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ISBM > Exam #3_Semester 2 > Flashcards

Exam #3_Semester 2 Flashcards

1
Q

blood - general roles

A

Transport vehicle: long distance

Defense: B-cells and phagocytes

Homeostatic role

  • buffering capacity: protein buffers; acid-base balance
  • osmotic balance: ECF oncotic pressure
  • heat distribution (disseminating heat load or conserving heat to core)
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2
Q

oncotic pressure

A

contribution made by proteins to overall osmotic pressure

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3
Q

multipotential hematopoietic stem cells

A

precursors to all cellular components of the blood (RBCs, WBCs, platelets)

  • produced by bone marrow
  • differentiate into myeloid precursors (RBCs and WBCs) and lymphoid precursors (lymphocytes - B’s, T’s, and NKC’s (natural killer cells))
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4
Q

functions of EPO (erythropoietin)

A

maintain constancy of HgB concentration

maintain constant of RBC mass

Ensure and speed recovery form hemorrhage

Note: great variation b/t individuals; diurnal fluctuations; higher at altitude (low PO2)

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5
Q

influences of EPO release

A

Hypoxia-inducible factor (HIF) synthesis is triggered by reductions in local PO2 and this is a function of:
o O2 carrying capacity: function of hemoglobin concentration (ex. anemia)
o O2 saturation: degree to which hemoglobin is saturated with O2
o O2 affinity: affinity of hemoglobin for O2 (factors that promote high affinity = low free O2 in plasma)

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6
Q

hemoglobin and glucose - HgB-A1c

A

erythrocytes, which contain hemoglobin, are entirely dependent on glucose to drive diffusion

Hgb can be irreversibly glycosylated with glucose (purely dependent on conc. of glucose in ECF), forming HgB-A1c

  • does not affect function in terms of O2 binding
  • marker of glycemic control
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7
Q

agglutinogens

A

cell surface glycosylated entities (sphingoipids) that define “blood type” phenotype

  • all sphingolipids are glycosylated (have carbohydrates attached), but A and B groups have a single, additional group attached
  • O group does not have an extra carbohydrate group attached
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8
Q

form of iron that can reversibly bind O2

A

ferrous form (Fe2+)

Note: ferric form (Fe3+) cannot bind O2

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9
Q

two things that affect blood O2 carrying capacity

A
  1. amount of O2 bound to Hgb - major contributor!
    - depends on degree Hgb is saturated with O2 (ability to associate with 4 O2) which depends on PO2
    - depends on amount of Hgb in system
  2. partial pressure of O2 (amount of O2 dissolved in plasma) - minor contributor!
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10
Q

fetal Hgb (HgbF)

A

γ/a (gamma/alpha) – alpha 2, gamma 2 expression: has higher affinity for O2 than adult

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11
Q

adult Hgb (Hgb A1)

A

a/b (alpha/beta) - beta chain increases following birth (gamma decreases); alpha chain remains
- can be conjugated with glucose (Hgb-A1c)

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12
Q

adult Hgb A2

A

when alpha chain associated with delta chain (usually small amount)

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13
Q

P50 value for Hgb

A

partial pressure of O2 at which 50% saturation of Hb exists

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14
Q

deoxyhemoglobin

A

no O2 bound

- 2,3-BPG can bind more readily to this form

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15
Q

alpha thalassemia

A

defect in alpha subunits (should be very high in fetus)
Left with gamma subunits only (gamma 4) – called Bart’s Hemoglobin
• P50 of 3 mmHg PO2 (vs. 21 mmHg normally)
• Hb Bart’s has a very high affinity for O2 - will not let go of it

Devastating to newborn (fetus starved of O2)

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16
Q

Bart’s hemoglobin (Hb Bart’s)

A

Hb Bart’s has a very high affinity for O2 - will not let go of it

P50 of 3 mmHg PO2 (vs. 21 mmHg normally)

Devastating to newborn (fetus starved of O2)
- see in alpha thalassemia

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17
Q

methemoglobinemia

A 
excess metHb (methemoglobin) - possesses oxidized iron in ferric state (Fe3+) instead of ferrous state (Fe2+)
 - Fe3+ state does not bind O2 (no reversible association occurs)

metHb typically present at 1% of total Hgb

Chemical agents can oxidize iron in Hb to ferric state and cause too much metHb = methemoglobinemia

