Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BMSC 208 > Renal 3 > Flashcards

Renal 3 Flashcards

Renal Lecture 8 and Acid-Base Lecture

1
Q

where is K reabsorbed and secreted

A

reabsorbed-proximal tubule and ascending loop of henle
secreted-distal tubule and cortical collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

excretion % at normal K conc

A

10-20% of filtered load (reabsorption is less than filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

excretion % at low K conc

A

decrease aldosterone release
reduce secretion = reduce excretion, 2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

excretion % at high K conc

A

stimulates aldosterone release
increase secretion and excretion, 10-150%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

K level conditions and AP effect

A

hyperkalemia: depolarize cells
normal: conc is 3.5-5mM
hypokalemia: hyperpolarize cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

tissues where K balance is important

A

excitable tissues: heart, skeletal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hypokalemia effects

A

muscle weakness bc more difficult for hyperpolarized motor neurons and muscles to fire APs

failure of cardiac and resp muscle concerning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hyperkalemia effects

A

more dangerous, initially hyperexcitability
eventually cells unable to repolarize and become less excitable

life threatening arrythmias in heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why might K imbalances occur

A

kidney disfunction, eating disorders, loss of K in diarrhea, use of diuretics that prevent kidneys from properly reabsorbing K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

behavioural mechanisms of salt and water balance

A

behavioural responses critical in restoring normal state, ECF volume decreases or osmolarity deviates
-drinking water is normally only way to replace lost water and eating salt is only way to replace body’s Na content
- act of drinking relieves thirst, water doesn’t actually have to be absorbed
-receptors in mouth/pharynx respond to w ater by decreasing thirst and decreasing AVP release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

major stimulus of thirst

A

increase in osmolarity of body fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

physiological changes that influence sodium appetite STIMULATE

A
  • increase aldosterone
  • increase ANG2
  • decrease Na conc
  • arterial/venous baroreceptors, stim or inhibit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

physiological changes that influence sodium appetite INHIBIT

A
  • increase Na conc in plasma or cerebrospinal fluid
  • post-ingestive signals from gut (increase Na, distension) sensed via vagus nerve
  • circulating and CNS peptide hormones/neuromodulators
  • arterial/venous baroreceptors, stim or inhibit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are avoidance behaviours

A

help prevent dehydration
ex) desert animals avoid daytime heat and become active at night
midday nap “siesta” in tropical countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are integrated controls of volume and osmolarity

A

CV system responds to change in blood volume and bp

renal system responds to changes in blood volume and or osmolarity

behavioural mechanisms respond to both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

increase volume, increase osmolarity: cause?

A

eating salty foods and drinking at same time, net results = more Na than water, hypertonic saline

  • need to excrete solute and liquid to match what was taken in
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

increase volume, no change osmolarity, cause?

A

salt and water ingested is equivalent to isotonic solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

increase volume, decrease osmolarity

A

pure water without ingesting solute
-kidneys can’t excrete pure water, some solute lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

no volume change, increase osmolarity

A

eating salt without drinking water, increases ECF osmolarity, shifting water from cells to ECF

  • trigger intense thirst and kidneys make concentrated urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

no change in volume, decrease osmolarity

A

water and solutes lost in sweat or feces but only water is replaced

  • lead to hypokalemia or hyponatremia (low Na)
  • sports drinks, electrolyte drinks help replace fluid and solutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

decrease volume, increase osmolarity

A

dehydration
due to heavy exercise (water loss from lungs doubles, sweat loss) or diarrhea
-can result in inadequate perfusion (decreased blood volume) and cell dysfunction
- increase water intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

decrease volume, no change in osmolarity

A

hemorrhage, need blood transfusion or ingestion of isotonic solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

decrease volume, decrease osmolarity

A

result from incomplete compensation for dehydration, uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

