydrostatic pressure |
|
primary extracellular cation |
sodium |
|
primary intracellular cation |
potassium |
|
what is the gibbs donnan effect? |
albumin as the major determinant of COP |
|
what are the 3 additional starling forces? |
1. permeability of capillary wall
2. reflection coefficient of capillary wall - how easy it is for albumin to move
3. lymph flow |
|
what is starling's equation/law? |
F = Lp [(Pcap-Pint)-o(pi-plasma-pi-int)] - Qlymph
F = net filtration Lp = permeability of cap wall o = reflection coefficient of proteins Qlymph = lymp flow removing excess ISF pi = oncotic pressure |
|
what typically causes increased colloid osmotic pressure?
what does it cause? |
iatrogenic
hypervolemia and increased hydrostatic pressure leading to edema |
|
2 types of intravenous fluids |
1. crystalloids - electrolyte solutions which easily leave vessels
2. colloids - contain large molecules such as protein or starch and stay within vessels, attracting water to them |
|
describe administration of isotonic fluids |
- tonicity close to plasma - 0.9% saline or LRS - used to expand ECF volume - no net mvmt of water |
|
describe administration of hypotonic fluids |
- tonicity less than plasma - 0.45% saline (1/2 strength) - used to expand ECF volume & supply free water - draws fluid from ECF to ICF - used for dehydration in hypertonic patient - hypernatremic or hyperglycemic |
|
describe administration of hypertonic fluids |
- tonicity greater than plasma - 3 or 7.5% NaCl - used to treat severe hyponatremia - increases osmolality in both ECF & ICF - draws water from ICF to ECF - MUST follow with hypotonic solution - used only in emergencies |
|
describe administration of colloid fluids |
- plasma (albumin) or hetastarch (starch) - stays within IVF space - increases oncotic pressure - metabolized in 1-2 days - treates hypovolemia & hyperprotenemia |
|
describe administration of dextrose |
- effective osmole so when it is given, it pulls water towards it (hypertonic)
- as the body uses it up, the free water left is hypotonic |
|
what is the major site of filtration in the kidney? |
glomerulus |
|
list the 3 layers of the glomerular membrane and what they filter |
1. capillary endothelial cells (fenestrated) - prevents blood cells 2. basement membrane - highly negative charge; prevents most plasma proteins (albumin) 3. distal foot process of podocytes - prevent mvmt of large molecules (30 angstroms) |
|
where is the site of injury in glomerular disease? |
glomerular basement membrane |
|
glomerular filtration is a [active/passive] prrocess |
passive |
|
3 reasons glomerulus is more efficient than other capillary beds |
1. huge surface area
2. very permeable to water & solutes
3. higher blood pressure |
|
"the amount of filtrate formed per unit time" |
glomerular filtration rate (GFR) |
|
what is the first step in the formation of urine |
ultrafiltrate |
|
while the ____________ pressure gradient predominates in the glomerular capillaries, leading to an efflux of fluid, the ____________ pressure predominates in the peritubular capillaries allowing a net influx of fluid |
hydrostatic
colloid osmotic pressure |
|
3 factors affecting GFR
(which one is most important?) |
1. surface area of filtration
2. filtration membrane permeability
3. net filtration pressure*** |
|
what is clearance? |
a measure of the rate at which a substance is filtered |
|
what are some substances that are used to measure GFR? |
inulin, BUN, creatanine |
|
drawbacks of using inulin to calculate GFR |
1. administered IV
2. bladder must be empty
3. accurate but not convenient
4. urine has to be collected over time |
|
what is the most widely used substance to estimate GFR? |
creatinine |
|
in what situations are creatinine levels altered? |
- hyperthermia
- muscle wasting
- muscle damage |
|
an increase in protein will cause an [increase/decrease] in BUN |
increase |
|
"the accumulation of nitrogenous waste in the blood" |
azotemia |
|
"azotemia that produces clinical disease" |
uremia |
|
T/F - by adjusting resistance to blood flow, the kidney can maintain a nearly constant GFR despite changes in systemic blood pressure |
true |
|
what do myogenic receptors do? |
sense blood pressure changes through stretch receptors in arterioles and response by constriction or dilation |
|
describe the actions of the macula densa |
1. high GFR - cells swell - release ATP - afferent constriction - lower GFR
2. low GFR - cells shink - decreases ATP - afferent returns to normal |
|
3 extrinsic factors effecting autoregulation |
1. sympathetic innervation (vasoconstriction)
