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APEX > Kidney & Diuretics & Liver > Flashcards

Kidney & Diuretics & Liver Flashcards

1
Q

What is contained in the renal cortex?

A

Most parts of the nephron
Glomerulus, Bowman’s capsule, proximal and distal tubule

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2
Q

What is contained in the renal medulla?

A

The inner part of the kidney. (more @ risk for hypoxia)
Loop of Henle & Collecting Ducts

-The medulla is divided into pyramids. The APEX of each pyramid is called the papilla. This part has a lot of collecting ducts.

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3
Q

Discuss the drainage of the papilla

A

Papilla drains urine > minor calyxes > major calyces > renal pevlics > ureter

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4
Q

What are the 2 key hormones that govern how the kidney regulates ECF volume and composition?

A

-Aldosterone controls na+ and h2O reabsorption (together)
-ADH controls plasma osmolarity

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5
Q

What is calcitrol?

A

Calciferol is synthesized from Vit. D ingestion or following UV light exposure. In the liver its converted to inactive vit d.

In the kidney under control of parathyroid hormone vid d is converted to the active form.

Calicitriol = 3 functions = absorb calcium in intestines, bone to store calcium, and kidney to reabsorb calcium and phosphate

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6
Q

how much blood flow do kidneys receive

A

20 - 25%

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7
Q

Discuss blood flow of kidneys

A

renal artery > renal segmental artery > interlobar artery > arcuate artery > interlobular artery > afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed > venules

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8
Q

Discuss TG feedback

A

JG apparatus is located in distal tubule
Specifically the region that passes btw afferent and efferent arterioles. JG cells recognize changes in sodium/water concentration. & Release renin

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9
Q

Discuss the surgical stress response on kidneys

A

Transient state of vasoconstriction and sodium retention. This persists for several days resulting in oliguria and edema.

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10
Q

What contributes to vasodilation

A

Kinins
Prostaglandins
ANP

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11
Q

What casues the release of renin by the JG cells

A
  1. decreased perfusion
  2. sns activation (B1)
  3. TG feedback
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12
Q

What converts angiotensinogen to AT1

A

RENIN

and ACE converts AT 1 to AT 2

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13
Q

List the effects of AT 2

A

Vasoconstriction of peripheral vessels and efferent arteriole
Aldosterone and ADH release
Na+ reabsorption in the PCT
Thirst

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14
Q

Where is aldosterone produced?

A

Zone GLOMERULOSA of the adrenal gland.

It stimulates the Na/K ATPASE pumps in the distal tubules and collecting duct.

Results in = sodium/water reabsorption, k and h excretion

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15
Q

Where is ADH produced?

A

Suproptic and paraventricular nuclei of the hypothalamus. Released from posterior pituitary gland.

Increased blood volume from V2 stimulation in collecting ducts (incr’d cAMP)

Increased SVR from V1 stimulation in the vasculature (IP3, DAG, CA)

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16
Q

DA1 vs DA2 receptors

A

DA 1 @ renal vasculature, renal tubules
= increased cAMP = vasodilation, diuresis

DA2 @ presynaptic SNS nerve terminal
= decreased cAMP and decr’d NE release

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17
Q

Fenoldopam

A

= selective DA1 receptor agonist that increases RBF.

0.1 - 0.2 mcg/kg/m

may offer renal protection during aortic surgery and during CPB

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18
Q

How much of the RBF is filtered at glomerulus?

A

RBF = 1000 - 1250 mL/m
GFR = 125 ml/m ~ 20% of RBF

The remaining 80% is delivered into the peritubular capillaries

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19
Q

What are the 3 determinants of glomerular hydrostatic pressure?

A

MAP, afferent arteriole resistance, efferent arteriole resistance

glomerular hydrostatic pressure is the most important determinant of GFR!!

