Renal A+P Flashcards

1
Q

What are the 3 functions of the kidney?

A

1) Excretory
2) Regulatory (Electrolytes, acid base, BP, glucose)
3) Hormone production (Erythropoietin, renin)

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2
Q

What is the significance of erythropoietin?

A

Produced in peritubular capillaries, stimulates bone marrow to increase production of erythrocytes which increases RBCs.

When O2 perfusion decreases to kidneys, kidneys produce erythropoietin or enzymes that catalyze erythropoeitin formation.

Erythropoietin deficiency is primary cause of anemia in CKD pts

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3
Q

What two types of nephrons are in the cortex?

A

1) Cortical nephrons (85%), entire nephron located in the cortex. Includes BC, PCT, DCT, LOH. Function to produce urine
2) Juxtamedullary nephrons (15%), some parts in cortex but LOH in medulla. Concentrates urine

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4
Q

What happens in the major and minor calyx?

A

Contains urine from collecting ducts

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5
Q

What happens in the medulla regarding renal function?

A

Houses LOH, concentrates urine

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6
Q

What does the renal pelvis do?

A

Uses peristalsis to move urine onwards

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7
Q

How does the bladder function?

A

As bladder fills, stretch receptors and PSNS nerves stimulate spinal reflex causing bladder contraction in relaxation of internal sphincter (involuntary). We are in control of the external sphincter which lets urine out

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8
Q

What is the normal range for Na+ and how is it regulated?

A

Normal: 135-145mmol/L

Mostly reabsorbed at PCT, throughout nephron

Increased aldosterone increases Na+ reabsorption

Decreased GFR leads to increased Na+ reabsorption and H2O follows

Loop diuretics block Na+ reabsorption

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9
Q

What is the normal range for K+ and how is it regulated?

A

Normal: 3.5-5.5 meq/L

Mostly secreted at DCT and reabsorbed in PCT

In metabolic alkalosis/acidosis, both K+ and H+ removed at DCT.

Flow rates can effect secretion in DCT

Increased serum K+ increases aldosterone and increases K+ secretion

Loop diuretics lead to Na+ loss, causes aldosterone to reabsorb Na leading to K+ s secretion and loss as a result of trade

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10
Q

How is K+ affected by metabolic acidosis and alkalosis?

A

In acidosis, K+ excretion decreased as H+ excretion is preferential.

In alkalosis, K+ excretion increased as holding on to H+ is preferential ​

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11
Q

How do loop diuretics affect K?

A

Loop diuretics lead to Na+ loss, causes aldosterone to reabsorb Na leading to K+ s secretion and loss as a result of trade

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12
Q

What is the normal range of calcium and how is it regulated?

A

Normal: 2.2 - 2.6 mEq/L

Filtered at glomerulus, most reabsorbed in PCT

In acidosis, inhibition of parathyroid hormone causes Ca++ excretion and decreased reabsorption from bone, GIT, kidneys

Decreased serum PO4 (required to bind Ca++ to be stored in bone) causes Ca++ excretion

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13
Q

What is the normal range of urea and how is it regulated?

A

Normal: BUN 3.0 - 7.0 mmol/L

Waste product of protein metabolism, filtered at glomerulus, reabsorbed in PCT, CD, secreted in LOH

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14
Q

Is BUN a reliable indicator of GFR?

A

No. Increased protein intake, pregnancy, DM can increase urea excretion

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15
Q

What is normal range of creatinine and why is it significant?

A

Normal: 60-110 umol/L for males, 50-90 umol/L for females

Filtered at glomerulus with rate of GFR, not reabsorbed or secreted. Great indicator of renal function as long as no muscle breakdown exists *rhabdomyolysis)

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16
Q

What is urine creatinine clearance?

A

Urine clearance should be proportional to serum creatinine

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17
Q

What is the function of the afferent arteriole?

A

Divisions from the renal arteries, brings oxygenated blood to nephron (to glomerulus)

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18
Q

Which arteriole is wider, afferent or efferent?

A

Afferent to allow easy blood flow to glomerulus

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19
Q

What is the function of the bowmans capsule?

A

Cup shaped structure in the cortex for cortical and juxtamedullary nephrons. Glomerulus to one side and proximal convoluted tubule on the other, allows filtration

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20
Q

What is the function of the glomerulus?

A

Tuft of capillaries nested in the BC, glomerular filtration forces fluids and solutes through the glomerular capsular membrane into the BC

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21
Q

What is the glomerular filtration rate?

A

Clinical measure of renal function, reflects CO. Comparison of serum and urine Cr.

22
Q

What is eGFR?

A

Estimation used to screen early kidney damage

<60 ml/min/1.73m2 = kidney disease
< 15 = kidney failure

23
Q

What is the function of the efferent arteriole?

A

Blood leaves glomerulus via efferent arteriole and into capillary network. Are smaller in diameter, increasing glomerular pressure and creating more effective filtration at BC.

Cortical nephrons go to peritubular capillary

Juxtamedullary nephrons go to vasa recta

24
Q

What is the function of the proximal convoluted tubule (PCT)?

A

REABSORPTION

Drains BC with hundreds of microvilli. 65% of glomerular filtrate is reabsorbed here, mainly H2O but also electrolytes, glucose, etc. Fluid leaves the PCT in an ISOTONIC state

25
Q

What happens at the PCT if serum glucose > 10.5?

