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Therapeutics I > Exam 2 (renal, ANS) > Flashcards

Exam 2 (renal, ANS) Flashcards

1
Q

What part of the kidney are the nephrons found?

A

The cortex–outer edge

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2
Q

What order does urine move through the parts of the kidney?

A

Cortex –> Calyx –> Renal pelvis –> ureter

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3
Q

Where does filtration of blood/formation of urine first occur?

A

Bowman’s capsule

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4
Q

What are the major functions of the kidney?

A

Filter out waste and toxins
Control ion concentrations
Control Blood pressure

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5
Q

What are fenestrae?

A

Holes in the endothelium of the kidney that allow things to be filtered out of the blood

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6
Q

What happens if the basement membrane of the kidney breaks down?

A

Protein or blood is released into the urine

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7
Q

What does a mesingeal cell do?

A

Maintain structure and growth of a kidney

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8
Q

What is azotemia?

A

Increased BUN and creatinine related to decreased GFR

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9
Q

What is uremia?

A

An excess of urea and other nitrogenous waste in the blood; toxic

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10
Q

What causes uremia?

A

Failure of renal excretion from (usually) a secondary condition–GI, neuromuscular, or cardiovascular

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11
Q

What is proteinuria?

A

Protein in the urine

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12
Q

What is albuminuria?

A

Protein in the urine–specifically albumin

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13
Q

What is hematuria?

A

Blood in the urine; can be gross (visible to the eye) or microscopic

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14
Q

What is naturesis?

A

Sodium excretion

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15
Q

What can altered naturesis cause?

A

Hypertension

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16
Q

What is circulatory congestion?

A

Build up of plasma volume from decreased renal function

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17
Q

What is the major characteristic of acute kidney disease/failure/injury?

A

Abrupt decrease in GFR and creatinine clearance

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18
Q

What does creatinine clearance measure?

A

How well the kidneys are clearing substances from the blood

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19
Q

How is acute kidney disease classified?

A

RIFLE

Risk, Injury, Failure, Loss of function, End-stage kidney disease

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20
Q

How are the causes of acute kidney disease classified?

A
  1. Prerenal (low blood flow to the kidneys)
  2. Intrinsic (structure within the kidney damaged–nephron)
  3. Postrenal (obstruction in urine collection system)
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21
Q

What are some possible causes of acute kidney disease/injury/failure?

A

Vascular damage
Drugs
Dehydration
Infection

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22
Q

Where does acute kidney failure occur?

A

Many different levels

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23
Q

Where does chronic kidney disease occur?

A

Damage to the glomerulus

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24
Q

What is the distinguishing feature of Chronic Kidney Disease?

A

Progressive loss of function over several months or years; gradual replacement of normal kidney structure with parenchymal fibrosis (cells change into fiber which causes them to lose function)

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25
Q

What causes Chronic Kidney disease?

A

Damage to the glomerulus, usually from another disease (DM, HTN, hyperlipidemia) that changes blood

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26
Q

What is glomerulosclerosis?

A

The process of glomeruli turning into fibrotic tissue

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27
Q

What is hemodialysis?

A

Blood is removed from the body and put into a dialyzer (which has dialysate and blood on opposite sides of the membrane). Dialysater removes the ions (through diffusion and convection) and water from blood (through ultrafiltration)

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28
Q

What is Peritoneal dialysis?

A

A tube is put into the peritoneal cavity, fills it with fluid, draws out ions and water, and drains it from the body

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29
Q

What is the semipermeable membrane in peritoneal dialysis?

A

The peritoneal membrane that lines the vascularized bdominal viscera

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30
Q

What particles are in peritoneal dialysis solution to draw plasma water out?

A

Dextrose or icodextrin

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31
Q

What drugs cause drug-induced kidney disease?

A

Antibiotics
NSAIDs
Thiazide diuretics
Analgesics (aspirin and APAP together)

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32
Q

What is analgesic nephropathy

A

Inflammatory reaction to aspirin/APAP in high or combined doses that causes damage to renal structure

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33
Q

What causes glomerular diseases?

A

Immune reactions!

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34
Q

What are the 3 types of immune reactions that can cause glomerular diseases?

A
  1. Antibody-associated injury
  2. Cell-mediated injury
  3. Other mechanisms of glomerular injury..
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35
Q

What is chronic glomerulonephritis? (GN)

A

One of the most common causes of renal failure

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36
Q

What are the two classifications of GN?

A

Primary or secondary (often from systemic diseases like SLE, HTN, DM)

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37
Q

How does complex deposition cause glomerular injury?

A

Antibody + antigen complexes deposit in the membrane of the kidneys, causes it to break down

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38
Q

What are anti-GBM antibodies?

A

Antibodies against specific antigens on the glomerular membrane

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39
Q

What can anti-GBM antibodies cause?

A

The immune system to attack the GBM, which causes damage to the membrane

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40
Q

How can T cells cause glomerulonephritis?