2. prostaglandins (dilate afferent arteriole) *NSAIDs inhibit prostaglandin
3. atrial natriuretic peptide (vasodilation of efferent - increase GFR) |
|
3 major processes accomplished by the nephron |
1. ultrafiltration of plasma by glomerulus
2. reabsorption of water and solutes
3. secretion of solutes into tubular fluid |
|
60% of filtered substances happens.... |
proximal tubule |
|
describe physical characteristics of proximal tubule |
- cuboidal epithelial cells
- lots of mitochondria
- dense microvilli (brush border) |
|
physical characteristics of descending henle's loop |
- simple squamous
- few mitochondria (not much active transport)
- passive permeability for water to move into interstital space |
|
physical characteristics of ascending henle's loop |
- cuboidal epithelium
- no aquaporins
- active & passive reabsorption of solutes |
|
physical characteristics of distal convoluted tubule |
- cuboidal
- thinner with little microvilli
- active transport of Na
- water reabsorbed in response to ADH |
|
physical characteristics of collecting ducts |
- intercalated cells > microvilli & acid-base regulation
- principle cells > less microvilli & Na/K regulation |
|
3 barriers of tubular reabsorption |
1. luminal membrane of tubule
2. basolateral membrane of tubule
3. endothelium of capillary |
|
what is cell death? |
the inability to maintain electrolyte gradient |
|
what is the cutoff for GFR function when there is an altered ability to modify urine concentration? |
20% |
|
4 ways that sodium moves |
1. passively down gradient
2. coupled to mvmt of glucose, aa, organic acids or phosphates
3. actively pumped
4. exchanged |
|
what is the primary determinant of ECFV volume |
sodium |
|
T/F - sodium needs a carrier molecule to move from lumen into cell |
true |
|
where is the only place in the nephron where there is no sodium reabsorption? |
ascending loop of henle |
|
total body (extrinsic) factors that affect sodium excretion (3) |
1. GFR (higher GFR = more sodium filtered)
2. ANP (increased GFR & decreases sodium reabsorption in DCT & collecting tubule)
3. angiotensin II (increases reabsorption of Na * HCO3 at proximal tubule) |
|
hyponatremia can lead to cell [swelling/shrinking] |
swelling |
|
hypernatremia can lead to cell [swelling/shrinking] |
shrinking |
|
where is glucose reabsorbed? |
proximal tubule |
|
describe removal of glucose from urine by secondary active transport |
1. glucose + 1 Na -> SGLT2 carrier into early proximal tubule cell
2. glucose transported by GLUT2 into interstitial fluid |
|
what happens when plasma glucose levels are elevated? |
the transport mechanisms can be overwhelmed and not all glucose will be transported/reabsorbed |
|
what is the threshold for transport of glucose in dog? cat? |
dog = 180 mg/dl
cat = 200 mg/dl |
|
3 things regulated by potassium |
1. cellular function
2. normal cardiac rhythm
3. proper neuromuscular transmission |
|
T/F - hyperkalemia is common when renal function is normal |
false - it rarely occurs unless there is a defect in renal excretion |
|
the most important route of excess potassium elimination is by..... |
renal excretion |
|
the number of available channels for Na reabsorption and K elimination is dependent on the presence of..... |
aldosterone |
|
aldosterone is secreted in response to [hypo/hyper]tension |
hypo |
|
normal K concentration in the ECFV
what is hyper? hypo? |
~4 mEq/L
hyper = K>5 hypo = K<3.5 |
|
[hyper/hypo]kalemia is a potentially fatal condition |
hyper |
|
what are cardiac signs of hyperkalemia? |
- arrhythmias & potentially cardiac arrest - bradycardia - elevation of T wave - lost P wave - QRS looks like sign wave - fibrillation soon follows
|
|
CO2 is primarily regulated by the ___________ and HCO3 is primarily regulated by the _____________ |
lungs
kidney |
|
2 ways H ions are removed |
1. binding with bicarb
2. actively pumped into filtrate where they combine with other urinary buffers in collecting ducts |
|
2 places where H ions are moved in or out of nephron |
1. proximal tubule - secretion of H in exchange for Na
2. distal tubule & collecting duct - K reabsorbed in exchange for K at intercalated cells |
|
where is bicarbonate retrieved? |
proximal tubule |
|
sequence of steps needed to resorb bicarbonate in proximal tubule |
1. H is exchanged for Na 2. HCO3 binds with secreted H 3. carbonic anhydrase catalyses formation of CO2 4. carbonic anhydrase catalyzes regeneration of HCO3 5. both Na & HCO3 are then resorbed into ECFV |
|
3 other things that can affect the rate of HCO3 reabsorption |
1. ECF volume
2. angiotensin II
3. increased CO2 |
|
