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Physiology And Pharmacology > Kidneys > Flashcards

Kidneys Flashcards

1
Q

Glomerular filtration rate and % of plasma filtered in glomerulus

A

The volume of fluid filtered into the glomerulus per minute.

Normal 125 ml/min. 20% of plasma

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2
Q

Renal clearance/ osmotic clearance and equation

A

Volume of blood cleared of a substance over time U x V / P

Osmotic clearance is the volume of plasma cleared of all osmotically active particles per unit time.

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3
Q

Renal plasma flow

A

Volume of plasma going into kidney over time 600 ml/min Renal blood flow = 1100 ml/min

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4
Q

Glucose reabsorption

A

Occurs in proximal convoluted tubule

Enters with sodium glucose cotransport

Exits with glut facilitated transport

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5
Q

Amino acid reabsorption

A

8 amino acid transporters, 6 of which sodium dependent

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6
Q

molecules that get reabsorbed via Na Coupled transporters and passive reabsorptions in the proximal convoluted tubule:

Urea, amino acids, phosphate, glucose, chloride, calcium, sulphate, potassium

A

Na Transporters: Glucose, amino acid, phosphate, sulfate

Passive diffusion: Urea, chloride, potassium, calcium

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7
Q

Secretion of organic acids anions (where how)

A

Proximal tubule

  1. Organic anion p enters in exchange for dicarboxylate through organic anion transporter
  2. OA enters tubule via ATP dependent transporters Dicarboxylate comes from sodium coupled Transporters
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8
Q

Organic cation secretion

A

Occurs in proximal convoluted tubule

  1. Enters via facilitated organic cation transporter (OCT2)
  2. Enters tubule via multi drug and toxin extrusion protein (MATE2-K/MATE1) in exchange for H+
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9
Q

Osmolality

A

Osmoles of solute per kg of solvent

measure of water concentration- if low, water is high

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10
Q

Normal urine osmolality

Normal plasma osmolality

Normal plasma sodium concentration

A

Urine: 50-1400 mosm/kg

Plasma: 285-295 mosm/kg

Sodium: 135 -145 mmol/l

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11
Q

Sodium reabsorption in proximal tubule

A

In: Na nutrient symporter, Na H exchanger

Out: Na/K pump Cl passively diffuses our

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12
Q

Sodium reabsorption thick and thin ascending limb

A

In: Na K CL cotransporter

Out: sodium potassium pump Cl passively diffuses out

Thin: passive diffusion

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13
Q

Sodium reabsorption distal tubule

A

In: Na Cl cotransporter

Out: sodium potassium pump Cl passively diffuses out

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14
Q

Sodium reabsorption in collecting duct

A

In: Na channel Out: Na k pump (principal cell)

In: Na/ H+ transport Out: Na K pump (intercalated cells)

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15
Q

Urea movement (pCT, Henle, CD) and effect of ADH on their reabsorption.

A

Proximal tubule: passive reabsorption

Loop of henle: apical secretion via urea transporter 2 (UT2)

Inner medullary collecting duct: apical reabsorption via UTA1

Net movement: 40 filtered is excreted, 60% reabsorbed\

ADH increases reabsorption

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16
Q

ADH action on collecting duct

A

ADH binds to V2 receptors on collecting duct, causing the activation of cAMP pathway and migration of aquaporin protein to luminal membrane Water can be reabsored through channels

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17
Q

Polyuria/ oliguria

A

Polyuria: excessive urine output

Oliguria: too low urine output -> less than .428L/day (obligatory water loss for all waste to be excreted)

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18
Q

Free water clearance calculation

A
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19
Q

Diuresis vs antidiuresis pathway

A
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20
Q

Production of ADH in posterior pituitary

A

Osmoreceptors in hypothalamus signal to magnocellular neurosecretory cells in paracentricular and supraoptic nuclei. These produce precursors to ADH that enter posterior pituitary and produces ADH

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21
Q

Effects of alcohol, nicotine BP and blood volume on ADH secretion

A

Alcohol inhibits ADH Nicotine stimulates ADH

BP: lower pB increases secretion

Volume: lower volume increases secretion

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22
Q

Neurogenic diabetes insipidus origins and what it is

A

excessive urination

No ADH secretion

Can be congenital or due to an injury

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23
Q

Nephrogenic diabetes insipidus origin and what it is

A

Excessive urination because no water reabsorption

Issue at level of kidney:

Inherited (mutated V2 receptor or aquaporin)

Acquired (infection or side effect of drug)

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24
Q

Mechanism of osmotic diuresis

A

Increased blood glucose

Increased glomerular filtration of glucose

Increased osmolality

Reduced reabsorption if water because smaller conc. gradient so greater water loss in urine

25
Q

K reabsorption in proximal tubule

A

Passively diffuses out (channels)

26
Q

K reabsorption in thick ascending limb and distal tubule

A

In: Na K Cl cotransporter

Out: facilitated diffusion In distal tubule via k H exchanger

27
Q

K transport in collecting duct

A

Reabsorption in intercalated cells: k h exchanger K

secretion by principal cells

Out: k channels (ROMK, BK) and K CL co transporter

28
Q

Factors affecting k secretion in principal cells of collecting duct (Na, aldosterone, tubular flow, pH)

A
  1. Factors affecting Na entry through ENaC channels (if more Na in cells, more k will flow out)
  2. Aldosterone stimulates k channels
  3. High tubular flow rate favors secretion (+ charges washed away in lumen so K+ has more space to go in)
  4. Acidosis inhibits, alkalosis enhances it
29
Q

Hypokalemia causes and level at which it becomes hypokalemia

Main issues caused by hypokalemia

A

Less than 3.5mM

Resting membrane potential becomes more negative. So nervous symptoms (Cardiac, skeletal muscle, GI, renal)

30
Q

Hyperkalemia causes and signs

A
  1. Decreased external loss (renal failure, hYpoaldosteronism) 2. Redistribution out of cells (acidosis, tissue destruction)

Can cause hyperreflexes, vomiting, nausea, dysrythmias because resting membrane potential is increaed so easier to depolarise cells.

31
Q

Main solutes in body

A

Sodium, potassium, glucose

32
Q

Pathways controlling sodium reabsorption

A

stimulate renin release (angiotensin)

aldosterone

atrial natriuretic peptide

dopamine

33
Q

Causes of renin release (4) and where it is released from

A

Decreased sodium delivery to macula densa

Decreased wall tension in afferent arteriole (baroreceptors)

Sympathetic activity

Low blood volume

Released from juxtaglomerular cells

34
Q

Formation of angiotensin

A

Plasma angiotensinogen -> angiotensin I (due to renin)

Angiotensin I (10 peptide) to angiotensin II (8 peptide) via converting enzyme.

35
Q

Effects of angiotensin (5)

A
36
Q

Effects of aldosterone

A

Stimulates expression of ENaC channels, ROMK channels and sodium potassium pumps in collecting duct principal cells.

Stimulates K secretion and sodium reabsorption

37
Q

Natriuretic peptide (what they are and what they do)

A

Hormones released when the heart is stretched.

Natriuretic effects: Inhibit ENaC in collecting duct. (sodium reabsorption). Inhibits Na/K pump activity. Inhibit aldosterone production

Diuretic effects: Inhibit renin release

Hypotensive effects: Decrease blood pressure/ volume, vasodilate afferent arterioles

38
Q

pH of buffer solution with Henderson hasselbach equation

A

pH= pK + log[HCO3]/[H2CO3]

39
Q

Where bicarbonate reabsorption occurs

A

Proximal tubule Ascending loop of henle Cortical collecting ducts (intercalated cells)

40
Q

HCO3 reabsorption

A

Bicarbonate is filtered in glomerulus

It binds to an H+ in lumen

It becomes water and CO2 and passively diffuses into interstitial cell

It can then be broken back down to H+ and HCO3- HCO3 is reabsorbed and H+ goes back into lumen

41
Q

Importance of HCO3

A

It is an essential body buffer that binds with H+ to form water and CO2. CO2 can then be excreted by lungs.

42
Q

H+ excretion

A

H combines with non bicarbonate ion and is excreted Or Glutamine in tubule enters epithelial cells and gets broken down to Nh4 nd bicarbonate. Bicarbonate is reabsorbed

43
Q

Acute vs chronic respiratory acidosis

A

Acute: abrupt failure in respiration ph less than 7.35

Chronic: secondary to many disorders, less abrupt but longer lasting

44
Q

Response to acidosis

A

Chemical (bicarbonate buffer)

Respiratory (to expel CO2)

Renal (increased glutamine metabolism, secretion of H + ions)

45
Q

Response to alkalosis

A

Chemical buffers: some bicarbonate reacts with H+ to produce CO2, this gets rid of some bicarbonate but still causing pH to decrease.

Respiratory: reduce ventilation

Renal compensation: reduction in H secretion, bicarbonate is therefore excreted in urine. Type B intercalated cells also add H to blood using pendrin and CO2 and water

46
Q

Structure of the glomerolus filtration membrane (3 layers) and role of this last layer.

A
  1. Widely fenenestrated capillary
  2. basement membrane (protein layer)
  3. podocytes and filtration slits. These serve to only let certain molecule sizes get through.
47
Q

Cortical vs juxtamedullary nephrons

A

Cortical: mostly in the cortex, shorter loop of henle - produces more dilute urine

Juxtamedullary: longer loop of henle descending into medulla - produces more concentrated urine

48
Q

Vasculature of the kidneys; pathway

A

Interlobular artery to glomerulus, the peritubular capillaries drain to interlobular vein.

49
Q

Size of molecules at which filtration through bowman’s capsule becomes difficult

A

7kDa

50
Q

Do anions of cations cross the glomerular filtration membrane better? Why?

A

Cationns: because negative charges fixed on basement membrane

51
Q

How starling forces influence glomerular filtration rate

A

Starling forces:

  1. hydrostatic pressure: fluid pressure pushing it into glomerulus (can be controlled by vasodilation/ constriction of afferent and efferent arterioles)
  2. oncotic pressure: pressure generated by solvents pushing it into capillaries
52
Q

How inulin is used to measure GFR and why it is good for this. What PAH is good for measuring

A

Inulin concentrations in urine and plasma over time can be used to measure clearance, which is equivalent to the GFR because:

It gets fully filtered at glomerus

Does not get secreted in proximal tubule

Does not get reabsorbed

Does not get metabolised

PAH gets fully secreted so it’s clearance is approx equivalent to Renal blood flow

53
Q

Concept of countercurrent and how this explains water reabsorption and generation of a concentrated urine

A

In ascending limb of the loop of henle, Na is pumped out via triporter, which causes water in the descending loop to flow out to match this osmolarity. When it gets to the ascending loop, there is less of it but water cannot flow back in because ascending loop is impermeable to water. Water volume is therefore reduced.

54
Q

Mechanism of Extrinsic control of GFR (when BP is too low)

A

Extrinsic: maintains arterial blood pressure by activation the sympathetic nervous system, which vasoconstricts the afferent arterioles. Also reduces filtration barrier via mesengial cells (

Intrinsic: Protexts renal capillaries from hypertensive damage and maintains healthy GFR

55
Q

Reaction of carbon dioxide and water forming H+ and bicarbonate and what diahrrea and vomitus effects on these products

A
56
Q

Important buffers in urine

A

Phosphate and ammonia

57
Q

Role of glutamine as an additional mechanism for adding HCO3 to plasma

A
58
Q

changes in these for the following disorders

A
59
Q
A

Physiology And Pharmacology (5 decks)

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