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Renal Holy Grail > PH, BG, PR > Flashcards

PH, BG, PR Flashcards

1
Q

Physiological functions of mineralocorticoids

A
  1. Increase sodium and water uptake.
  2. Increases blood glucose.
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2
Q

Analysis of acid base status

A

.

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3
Q

Cell types in the nephron­ properties of principal cells

A

Principal cells reabsorb NaCl, water into the blood and secretes K into the lumen. This reabsorption of Na yield a negative lumen which drives the absorption of Cl.

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4
Q

Comparison of the clearance of a substance with inulin clearance

A

Clearance of inulin is e​qual to GFR​: (Cx/Cinulin)=(Cx/GFR)

If Clearancex = 0­-1 → lower than GFR (inulin) = ABSORBED

If Clearancex = 0­-5 → higher than GFR (inulin) = SECRETED

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5
Q

Control of renin release in kidneys

A

Renin released to INCREASE blood pressure to the kidneys. If there is too little pressure, renin activates the angiotensin pathway. If there is too much pressure, this happens:

↑ GFR­­ = ↑ NaCl to m​acula densa­​­ = Macula densa cells begin uptaking NaCl via with Na/Cl/K symporter­​­ = ↑ of ATP and ADO(inactive ATP) in the cell­­ = A​TP binds to P​2x receptor* ​and​ADO​binds to A​1 receptor*­​­ (on arteriole) = ↑ Increase in calcium of Afferent A­­rteriole = CONTRACTION = ↓ GFR & ↓ RENIN

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6
Q

Compensation of respiratory alkalosis

A

BE = NEGATIVE for compensation

1 HCO3 / 10 pCO2

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7
Q

Factors affecting O2 affinity of the blood

A

Hydrogen ion:​ as H concentration changes, O2 affinity changes because hydrogen ions bind. High Hydrogen shifts the equilibrium and dissociation curve to the right. Low H shifts the equilibrium to the left.

Carbon dioxide:​ High PCO2 lowers the affinity (right shift).

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8
Q

Calculation of filtration pressure

A

.

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9
Q

correction of metabolic acidosis

A

base required = -BE x 0.3 x body weight

1 HCO3 / 10 pCO2

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10
Q

correction of metabolic alkalosis

A

base required = +BE x 0.2 x body weight

1 HCO3 / 10 pCO2

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11
Q

Effects mediated by constriction of renal afferent arterioles

A
  1. Changes in afferent arteriolar resistance: ↓ resistance ↑ PGC and GFR….↑ in resistance ↓ both.
  2. Changes in efferent arteriolar resistance: ↓ resistance ↓ PGC and GFR
  3. Changes in renal arteriolar pressure (secondary to changes in MAP): ↑ blood pressure ↑ PGC (which enhances GFR), whereas ↓ blood pressure ↓ PGC (which reduces GFR).
  • Constriction of the afferent arteriole (A) decreases PGC because less of the arterial pressure is transmitted to the glomerulus, thereby reducing GFR.
  • In contrast, constriction of the efferent arteriole (B) elevates PGC and thus increases GFR. Dilation of the efferent arteriole (C) decreases PGC andthus decreases GFR.
  • Dilation of the afferent arteriole (D) increases PGC because more of the arterial pressure is transmitted to the glomerulus, thereby increasing GFR.
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12
Q

SNS affects on renal arterioles

A

↑ SNS = efferent and efferent arteriolar vasoconstriction = ↓ GFR and RBF.

Not only does this allow blood volume to be redirected to more critical organs, such as the brain, the reduced GFR decreases the capacity of the kidney to filter and thus potentially excrete critical ECF volume.

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13
Q

Effect of ADH on osmolarity of tubular fluid

A

ADH is released in response to increased osmolarity in the blood (remember ADH keeps WATER)

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14
Q

Parameters needed for calculation of clearance

A

Cx= V*Ux/Px

the amount of substance cleared from blood = urine volume x amount of substance in urine / plasma concentration on substance

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15
Q

Substances used to determine renal plasma flow

A

To find RPF, find out what was coming in and going out

RPF (Pa-­Pv)=V*U

RBF x (1-hematocrit)

the amount of plasma/concentration of filtrates in the blood that passes thru nephron

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16
Q

Tubular function­changes in TF/P ratio for filtered solutes along the proximal tube

A

SODIUM CONCENTRATION DOESN’T CHANGE ​even though it’s reabsorbed. This is because water is absorbed with it . I​nulin and Cl ­ increase

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17
Q

Urine concentration and dilution­role of vasa recta

A

Vasa Recta produces​ hyperosmotic (​concentrated) urine ​if ADH is present

Vasa Recta produces​ hypoosmotic (​diluted) urine ​if ADH is absent

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18
Q

Hormones that regulate calcium homeostasis

A

PTH increases blood Ca+ levels, decreases PO4

Calcitonin decreases Ca+ levels
Calcitriol increases Ca+ levels and PO4

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19
Q

Stimuli for the release of ADH

A

Hypovolemia

Low blood pressure

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20
Q

Mass balance by renal handling of a substance

A
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21
Q

Reabsorptive functions of nephron segments­proximal tubule

A

Proximal tubule is p​ermeable to water​ (ascending loop and distal tubule aren’t)

  • First half: ​absorb Na+ via a Na/H antiporter and a Na/X symporter. Pump out Na out into blood and K in. Water is absorbed, leaving CL- behind
  • Second Half: A​bsorb n​egative ions and ​also the leftover Cl. water follows = positive lumen POSITIVE

At the end of the proximal tubule:​ Bicarbonate and glucose and AA are low ​because they were absorbed. Creatinine and Urea still high. Cl slightly high.

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22
Q

Effections of dilation of efferent arterioles on renal hemodynamics

A

Efferent arteriole is AFTER the glomerulus

Glomerular pressure INCREASE because its backed up.

RPF DECREASE because of increased resistance

GFR is depends at which point you are at

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23
Q

Evaluation of buffer capacity

A

Phosphate buffer: intracellular and extracellular buffer (not available in erythrocytes!!!)

Proteins are a good buffer but are not available it has a very low intracellular concentration. They are many proteins which can be a buffer for a wide range of pHs. The one’s closest the neutral are histidine, cysteine, and ammonia.

Bicarbonate/Co2 buffer is a good intracellular buffer but not a good extracellular buffer. It can be a good extracellular buffer if it’s open to the body.

24
Q

Effect aldosterone as a hormone replacement

A

Increase Na/H2O absorption
Can cause hypokalemia and alkalosis

25
Q

Actions of aldosterone­effects of increased plasma levels on plasma K+ and pH

A

Aldosterone ​increases K secretion​ across the apical membrane (there’s increased K in the tubular fluid, less in the blood)
Increased K plasma levels drive aldosterone production.

Too much aldOsterone can lead to hypOkalemia and alkalOsis.

26
Q

Changes in ion concentration along the proximal tubule

A
27
Q

Renal handling or organic anions and drugs

A

High AG: n​ew unmeasured anion exogenous acid. Chlorine and low bicarbonate.

→ Examples would be lactic acidosis, ketoacidosis, chronic renal failure, methanol, ethanol, and rhabdomyalysis.

Normal AG: h​igh chlorine replaces the lost HCO3­ which is why we don’t see it.

→ Ex. Diarrhea, RTA, HCl ingestion, and CA inhibitors.

28
Q

The corticopapillary osmotic gradient and urine concentrating ability

A

Plasma ADH levels will set the urine osmolality, ­high urine osmolality AND high plasma osmolarity­ increases thirst, through osmoreceptors­ increase ADH release and increase in H20 reabsorption.

Plasma osmolarity is the primary regulator of ADH release.

29
Q

primary regulator of ADH release.

A

Plasma osmolarity is the primary regulator of ADH release.

30
Q

Intestinal effect of aldosterone

A

Absorption in the colon is lower quantity and under fine control. Its product, fecal material, is typically quite dry containing about 100 mL of water excreted this way per day. Aldosterone increases absorption. Thus aldosterone can act on colonocytes in much the same way it does in the kidney to increase colonic fluid absorption of sodium and water therefore to maintain blood volume and pressure. The colonic response to aldosterone is not nearly as important a process for water balance as the response of the kidneys to this hormone.

31
Q

Response of renin­-angiotensin system to renal ischemia

A

Renin is secreted by the juxtaglomerular cells when the intraglomerular pressure is too low.

Angiotensin 2 upregulates the blood pressure by constricting the blood vessels and potentiating the effects of NE on vascular tone.

It releases aldosterone from the adrenal cortex.

ACE inhibitors are standard antihypertensive drugs. In addition to preventing angiotensin synthesis they also inhibit the breakdown of the vasodilator peptide bradykinin.

Also available are angiotensin receptors blockers and renin inhibitors.

32
Q

Amino acid disease causing black diapers

A

Alkaptonuria­­ → can’t digest tyrosine

Mutation in h​omogentisate oxidase

Defect in Tyrosine Catabolism

33
Q

Amino acid metabolized by kidneys in acidosis

A

Glutamine ​

(EASY POINT, REMEMBER THIS)

34
Q

Use of Benzoic acid and phenylacetic acid in hyperammonemia

A

Benzoic acid​ is also called h​ippuric acid.​ It provides an alternative route of nitrogen excretion

Phenylbutyrate a​ka phenylacetic acid removes t​wo nitrogens​ at a time so it’s the ​preferred method.​

*b​oth of these “soak up” extra nitrogens in the body

35
Q

Enzyme producing melanin

A

N actelytransferase

36
Q

Tyrosine requirement in PKU

A

Tyrosine is the precursor to make phenylalanine, which is what PKU people lack

37
Q

Reduction of phosphate foods in chronic renal failure

A

Reduction of phosphate foods in chronic renal failure

38
Q

Identify defective enzyme in patient with PKU despite normal Phe hydroxylase

A

Other possibilities: Don’t have BioH4

OR (more likely)

dihydropteridine reductase

39
Q

restriction for PDH deficiency

A

ALANINE

40
Q

Actions of angiotensin converting enzyme

A

Converts angiotensin I (in lung) into angiotensin II. Angiotensin II works in the kidney to increase ADH levels, increasing water uptake.

This increases blood pressure.

41
Q

Mechanism of action of drugs used to treat heart failure

A

Loop diuretics: ​Furosemide­­ → inhibition of Na/Cl/K symporter in thick ascending loop

42
Q

Adverse effects of tolvaptan

A

Vasopressin (antidiuretic hormone) a​ntagonists nausea, xerostomia (dry mouth) hypotension, hypokalemia

taken at home

43
Q

Molecular mechanism of action of acetazolamide

A

‘zolamide’
Carbonic anhydrase inhibitor; decreases bicarbonate

44
Q

Urinary electrolyte porile produced by loop diuretics

A

Loop diurectics decrease kidney’s ability to concentrate urine
Increased renal excretion of Na, CL, K, H, Ca

Urine will be a​cidic

45
Q

Adverse effects of furosemide
­

A

used in heart failure -loop or high ceiling diuretics

MOA: inhibiting the Na/K/2Cl cotransporter in the loop of Henle thick ascending loop specifically

Pharmacological effects: promotes excretion of NaCl, H, K, Mg, and Ca

Side Effects: hyperuricemia, hypokalemia, hypocalcemia, hypomagnesium, and h​earing impairment

46
Q

Diuretics used to treat nephrolithiasis

A

Thiazide diuretics

47
Q

Pharmacological actions/effects and clinical uses of hydrochlorothiazide

A

MOA: blocks the action of Na/Cl cotransporter in the luminal of the distal convolute tubule

  • ­inhibits NaCl reabsorption in the DCT
  • ­produces diuresis
  • ­promotes renal excretion of K and H
48
Q

Adverse effects of indapamide

A

Indapamide is a thiazide

  • Hypokalemia
  • metabolic alkalosis
  • Hypovolemia
49
Q

Appropriate drugs for the treatment of ascites associated with right sided heart failure

A

Furosemide

50
Q

Molecular target of furosemide

A

Inhibition of Na/K/Cl symporter in the ascending loop of Henle

51
Q

Mechanism of action of desmopressin

A

V2 receptor agonist, used for central diabetes insipidus.

Can’t use it for nephrogenic diabetes because V2 receptors are unresponsive.

For nephrogenic diabetes, use thiazides.

52
Q

Adverse effects of mannitol

A

Think of mannitol as a sugar we use to “soak up” any excess fluid in our patient (like cerebral edema)

  • Adverse effect in patients with normal kidney function: extracellular volume contraction (losing too much fluid) which leads to h​ypovolemia, dehydration, hypernatremia
  • Adverse effect in patients with cardiac or renal disease: volume expansion (because they can’t pee out the excess fluid) which can cause hypervolemia, hyponatremia, pulmonary edema
53
Q

Appropriate treatment for lithium induced nephrogenic diabetis insipidus

(hint: thiazides)

A

Thiazides and thiazide­-like:

  • Hydrochlorothiazide
  • Indapamide
  • sulfonamides

Work in early distal convoluted tube and d​ecrease absorption of NaCl

Mechanism of action: Thiazide and thiazide like diuretics inhibit Na/Cl symporter.

Results in reduced reabsorption of NaCl.

Some thiazides (including hydrochlorothiazide and indapamide) are also weak inhibitors of carbonic anhydrase.

Therapeutic use: hypertension, edema in the heart or kidneys, and nephrogenic diabetes insipidus (seems­paradoxical­likely mediated via extracellular volume contraction promotes proximal tubule Na and water reabsorption. Therefore, a reduced volume is delivered to the distal tubule)

54
Q

Molecular mechanism of action of dorzolamide

A

Carbonic androhyde inhibitor → ​decreases the synthesis of H3CO2 (bicarbonate) from H2O and CO2

Since it works on pH we use it for any condition dealing with pH homeostasis: mountain sickness, epilepsy, alkalosis due to thiazide or loop diuretic use

Works in the p​roximal tubules

55
Q

Use of diuretics in treatment of acute pulmonary edema

A

Loop Diuretics

  • Furosemide
  • ethacrynic acid

Inhibit Na/K/Cl symporter in (Ascending?) loop; There’s no negative charge on the lumen side so no Mg/Ca paracellular transport, no water follows.

Renal Holy Grail (2 decks)

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