A

Active glucose reabsorption transport maxes out and glucose spills into urine

26
Q

What is the function of the loop of henle (LOH)?

A

CONCENTRATION

Concentrates urine primarily by juxtamedullary nephrons. Goes deep into the hypertonic medulla region and H2O moves from tubule to interstitium

Has a descending and ascending limb

27
Q

What is the function of the descending limb of LOH?

A

H2O permeable, allows for movement of H2O

28
Q

What is the function of the ascending limb of LOH?

A

H2O impermeable, actively transports Cl-, and Na+ passively follows maintaining concentration gradient

29
Q

What is the counter current mechanism in the LOH?

A

Filtrate going down one arm of the loop interacts with blood going up the other arm in opposing direction, increases diffusion

30
Q

What do the NKCC2 transporters do and where are they?

A

Located in ascending LOH, actively reabsorb Na, K, and CL. Entire transporter blocked by loop diuretics (lasix)

Lasix causes Na, K, and 2Cl to remain in LOH causing filtrate to become hypertonic. This increases excretion of H2O along with all lytes that don’t get reabsorbed.

31
Q

What are risks with potassium wasting diuretics?

A

Arrhythmias due to hypokalemia

Metabolic alkalosis as body excretes too much Cl- in proportion to HCO3

32
Q

What is the function of the distal convoluted tubule (DCT)?

A

SECRETION

Final regulation of electrolytes, H2O using hormonal influence (ADH removes excess H2O, Aldosterone regulates lytes)

33
Q

What is the function of the collecting duct?

A

Only minor changes in H2O occur here only with ADH influence. After urine leaves here, no further changes

34
Q

What is the juxtaglomerular apparatus?

A

1) Juxtaglomerular cells (on the inner wall of the afferent arteriole)
Secretes RENIN

2) Medulla densa cells
Senses decrease in Na+ or decrease in GFR, signals juxtaglomerular cells to secrete RENIN

35
Q

How is the RAAS system activated?

A

As blood approaches nephron via the afferent arteriole, depending on BP the GFR may be low resulting in low Na+ being sensed at the macula densa. Juxtaglomerular cells will then secrete renin which activates angiotensinogen (from liver) to form angiotensin I and with converting enzyme from the lungs, forms angiotensin II

36
Q

What is the steps of the RAAS system?

A

1) Angiotensinogen formed in the liver
2) Renin from juxtaglomerular cells
3) Renin activates angiotensinogen to form angiotensin I
4) Lungs create converting enzyme
5) Angiotensin I converts to Angiotensin II

37
Q

What is the role of angiotensin II?

A

Powerful vasoconstrictor, main compensatory mechanism for dehydration to maintain BP. Increases venous return, preload, CO, and GFR

Efferent arteriole is more sensitive to AGII, will decrease U/O to increase GFR

As GFR increases, more Na noted at macula densa cells and renin stops being created

38
Q

What are the 3 factors affecting GFR?

A

1) Glomerular capillary pressure (GCP)
Result of MAP, filtrates, fluid from glomerulus to BC

2) Colloid oncotic pressure (COP)
Plasma proteins in glomerular blood attract H2O

3) Bowman’s capsule pressure (BCP)
Physical presence of wall creates opposing force for filtration

39
Q

Which factors affecting GFR must be balanced to have a good GFR?

A

Colloid oncotic pressure and Bowmans capsule pressure must be lower than Glomerular capillary pressure in order to have a good GFR

If GCP = Sum of COP and BCP, no urine output

40
Q

How is GFR affected by blood protein concentration?

A

Initially decreased blood colloid pressure will increase GFR

Later, decreased GFR due to decreased SBP and decreased preload `

41
Q

How do tubular occlusions affect GFR?

A

Increased capsular pressure decreases GFR

42
Q

How do damaged cell membranes impact GFR?

A

Initially, increased capillary permeability increases GFR

Later, decreased GFR due to lower SBP

43
Q

How does SNS stimulation impact GFR?

A

Constricting afferent and efferent arterioles will cause excessive vasoconstriction. This decreases GFR

44
Q

What is renal autoregulation?

A

Compensatory vasodilation or constriction in response to fluctuations in BP that is independent of nervous system or hormones

45
Q

How is thirst regulated renally?

A

Osmoreceptors in the anterior hypothalamus

In hyperosmolar states, osmoreceptors shrink and thirst increases

In hypo-osmolar states, osmoreceptors swell and thirst decreases

46
Q

Where are the thirst regulating osmoreceptors found?

A

Hypothalamus

47
Q

How is ADH regulated renally?

A

Is stored and released from the posterior pituitary, controls extracellular fluid and Na+ concentration

48
Q

What is normal serum osmolarity?

A

285-295 milliosmoles

49
Q

How do nephrons maintain filtrate homeostasis? 3 ways

A

1) Glomerular filtration (filtrates move to BC)
2) Tubular reabsorption (movement of filtrates from tubule to blood)
3) Tubular secretion (movement of filtrates from blood to tubule)

50
Q

How are solutes and filtrates moved from blood to tubule and vice versa?

A

1) Passive transport along concentration gradients:
Diffusion –> Movement of solute
Osmosis –> Movement of solvent

2) Active transport against a concentration gradient