loss of the ability to resorb HCO3 results in... |
proximal renal tubule acidosis |
|
loss of ability to excrete H results in.... |
distal renal tubular acidosis |
|
3 steps in the secretory pathway |
1. mvmt of organic solute from peritubular capillary into interstitium by diffusion 2. transport of solute into cell across basolateral membrane by specific transporters (facilitated diffusion) 3. secretion from cell into lumen driven by cation or anion exchangers |
|
what is fanconi syndrome? |
- proximal renal tubule does not reabsorb electrolytes & amino acids
- often PU/PD, glucose, aa & HCO3 in urine
- loss of bicarb results in acidemia
- often misdiagnosed as having diabetes |
|
what is the countercurrent multiplier? |
- governs creation of osmotic gradient for urine filtration
- counter current = loops of henle interact w/parallel blood from vasa recta
- multiplier = many thousands of tehse packed together |
|
3 reasons the countercurrent multiplier works |
1. desc loop of henle is impermeable to solutes but permeable to water (conc. filtrate) 2. ascending loop of henle is permeable to solutes but impermeable to water (conc. interstitium & diluets filtrate) 3. urea recycling contributes to medullary osmotic gradient |
|
T/F - the urine formed can only be as concentrated as the interstitial fluid |
true |
|
specific gravity of isothenuric urine |
1.008-1.012 |
|
what goes in & out of urea cycle? |
ammonia goes in
urea comes out
*requires ATP |
|
what % of urea is excreted? |
50% |
|
ADH [increases/decreases] urea recycling |
increases |
|
what 3 mechanisms regulate osmolality? |
1. ADH secretion
2. thirst
3. salt appetite |
|
disorders of water balance manifest by changes in .... |
body fluid osmolality |
|
where are osmoreceptors located?
what do they respond to? |
hypothalamus
changes in osmolality of blood- effective osmoles |
|
what controls the release of ADH? |
osmoreceptors |
|
the result of increased ADH is __________ urine and ___________ plasma osmolarity |
concentrated
decreased |
|
the absence of ADH results in _______ urine and _________ plasma osmolarity |
dilute
increased |
|
describe ADH receptors |
V2 - located in collecting ducts
V1 - located in blood vessels > mediate vasoconstriction |
|
what 2 changes causes release of ADH?
how much change is required in each? |
1. osmolality (primary trigger) - 1%
2. hemodynamic (secondary) - 5-10% |
|
"production of large volumes of dilute urine" |
polyuria |
|
"ingestion of large volumes of water" |
polydipsia |
|
2 types of diabetes insipidus |
central: inadequate release of ADH - treated with exogenous ADH
nephrogenic: collecting ducts do not respond normally to ADH - no effective treatment |
|
what stimulates thirst? |
1. osmoreceptors - stimulated by changes in osmolality
2. baroreceptors - stimulated by decreased blood volume/pressure |
|
extracellular fluid volume is controlled by.... |
sodium |
|
NaCL and water are controlled by what 4 systems? |
1. renin-angiotensin-aldosterone
2. antidiuretic hormone
3. atrial natriuertic peptide
4. renal sympathetic nerves |
|
where are low pressure baroreceptors located?
what do they respond to? |
walls of cardiac atria & pulmonary vessles
change in stretch |
|
where are high pressure baroreceptors located?
what do they respond to? |
walls of aortic arch, carotid sinus& afferent arteriole of kidney
change in blood pressure |
|
what 3 things cause renin release? |
1. decrease in perfusion pressure
2. stimulation of sympathetic nervous system
3. decrease in NaCl to macula densa |
|
where is renin produced? |
granular cells of afferent arteriole in kidney |
|
what does renin do? |
converts angiotensinogen to angiotensin I |
|
what does angiotensin I do |
nothing! |
|
where is angiotensinogen produced? |
liver |
|
what converts angiotensin I to angiotensin II? |
angiotensin converting enzyme (ACE) |
|
where is ACE produced? |
lung |
|
5 actions of angiotensin I |
1. increase sympathetic activity 2. tubular NaCL reabsoption & K excretion & H2O retention 3. stimulate adrenals to release aldosterone 4. efferent vasoconstriction = increased BP 5. stimulate pituitary gland to release ADH |
|
aldosterone secretion is [increased/decreased] by hyperkalemia |
increased |
|
patients with decreased aldosterone secretions present with [increased/decreased] Na concentration, which causes [increased/decreased] ECF volume |
decreased
decreased |
|
what Na:K ratio is highly suggestive of addison's? |
< 25 |
|
hyperkalemia =
hypokalemia = |
K>5
K<3.5 |
|
what balances the RAA system? |
atrial natriuretic peptide (ANP) |
|
what does atrial natriuretic peptide do? |