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18
Q

effect of Hb mutation increasing affinity for O2

A

decreased P50 = increased affinity

- more O2 bound tightly to Hb = blood not releasing enough O2 to body = tissues starved of O2

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19
Q

effect of Hb mutation decreasing affinity for O2

A

increased P50 = decreased affinity

- less O2 bound to Hb = less saturation = lower blood oxygen carrying capacity = blood not supplying enough O2 to body

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20
Q

haptoglobin

A

“suicide” protein that is a weak binder of hemoglobin in plasma (versus bilirubin synthesis in liver and spleen)

  • creates a non-reactive complex once bound to Hb
  • low levels = elevated hemolytic activity since most bound with heme
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21
Q

Can iron be cleared by body?

A

no, iron is an element - we cannot metabolize it

body has not evolved mechanisms to clear excess iron

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22
Q

fluid compartments of body

A

ECF: consists of blood and interstitial fluid (ISF)

  • Exchange with external environment mainly though ISF
  • kidney is only organ in steady stage with blood

ICF: largest volume of fluid (2/3)
- in stead state with transcellular fluids

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23
Q

secretion

A

active process of moving substances across membrane

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24
Q

excretion

A

ridding from body

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25
Q

substance handling - how are substances introduced into our systems and leave our systems?

A

ingested
produced via metabolism
consumed via metabolism
excreted

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26
Q

balance concept

A

To maintain balance in our systems (fluid volume homeostasis and electrolyte homeostasis):

substance amount produced and ingested = substance amount consumed and excreted

intake = output

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27
Q

“mu”

A

normal

ex. mu natremic state = normal homeostatic state for Na

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28
Q

types if nephrons

A

Superficial nephrons: have glomerulus/bowmen’s capsule at the more distal regions of the cortex
• Short loop of Henle – does not extent far into medulla

Mid-cortical nephrons:
• Loop of Henle is a bit longer

Juxtamedullary nephrons: glomerulus/bowman’s capsule very close to the medulla (still in cortex)
• Very lengthy loop of Henle that dips far into the medulla

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29
Q

importance of afferent and efferent arterioles on either side of glomerulus

A

Helps to maintain a relatively constant GFR

Sets up series resistance which effects flow rate and pressure gradients
-arterioles surrounded by smooth muscle (influenced by SNS)

30
Q

macula densa

A

group of cells located at intersection of LH and DCT right next to glomerulus; important for tubular glomerular feedback

31
Q

glomerular filtration rate (GFR)

A

volume of blood that is filtered by the glomeruli / time (volume / time)

Gold standard - use of inulin to establish

Represents net filtration pressure (NFP)

  • function of permeability constant and outward and inward Starling forces
  • note: oncotic pressure in Bowmen’s capsule not included (see equation)
32
Q

filtration fraction

A

fraction of blood traveling to kidney that will actually enter Bowmen’s capsule

  • 15-20% of plasma moves into urinary space
  • HUGE impact on fluid volumes

clearance of inulin (GFR) / clearance of PAH (renal plasma flow)

33
Q

freely filterable

A

nothing impedes ability of molecule to move from capillary into Bowmen’s capsule (e.g. water, electrolytes, urea, glucose, insulin)

34
Q

exchangeable pool

A

portion of total pool of electrolytes that is filterable (since electrolytes often association with larger molecules making them less filterable)

35
Q

average GFR

A

125ml/min or 180L/day
• 125 ml per minute is moving from plasma space into urinary space
• Meaning the plasma is filtered about 60 times per day (plasma vol = roughly 3 liters total)

36
Q

clearance

A

volume of plasma from which that substance is completely cleared by the kidneys per unit time
- problem: kidney cannot completely clear

represents the volume of plasma that contains the amount of our substance that is appearing in urine (cleared) per unit time

37
Q

filtered load

A

amount of a substance that is filtered per time
- function of GFR and conc. of the substance in the plasma

FL = GFR x Plasma conc. of substance

38
Q

anti-diuretics

A

decrease production of urine by chinning the permeability of the apical membrane to water