direct effect of decreased bp/volume

A

granular cells = renin secretion
glomerulus = decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
reflexes of decreased bp/volume
carotid and aortic baroreceptors: - CVCC- increase sympathetic output, decreased parasympathetic output - hypothalamus: 1. thirst stim 2. vasopressin secretion atrial volume receptors: - hypothalamus 1. thirst 2. vasopressin
26
direct effects of increased bp
glomerulus: increased GFR (brief) increased atrial filling= myocardial cells: natriuretic peptide secretion
27
reflexes of increased bp
carotid and atrial baroreceptors: - CVCC: decrease symp, increase parasymp - hypothalamus: 1. thirst inhibited 2. vasopressin inhibited atrial volume receptors: - hypothalamus: 1. thirst inhibited 2. vasopressin inhibited
28
increased osmolarity direct effects
pathological dehydration: adrenal cortex, decreased aldosterone secretion
29
increased osmolarity reflexes
osmoreceptors: hypothalamus - thirst stim -vasopressin secretion
30
decreased osmolarity direct effects
pathological hyponatremia: adrenal cortex, increased aldosterone secretion
31
decreased osmolarity reflexes
osmoreceptors: hypothalamus - decrease vasopressin secretion
32
homeostatic response to severe dehydration, what is severe dehydration physiologically
loss of ECF volume, decrease bp, increase osmolarity
33
what are the 4 compensatory mechanisms to overcome dehydration
1. CV system 2. renin-angiotensin system 3. renal mechanisms 4. hypothalamic mechanisms
34
what are the 3 ways that compensatory mechanisms aim to restore the 3 factors of dehydration
1. conserve fluid to prevent further loss 2. trigger CV reflexes to increase bp 3. stimulate thirst so normal fluid volume and osmolarity can be restored
35
aldosterone during severe dehydration
decreased ECF volume (bp) signals to increase aldosterone BUT at the same tome increased osmolarity overrides this and inhibits aldosterone release
36
CVCC and severe dehydration (signal and 5 steps)
carotid and aortic baroreceptors signal CVCC - heart rate goes ip as SA node control shifts from para to symp - force of ventricular contraction increase from sympathetic stimulation - symp input to arterioles increase peripheral resistance - symp vasoconstriction of afferent arterioles in kidney decreases GFR, conserves fluid - increased symp activity at granular cells increases renin secretion
37
renal mechanisms during severe dehydration (1 step)
decreased bp directly decreases GFR
38
RAS mechanisms during severe dehydration (2 steps)
paracrine feedback at macula densa cells causes granular cells to release renin (ANG path) granular cells respond to decreased bp by releasing renin
39
hypothalamic mechanisms to severe dehydration (1 step)
decreased bp and volume, increased osmolarity and increased ANG2 all stimulate vasopressin and thirst centers of hypothalamus ANG2 reinforces CV response
40
3 results of integrated mechanisms for severe dehydration
1. rapid attempt by CVCC to maintain bp (depending on volume loss, it may not completely restore pressure) 2. restored volume by water conservation and fluid intake 3. restored normal osmolarity by decreased Na reabsorption and increase water reabsorption and intake
41
how does change in pH denature proteins
changes in H+ conc results in disruptions of hydrogen bonds
42
symptoms of acidosis
CNS depression, confusion, coma
43
alkalosis symptoms
hyperexcitability in sensory neurons and muscles sustained resp muscle contraction
44
largest source of acid on a daily basis in the body?
CO2 aerobic metabolism
45
3 mechanisms for pH homeostasis
1. buffers (first line of defense) 2. ventilation (handles 75% of disturbances), chemoreceptors 3. renal regulation of H+ and HCO3- (slowest) excrete HCO3 instead of H
46
what is a buffer