- vasodilation of afferent arteriole - vasoconstriction of efferent arteriole - inhibits secretion of renin & aldosterone - inhibits reabsorption of NaCL - inhibits secretion of ADH - increase in GFR |
|
2 causes of intracellular edema |
1. iatrogenic - we gave fluids too fast
2. altered permeability of sick cells |
|
4 causes of extracellular edema |
1. increased hydrostatic pressure
2. decreased oncotic pressure
3. increased capillary permeability
4. lymphatic obstruction |
|
how do you treat edema? |
*increase NaCl excretion or prevent reabsorption
- diuretics - ACE inhibitors - treat underlying cause! |
|
what pH range is compatible with life? |
6.8 to 7.8 |
|
parameters for acidemia |
blood pH < 7.35 |
|
parameters for alkalemia |
blood pH > 7.45 |
|
what percent of total CO2 is in bicarbonate? |
95% |
|
2 types of acid |
1. volatile - organic acids that are easily evaporated (CO2)
2. non-volatile - fixed, non-gaseous acids - formed primarily from metabolism of AA |
|
how has more non-volatile acids typically - herbivores or carnivores? |
carnivores |
|
3 compensatory mechanisms for acid-base disturbances and their timing |
1. immediate chemical buffering (sec-min)
2. respiratory compensation (hours)
3. renal compensation (days) |
|
extracellular immediate body buffers |
- bicarbonate - bone - phosphates - ammonia |
|
intracellular immediate body buffers |
- hemoglobin - intracellular proteins - phosphates |
|
an increase in pCO2 is....
typically caused by....
how to treat? |
respiratory acidosis
alveolar hypoventilation
increase respiration |
|
a decrease in HCO3 is....
typically caused by....
how to treat? |
metabolic acidosis
consumption of HCO3; renal or GI wasting or bicarb (D+); rapid dilution of ECF
respiratory centers stimulate increase in ventilation, which decrease CO2 levels |
|
"the amount of acid that must be added to return 1 L of blood to a pH of 7.4" |
base excess (BE) |
|
if your patient is acidemic, your BE will be [positive/negative] |
negative |
|
"difference between measured cations and anions"
what does it tell us? |
anion gap
if we are losing bicarb or adding acid |
|
if metabolic acidosis is due to addition of acid, the anion gap is [increased/decreased] |
increased |
|
if acidosis is result of loosing bicarb, the anion gap will be [high/normal] |
normal |
|
a decrease in pCO2 is....
typically caused be....
how to treat? |
respiratory alkalosis
increased alveolar ventilation
renal decrease bicarb reabsorption or increase loss in urine (or both) |
|
an increase in HCO3 is....
typically caused by.....
how to treat? |
metabolic alkalosis
enhanced H ions (vomiting) or addition of alkali (antacids)
decreased ventilation increases CO2 |
|
metabolic acidosis: decrease in HCO3......PaCO2
respiratory acidosis: increase in PaCO2......HCO3 |
decreases
increases |
|
metabolic alkalosis: increase in HCO3.....PaCO2
respiratory alkalosis: decrease in PaCO2......HCO3 |
increases
decreases |
|
phases of acute kidney injury |
1. initiation
2. maintenance
3. recovery |
|
which phase of kidney injury can you do something for? |
initiation |
|
how many stages are there of acute kidney injury? |
5 |
|
definition of chronic kidney disease |
- > 2 weeks
- typically progressive over months to years
- irreversible injury |
|
how many stages of chronic kidney disease are there? |
4 |
|
what are 3 benchmarks in determining stages of chronic kidney disease? |
- serum creatanine level & clinical signs
- presence/absence & degree of proteinuria
- presence/absence of hypertension |
|
azotemia + isothenuria = |
renal disease |
|
azotemia + inappropriate urine conentration = |
renal disease |
|
4 causes of acute kidney injury |
1. hemodynamic
2. end/exogenous toxins
3. renal parenchymal disease
4. post-renal obstruction |
|
3 causes of chronic kidney disease |
1. acquired (did not recover)
2. congenital
3. familial |
|
what is the difference in clinical signs of acute vs. chronic kidney disease? |
acute: sudden illness; present very ill
chronic: chronic progression; lethargy; general wasting |
|
what is the difference in PE findings for acutve vs. chronic kidney disease? |
acute: normal wt & haircoat; enlarged & painful kidneys; not debilitated
chronic: wt loss; unkempt coat; oral ulcerations; small, nonpainful kidneys; debilitated |
|
what isthe difference on bloodwork for acute vs. chronic kidney disease? |
acute: increased K
chronic: decreased K; increased Ca |
|
what is the difference on CBC for acute vs. chronic kidney disease? |
acute: normal; possibly WBC if infection
chronic: normocytic, normochromic anemia |