39
Q

trans-cellular pathway

A

substances exit the lumen through the apical cell membrane, cross the cell, and exit the cell through the baso-lateral membrane
- primary mechanism of reabsorption

40
Q

para-cellular pathway

A

movement occurs through tight junctions between the tubular cells
- principle route of movement of some ions (e.g. Cl-) is through tight junctions

41
Q

carbonic anhydrase

A

enzyme within cells of kidney - important in acid/base balance and for contributing protons utilized in secretion and recapture of bicarbonate (via proton pumping) – HCO3 into plasma

42
Q

maximal transport rate

A

filtered load of a substance that saturates the transport mechanism
- protein-mediated transport mechanisms are saturable

43
Q

effective circulating volume (ECV)

A
  • regulated variable
  • dictated by ECF volume (plasma+ISF) and total Na and Cl play large role in dictation ECF
  • consequence of HP that exists within organ systems that is a sensed parameter by a variety of sensing mechanisms (monitored variables)
  • not calcuable - concept
  • sensors provide afferent to CNS which alters handling of NaCl (and water) at level of kidney
44
Q

autoregulation - two key mechanisms

A

GFR is held “constant” by holding renal blood flow constant through auto regulation, despite inc. or dec. in pressure

  1. myogenic response of vascular smooth muscle: increased in resistance (due to SM contraction of vasculature) keeps kidney flow relatively constant (stretch receptors on myocytes activate Ca channels)
  2. tubuloglomerular feedback: macula densa initiates cascade that affects contractile state of afferent and efferent arteriole SM
45
Q

obligatory water loss

A

(0.43 L/day) since we must get rid of 600mosmols of water-soluble waste products per day

46
Q

specific gravity

A

measure of the osmotic composition of a fluid relative to a reference fluid (pure water)

Urine SG = 1.001-1.028
Dilute: 1.001 = 50 mosmols/L
Concentrated: 1.028 = 1400 mosmols/L
Average = approx. 700 mosmols/L

Note: Function of ADH (higher ADH = higher SG) and hydration status

47
Q

aquaporin expression

A

results from hormones ADH

passive moment of water exclusively in accordance with osmotic differences

48
Q

diabetes insipidus

A

inability to produce or respond to ADH; inability to produce a concentrated urine

Problem: women suffered severing of pituitary stalk in car accident, resulting in inability to secrete ADH in response to central signals of increasing osmolarity

49
Q

natriuretic peptides

A

peptides (hormones) derived in atria and brain that respond to increased ECV (effective circulating volume)

  • sensors detect changes in pressure (volume) and activate ANP/BNP to promote NaCl and (consequently) water excretion
  • actions are to remove water and electrolytes (counter effects of ADH, aldosterone, and ANG-II)
50
Q

urea wash out effect

A

extreme hydration can decrease the osmotic gradient necessary for proper water reabsorption in order to create a concentrated urine
- minimizes concentrating ability

51
Q

low protein diet

A

low urea which can decrease the osmotic gradient necessary for proper water reabsorption in order to create a concentrated urine
- minimizes concentrating ability

52
Q

counter current multiplier

A

mechanism through which the medullary gradient is increased from outer to inner medulla

Depends on exchange of water and solute between vasa recta, ISF (and filtrate)?

53
Q

what happens we increase sodium intake

A

entering state of positive Na balance will elevate osmolarity and set off mechanisms that promote water retention (enhance thirst (ANG-II) and minimize water loss (ADH)

  • Fluid vol. and body weight will increase: inc. ECV
  • Inc. in ECV sensed by natriuretic peptides which work to excrete excess Na and body fluid
54
Q

actions of natriuretic peptides

A

o Vasodilator of afferent and efferent arterioles: inc. glomerular flow→enhance GFR
o Inhibits renin secretion: reduce ANG II levels
o Inhibits aldosterone secretion
o Inhibits NaCl reabsorption in DCT and CD
o Inhibits ADH secretion

All promote NaCl and (consequentially) water excretion

Peptides respond to increased ECV

55
Q

diuretics

A

effect water passively by regulating electrolyte balance

  • can alter urinary output fairly easily with diuretics (electrolyte wasting – water follows)
  • most act on TAL and DCT (not on PCT even though that is the point of maximal reabsorption)
56
Q

four main electrolytes in urine

A

Na+, K+, Cl-, HCO3-

57
Q

Mannitol - osmotic diuretic

A

osmotic diuretic: sugar that is freely filterable but not reabsorbed so makes filtrate very osmotic, drawing water out