a molecule that moderates but does not prevent changes in pH by combining with or releasing H+
47
what happens to a solution without a buffer when you add acid? With buffer?
sharp change in pH prescence of buffers the H+ added is bound and pH change is slightly moderated or unnoticiable
48
examples of intracellular buffers
cellular proteins (hemoglobin), phosphate ions (HPO4-2, H2PO4-)
49
cellular respiration results in
large amounts of HCO3, most important EXTRACELLULAR BUFFER, can now buffer H+ from non-respiratory sources
50
cellular respiration buffered by hemoglobin path
1. CO2 produced in tissues 2. 7% dissolved CO2 in plasma 3. Hb+ CO2 = HbCO2 (23%) 4. Hb+ CO2 = H2O + CO2 -> carbonic anhydrase --> HCO3- or H+ +Hb 5. HCO3- -> HCO3 out to plasma, Cl- into cell (70%)
51
CO2 + H2O <> H+ + HCO3, increase CO2
increase CO2, shift to right creating 1 H+ and 1 HCO3
52
CO2 + H2O <> H+ + HCO3, add H+ (lactic acid)
shift to left HCO3 acts as buffer creating carbonic acid = increase CO2 + increase H2O <> increase H + decrease HCO3
53
ventilation compensation for pH disturbances
peripheral and central chemoreceptors sense changes in plasma PCO2 and or H+ and signal to the resp control center to adjust ventilation
54
hypoventilation effect on pH
right shift increase CO2 + H2O -> increase H+ + increase HCO3
55
hyperventilation effect on pH
left shift decrease CO2 + H2O <> decrease H+ + decrease HCO3
56
kidney effect on pH
1. direct: altering rates of excretion or reabsorption of H+ 2. indirect: alter rate of HCO3- buffer is reabsorbed or excreted
57
kidneys during acidosis
excess H+ is buffered by ammonia in tubule cells or enters lumen and is buffered by phosphate ions
58
proximal tubule secretion of H+ and reabsorption of HCO3 pathway
1. HCO3 and Na filtered in. Na/H exchanger secretes H+ into filtrate 2. H+ in filtrate combines with filtered HCO3 to to form CO2 3. CO2 diffuses into cell 4. CO2 combines with H2O to form H+ and HCO3 5. H+ secreted again via Na/H exchanger 6. HCO3 reabsorbed with Na 7. glutamine is metabolized to ammonium NH4 and HCO3, taken into cell 8. NH4 is secreted and excreted
59
acidosis in collecting duct
type A intercalated cells function to increase H+ secretion Reabsorb HCO3 usually increase K reabsorption (hyperkalemia)
60
alkalosis in collecting duct
Type B intercalated cells increase H+ reabsorption increase HCO3 secretion usually increase K secretion (hypokalemia)
61
4 types of pH disturbances
1. Resp acidosis 2. Resp alkalosis 3. metabolic acidosis 4. metabolic alkalosis
62
resp acid
alveolar hypoventialtion results in CO2 retention and elevated plasma CO2 *increase CO2* + H2O -> increase H increase HCO3 -pulmonary fibrosis - skeletal muscle disorders (muscular dystrophy) because of rep origin compensation must occur from renal mechanisms excrete H+, reabsorb HCO3
63
resp alk
less common, hyperventialtion in absence of increased metabolic CO2 production *decrease CO2* + H2O <- decrease H + decrease HCO3 clinic: excessive artificial resp (ventilator) physiological: anxiety induced paper bag: rebreathing CO2 will raise plasma CO2 levels renal comp: HCO3 excretion, H+ reabsorption
64
metabolic acid
dietary or metab input of H+ exceeds H+ excretion lactic acidosis as a result of anaerobic metab ketoacidosis from excessive breakdown of fats and some aa or excessive HCO3 loss (diarrhea) increase CO2 + H2O <- *increased H+* + decrease HCO3 H+ enters blood, HCO3 enters intestine clinic: rare, usually resolved by resp and slow renal comp: HCO3 reabsorbed, H+ excreted
65
metabolic alk
excessive vomit, excessive ingestion of bicarbonate containing antacids decrease CO2 + H2O -> decreased H+ + *increase HCO3* usually rapidly resolved by decreasing ventilation, effectiveness limited bc can cause hypoxia renal comp: HCO3 excreted, H+ reabsorbed

BMSC 208 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions