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Therapeutics P2 > Exam 1 lecture 3 > Flashcards

Exam 1 lecture 3 Flashcards

1
Q

Name 6 physiological functions of kidney

A

Endocrine function
control of solutes and fluids
BP control
Acid/base balance
Drug metabolism and excretion
Metabolic waste excretion

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2
Q

What are the two big components of nephrons

A

Tubules
blood vessels

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3
Q

What is the relationship between tubules and blood vessels in kidney

A

There is reabsorption and excretion between tubules and blood vessels

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4
Q

What happens in glomerulus

A

Filtration (100% filtrate produced)

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5
Q

What structure is present after filtration in glomerulus

A

PCT

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6
Q

What happens in PCT

A

Major reabsorption site (both active and passive).
Glucose and aa reabsorbed.
Lots of blood vessels present for reabsorption

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7
Q

What structure is present after PCT

A

loop of henle

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8
Q

What are the two parts of loop of henle and what are their functions

A

descending (thin) limb- primary site for H2O absorption
Ascending (thick) limb- permeable to ions (salts reabsorption)

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9
Q

What is after loop of henle

A

DIstal tubule

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10
Q

Percent of filtrate reabsorbed at distal tubule

A

9%

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11
Q

What structure comes after distal tubule

A

collecting duct

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12
Q

Percent of filtrate reabsorbed at collecting tubule

A

4%

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13
Q

percent of filtrate reabsorbed from loop of henle

A

6%

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14
Q

Percent of filtrate reabsorbed from proximal tubule

A

80%

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15
Q

average kidney has how many nephrons

A

1 million

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16
Q

afferent vs efferent arteriole

A

afferent- brings blood to glomerulus
efferent- carries blood away from glomerulus

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17
Q

difference between PCT and proximal tubule

A

proximal tubule- secretions and reabsorption of organic acids and bases, uric acid and most diuretics

PCT- reabsorption of 65% of ions, 100 % of aa and glucose

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18
Q

function of thick ascending loop

A

active reabsorption of 15-25% of filtered NA/K/Cl.
secondary reabsorption of Ca and Mg

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19
Q

function of distal convoluted tubule

A

PTH control

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20
Q

Function of medullary collecting duct

A

Water reabsorption under vasopressin control

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21
Q

Water permeability of
Proximal tubule
Thick ascending loop
DCT

A

proximal- very high
thick ascending loop- very low
DCT- very low

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22
Q

What are some different ways of measuring kidney function

A

serum creatinine
blood urea nitrogen (BUN)
creatinine clearence
Glomerular filtration rate (GFR)

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23
Q

What does serum creatinine measure? How would an increase or decrease affect our body?

A

measures how well kidneys filter waste from blood.
Increase in this is bad

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24
Q

What does Blood urea nitrogen measure (BUN), how would change affect it?

A

Measures waste from liver breakdown of AA
increase is bad

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25
Q

What does creatinine clearence measure

A

Useful for predicting secretion and drug clearence

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26
Q

What are some markers for damage for kidney

A

Urinary abnormalities- protein, RBC in urine suggest membrane malfunction

Imaging abnormalities (MRI/CTI scans)

27
Q

Kidney functions decline with age due to

A

Decline in kidney mass (nephrons)

28
Q

How does renal injury lead to decrease in number of nephrons

A

Decrease in number of nephrons lead to compensatory rise in size and function of remaining nephrons

Increase in size and function of nephrons lead to glomerular and tubular lesions

lesions lead to loss of nephrons, leading to decline in GFR

decrease in GFR leads to azotemia and uremic syndrome (death)

29
Q

Criteria to determine acute kidney failure (AKF)

A

1.Increase in Scr of 0.3 or more

  1. Increase in Scr by 50% (1.5x) baseline, which is known to have occured within the prior 7 days
  2. A reduction in urine output of less than 0.5 ml/kh/h for 6 H
30
Q

How is normal GFR maintained under decreased perfusion pressure and reduction of GFR by drugs

A

The kidney has an internal mechanism for autoregulation.