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20
Q

Describe the fate of sodium at each location in the nephron

A

PCT = 65%
LOH = 20%
DCT = 5%
CD = 5%

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21
Q

What are the key functions of each part of the nephron

A

PCT = bulk reabsorption of solutes, water
LOH Descending= countercurrent mechanism (tubular fluid concentrated) and high permeability to H2O
LOH (Ascending) = countercurrent mechanism (tubular fluid diluted) and no permeability to water
Distale Tubule = fine tunes solute concentrations (ADH and aldosterone)
Collecting Duct = regulates final concentration of urine (aldosterone and ADH)

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22
Q

List 3 tests of GFR and give normal values

A

BUN (10 - 20)
Cr (0.7 - 1.5)
Cr Cl (110 - 150 mL/m)

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23
Q

List 4 tests of tubular function

A

Fractional excretion of Na+ % = 1 - 3%
Urine osmolaliity = 65 - 1400 msOsm/kg
Urine sodium concentration = 130 - 260 mEq/day
Urine specific gravity = 1.003 - 1.030

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24
Q

BUN

A

Urea is the primary metabolite of protein metabolism in the liver.

Amino acids - ammonia - urea

B/c urea undergoes filtration AND reabsorption, it is a better indicator of uremic symptoms than as a measurement of GFR>

25
Q

What is included in the differential diagnosis of a low BUN?

A

< 8

overhydration

d/t decreased urea production - malnutrition or severe liver dx

26
Q

High BUN?

A

20 - 40

dehydration
increased protein input, catabolism, or decr’d GFR

27
Q

What is the BUN:Creatinine ratio?

A

Helps us evaluate the status of hydration. Nml = 10:1
> 20:1 = prerenal azotemia

or non-renal causes of elevated BUN can cause this

28
Q

What is the best indicator of GFR?

A

CREATINE CLEARANCE

(140 - age) x kg/ 72x cr

if female multiply by 0.85

29
Q

How do you interpret the fraction excretion of sodium?

A

Fe(Na+) < 1% = prerenal azotemia b/c more sodium is conserved relative to the amount of creatine cleared
> 3% = impaired tubular function

30
Q

Carbonic anhydrase inhibitors

A

Acetazolamide, Dorzolamide

Noncompetitive inhibition of carbonic anhydrase in the PCT - net gain of H+, Cl- and loss of HCO3 and Na

ADR: metabolic acidosis and hypokalemia!

31
Q

Osmotic diuretics

A

-Mannitol, glycerin, isosorbide

Sugars that undergo filtration but not reabssorption. PCT and LOH are the primary sites.

32
Q

Loop diuretics

A

furosemide, bumetanide, ethacrynic acid

poison the Na/K/2CL transporter in the medullary region of the LOH. The amount of sodium remaining in the tubule overwhelms the distal tubule reabsorption capability. Thus, a large volume of dilute urine is excreted. Potassium, calcium, magnesium, and chloride are also lost to the urine.

ADR: hypokalemia, hypochloremic metabolic alkalosis, ototoxicity (ethacrynic acid > furosemide), reduced lithium clearance

33
Q

Thiazide diuretics

A

HCTZ, metolazone, indapamide

Inhibit the NaCl transported in the distal tubule

treats osteoporosis by reducing calcium excretion.

ADR: hyperglycemia, hypercalcemia, hyperuricemia, metabolic alkalosis (hypochloremic hypokalemia)

34
Q

Potassium sparing diuretics

A

Spironolactone, amiloride, triamterene

Inhibit k secretion and sodium reabsorption in the collecting ducts. (A&T) Thus, function is independent of aldosterone.

Spironolactone exists in a subclass called aldosterone antagonissts.

Treats secondary hyperaldosteronism.

ADR: metabolic acidosis, gynecomastia, decreased libido (spir), nephrolithiasis (triamterene)

35
Q

CKD and acid/base balance

A

Decreased excretion of non-volatile acid contributes to a gap in metabolic acidosis.

Gap acidosis = accumulation of nonvolatile acids

36
Q

Discuss pathophys of renal osteodystrophy

A

-D/t = decreased vitamin D production and secondary hyperparathyroidism

-inadequate supply of vit d impairs calcium absorption in GI.
-body increases PTH which gets ca+ from bones.

37
Q

What are the arterioles of the liver? Aka what is its blood supply?

A

Hepatic artery and portal vein

The central vein is the hepatic “vein” that actually drains blood.
The sinusoid is the capillary equivalent

38
Q

Describe the flow of bile from its site of production to release into the duodenum

A

-Hepatocytes make the bile
-Canaliculi drain bile into the bile duct
-The bile ducts converge to form the common hepatic duct
-The cystic duct (from the gallbladder) and the pancreatic duct join the common hepatic duct before it empties into the duodenum
-Sphincter of Oddi controls flow of bile released

39
Q

How much blood flow does the liver receive?

A

30% = 1500 mL

40
Q

Celiac artery provides blood flow to

A

Liver, Spleen, Stomach

Comes from aorta. Has a1 and b2 receptors

41
Q

Superior mesenteric artery provides blood flow to

A

Pancrease, SI, Colon

42
Q

Inferior mesenteric artery provides blood flow to

A

Colon

43
Q

Portal vein has what receptors on it

A

alpha 1 only

44
Q

What is normal portal vein pressure

A

7 - 10 mmHg

PORTAL HTN > 20 - 30 mmHg

45
Q

What is the hepatic arterial buffer response

A

Hepatic Artery Perfusion Pressure = MAP - Hepatic Vein Pressure

A reduction in portal vein flow is compensated by an increased hepatic artery flow. This is mediated by adenosine. Severe liver disease impairs this response.

46
Q

What coagulation factors are NOT produced by hepatocytes

A

Factor 3, 8, & vwF & factor 4

47
Q

What plasma proteins are produced by the liver

A

All except for immunoglobulins

Albumin & acidic drugs
Alpha 1 acid glycoprotein & basic drugs
Pseudocholinesterase metabolizes sux & esters

48
Q

Glycogenesis

A

Hyperglycemia - insulin releaased from beta cells - glucose stored as glycogen

49
Q

Glycogenolysis & Gluconeogenesis

A

Hypoglycemia - glucagon released from pancreatic alpha cells - glycogen broken into glucose

Epi released from adrenal medulla - non-carbs made into glucose

LIVER PLAYS IMPORTANT ROLE IN GLUCOSE METABOLISM

50
Q

Discuss bilirubin

A

Aged RBCS (> 120 d) are processed by reticuloendothelial cells in the spleen
-Hgb -> Heme -> Unconjugated bilirubin which binds with albumin
-Transported to the liver. Conjugated with glucuronic acid.
-Now it’s water-soluble, and it can be excreted into bile.

51
Q

AST/ALT

A

AST = 10 - 40
ALT = 10 - 50

AST/ALT > 2 = cirrhosis or alcoholic liver dx

52
Q

Name 3 tests of biliary duct obstruction. What. is the most specific?

A

5 Nucleotidase = 0 - 10 = MOST SPECIFIC
Y Glutamyl transpeptidase = 0 - 30
Alk phos = 45 - 115 (not v. specific b/c its in bone, placenta, tumors)

53
Q

Prehepatic lab dx

A

Unconjugated bilirubin will be high

caused by hemolysis, hematoma reabsorption

54
Q

Hepatocellular injury

A

Conjugated bilirbuin, AST/ALT/ PT all high

caused by cirrhosis, alcohol abuse, drugs, viral infection, sepsis, hypoxemia

55
Q

Cholestatic

A

Conjugated bilirubin, alk phos, y glutamyl all high
PT, AST/ALT albumin don’t change until late

Due to biliary tract obstruction and sepsis

56
Q

Which type of viral hepatitis has the highest incidence

A

Type A = 50%
Type B = 35%
Type C = 15%
Type D = coinfection w/B

57
Q

Anesthetic technique to maintain blood flow

A

Isoflurane
Liberal use of fluids
Normocapnia
Avoid: amio, PCN, tetracycline, sulfa

58
Q

MELD score

A

Low risk < 10
Intermediate risk = 10 - 15
High risk > 15

APEX (18 decks)

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