  • does not alter uptake of electrolytes
  • Na, Cl, K, and HCO3 follow water
  • inc. urine 10 fold!
58
Q

loop diuretics

A

inhibit Na/K/2Cl transport in the TAL (on apical membrane - typically draws electrolytes back into blood; when inhibited electrolytes stay in filtrate and attract H2O)

  • high loss of electrolytes (Na and Cl; HCO3 stays same), most notably potassium (see below – must monitor K when using these)
  • increase urine by 8 fold!

furosemide (Lasix), ethacrynic acid, mercurial

59
Q

what electrolyte must be monitors when using diuretics?

A

potassium (K+) - smalll amunt in ECF is very key for membrane potential
- patients can become hypokalemic very quickly due to small amount of K typically in ECF (compared to intracellular)

60
Q

two key cell types in late distal convoluted tubule (DCT)

A

principle cells: responsible for reabsorption of Na and secretion of K

Intercalated cells: pump protons and bicarbonate

61
Q

intercalated cells - two types

A

Type A: express transport mechanisms (ATP-driven H and K extrusion mechanisms – prime secretory mechanisms) on apical membrane
• Cl/HCO3 antiport mechanisms on baso-lateral membrane (moves HCO3 into ISF)
• Major type: HCO3 reabsorption

Type B: express transport mechanisms on baso-lateral membrane (ATP-driven H+/K antiport and proton ATPase – drive H+ into ISF)
• Cl/HCO3 antiport mechanisms on apical membrane (moves HCO3 into filtrate)
• Minor type (but key under alkalytic conditions – high pH): HCO3 can be secreted!

62
Q

titratable acidity

A

take urine specimen and determine pH; add known quantity of hydroxide ion (-OH) in form of NaOH and take urine back up to pH of 7.4

  • Measure amount of OH added to system = quantify proton conc. that had been added to urine to make acidic (how acidic is the urine)
  • Note, cannot have titratable acid if pH over 7.4 (alkalytic) – does not fit definition
63
Q

renal system maintains [HCO3-] in system

A
  1. Titratable acid production & excretion 2. NH4+ production & excretion
  2. Bicarbonate reabsorption

Key for acid-base balance (Henderson-Hasselbalch equation)

64
Q

urea

A
  • passively handled solute (small and not charged)
  • key for maintaining inner-medullary osmotic gradient
  • metabolic waste product (we cannot do anything with it); repository for amine groups
65
Q

urea in nephron and ultimately urine

A
  • concentration increases as you move through the nephron
  • transporters responsible for facilitated diffusion b/t filtrate and ISF (protein mediated and saturable)
  • urea levels very high in urine - contribute to majority of osmolarity of urine
66
Q

three purposes of iron chelation

A

chelation: binding of iron to transferrin
• Renders iron soluble under physiologic conditions (iron can precipitate – no good)
• Prevents iron-mediated free radical toxicity
• Facilitates transport into cells

67
Q

physiologic anemia of the newborn

A

decreased production of RBCs due to loss of stimulus to produce more EPO

Newborn improves O2 status:

  • occurs at 6-9 weeks for full-term infant
  • occurs at 4-6 week for premature infant
68
Q

recommended daily iron intake - infant

A

Newborn infant: born with 75 mg/kg of iron (adequate at first); however, rapidly expanding RBC mass

Adequate storage until birth weight doubles (usually 4-6 months)

During first year of life, RBC mass doubles
• Average increase in blood from 135 ml to 270 ml
• 1 mg elemental iron needed for each ml of blood
• Total of 135 mg needed during first year of life just to build RBC mass

69
Q

agglutinogens

A

cell surface glycosylation entities that define “blood type” phenotype
- form antibodies against when you do not have

70
Q

chelation

A

binding of iron to transferrin

Serves 3 purposes:

  • makes iron soluble
  • transports iron
  • prevents iron-mediated free radical toxicity
71
Q

what is driving force for mov’t of electrolytes from ISF into plasma/blood

A

oncotic pressure within capillaries (low)

ISBM (7 decks)

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