31
Q

how does the kidneys internal autoregulation of perfusion pressure work

A

Normal GFR is maintained by afferent vasodilation and efferent vasoconstriction

32
Q

How is afferent vasodilation maintained

A

Increased vasodilatory prostaglandins- dilation

33
Q

how is efferent vasoconstriction maintained

A

Increased angiotensin II

34
Q

How would taking NSADIs affect autoregulation of kidney

A

NSAIDs affect prostaglandin. This will affet vasodilation of efferent arterioles leading to low GFR

35
Q

We can use NSAIDs with renal injury t/f

A

False

36
Q

What drugs could affect angiotensin II levels

A

ACE inhibitors

37
Q

Major causes of intrinsic acute kidney injury

A

sepsis, ischemia, nephrotoxicity

38
Q

What are some causes of obstruction leading to post renal AKI (acute kidney injury)

A

Kidney- kidney stones, blood clots, tumor
Bladder- Prostate enlargement, blood clots, cancer
Urethra- obstructed foley catheter

39
Q

What are some common key elements of progressive nephropathies?

A

Increased glomerular capillary pressure
Proteinuria
Glomerulosclerosis

40
Q

2 main abnormalities that give rise to CKD-MBD (chronic kidney disease- mineral bone disease)

A
  1. impaired phsophate excretion
  2. decreased production of 1,25 dihydroxy vitamin D3
41
Q

why cant patients with CKD produce active vit-D3

A

Vitamin D3 becomes active invivo. goes through liver and then kidney to become activated. CKD patients can not undergo kidney portion.
That is why CKD patients require Ca homeostasis checks

42
Q

What is uremia

A

Uremic illness due to buildup of organic waste products

43
Q

signs and symptoms of uremia

A

Endocrine and metabolic
neural and muscular

44
Q

nephropathy meaning

A

Damage or disease of kidney

45
Q

Name 5 nephropathies

A

Nephritic syndromes
nephrotic syndromes
Cystic disease of kidney
nephrolithiasis
contrast induced nephropathy

46
Q

differentiate nephritic and nephrotic syndromes

A

Nephritic- INFLAMMATION distrupting glomerular basement membrane (hematuria, cola colored urine)

Nephrotic- pOdocyte damage leading to glomerular charge barrier disruption (massive proteinuria)

47
Q

Which has more proteinuria nephritic or nephrotic

A

Nephrotic

48
Q

How does proteinuria affect serum albumin?

A

lowers serum albumin

49
Q

How does low albumin affect the body?

A

Edema

proteinuria–>low albumin–>edema

50
Q

What is generally observed with nephritic syndrome

A

Hematuria

51
Q

What is glomerulonephritis? two forms?

A

inflammation of glomerulus. Can have chronic or acute. Presents with both proteinuria and hematouria

52
Q

cause of glomerulonephritis

A

Primary- genetics
secondary- infection, drugs etc

53
Q

pathogenesis of glomerular disease

A

antibody associated immune rxn
cell mediated immune rxn

54
Q

what is pyelonephritis

A

Inflammation of kidney caused by bacteria from blood or UTI

55
Q

clinical presentation of pyelonephritis?

A

Painful urination, white cells in urine

56
Q

What is the major cause of pyelonephritis

A

Bacteria from UTI go against the floe of urine using flagella and go into the kidney.

57
Q

What is interstitial nephritis? what is AIN (acute interstitial nephritis caused by?)

A

Interstitial nephritis is the primary injury to renal tubules and interstitium. It has several different causes.
70-75% Drugs- penicillin and diuretics
4-10% Infections
10-20% autoimmune infections

58
Q

What is the most common form of cystic renal disease

A

cystic disease of kidney

59
Q

2 forms of cystic disease

A

APKD- autosomal dominant polycystic kidney disease (adult)

autosomal recessive polycystic kidney disease (childhood)

60
Q

What is the difference between autosomal dominant polycystic kidney disease and autosomal recessive polycystic kidney disease

A

autosomal dominant affects adults
autosomal recessive affects children

autosomal dominant is characterized by multiple expanding cysts of both kidneys that ultimately destroy the parenchyma.

autosomal recessive is ultimately fatal, those who survive will have liver disease

61
Q

what is nephrothiasis

A

Kidney stones

62
Q

what percent of men and women are affected by nephrothiasis

A

10% of men, 5% of women

63
Q

how does nephrothiasis occur?

A

supersaturation of calcium (kidney stones are predominantly calcium phosphate)

Therapeutics P2 (41 decks)

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