A

They can attach to mesangial cells and release a variety of substances–protease, growth factors, eicosanoids, nitric oxide

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41
Q

How can epithelial cell injury cause glomerulonephritis?

A

The epithelial cells are injured and detach from the basement membrane, causing protein leakage through defective GBM and filtration slits

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42
Q

What is nephrotic syndrome?

A

Protein leakage only; caused by leaky glomeruli

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43
Q

What is nephritic syndrome?

A

Protein and RBC leakage; collection of signs associated with disorders affecting the kidneys, specifically glomerular disorders

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44
Q

What is nephrosis?

A

Nephropathy (any disease of the kidney)

Degeneration of renal tubular epithelium

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45
Q

What is nephritis?

A

Inflammation of the kidney

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46
Q

What usually causes glomerular disease?

A

The immune system

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47
Q

What is associated with nephritic syndrome?

A

Hematuria, oliguria (sugar in urine), azotemia, HTN

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48
Q

What is associated with Nephrotic syndrome?

A

Hypoalbuminemia, proteinuria, hyperlipidemia

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49
Q

What can cause nephrotic syndrome?

A

Infections
Toxins
DM

50
Q

Do nephritic and nephrotic syndrome have different causes?

A

Yes

51
Q

What are the three cystic disease of the kidney?

A

Simple Cysts
APKD (acute polycystic kidney disease)
ARPKD

52
Q

What is APKD?

A

Multiple expanding cysts of both kidneys that destroy the intervening parenchyma (functional part of kidney)

53
Q

What causes APKD?

A

Mutation in PKD1 or PKD2 gene in renal tubular cells that makes a mutated polycstine 1/2, which disrupts tissue structure

54
Q

How do you treat APKD?

A

Renal transplant

55
Q

What are some complications with APKD?

A

Hematuria, hypertension, urinary infection

56
Q

What is autosomal recessive polycystic kidney disease?

A

Mutation in PKHD1 (fibrocystin) that fails to maintain normal structure of the kidney

57
Q

What determines the severity of ARPKD?

A

The type of mutation that the patient has–different mutations can cause the disease

58
Q

What are the clinical features of ARPKD?

A

Present from birth
Young infants die quickly from pulmonary/renal failure
Patients who survive develop liver cirrhosis

59
Q

What is diuresis?

A

An increase in urine volume

60
Q

What is natriuresis?

A

An increase in renal sodium excretion

61
Q

What are some uses of diuretics?

A

hypertension, renal failure, edema, CHF, diabetes insipidus, hypercalcemia, hepatic cirrhosis

62
Q

In the context of the kidney, what does it mean to excrete something?

A

Move it from the body/blood into the urine

63
Q

In the context of the kidney, what does it mean to reabsorb something?

A

Bring it from the urine back into the body

64
Q

What are the major functions of the proximal tubule?

A 
Bicarbonate reabsorption
Water reabsorption (60%)
NaCl reabsorption (40%)
65
Q

What are the major functions of the descending loop of henle?

A

Water excretion

66
Q

What are the major functions of the thick ascending Loop of Henle?

A

Dilute the urine–reabsorb ions (K, NaCl-33%, Mg, Cl, Ca) but not water

67
Q

What are the major functions of the distal convoluted tubule?

A 
NaCl reabsorption (10%)
Ca reabsorption (controlled by PTH)
68
Q

What are the major functions of the macula densa?

A

Detect NaCl concentration to signal control of blood pressure

69
Q

What are the major functions of the collecting duct?

A

NaCl reabsorption (5%)
Water reabsorption
K and H excretion

70
Q

Where does potassium wasting occur?

A

The collecting duct

71
Q

Where do thiazides act?

A

Distal convoluted tubule

72
Q

Where do loop diuretics act?

A

Thick ascending limb of the Loop of Henle

73
Q

Where do potassium-sparing diuretics act?

A

Collecting duct

74
Q

Where does carbonic anhydrase act?

A

Proximal tubule

75
Q

What are thiazide diuretic examples?

A

Hydrochlorothiazide and chlorthalidone

76
Q

What are loop diuretic examples?

A

Furosemide
Bumetanide
Ethacrynic acid

77
Q

What are potassium-sparing diuretic examples?

A

Spironolactone
Triamterene
Amiloride

78
Q

What are carbonic anhydrase inhibitors?

A

Acetazolamide

79
Q

What does aldosterone do?

A

NaCl reabsorption (for water reabsorption) in the collecting dut

80
Q

How do thiazides work?

A

Block the NaCl transport system

81
Q

What is convection?

A

Solute moves across membrane with the solvent; moving down concentration gradient

82
Q

Acetazolamide mechanism

A

Carbonic anhydrase inhibitor–inhibits bicarbonate reabsorption, H+ excretion, Na+ reabsorption

83
Q

Acetazolamide clinical uses

A

Acute mountain sickness
Metabolic alkalosis
Urinary alkalinization
Glaucoma

84
Q

Acetazolamide Toxicities

A

Hyperchloremic metabolic acidosis
Renal stones
Renal potassium wasting
Drowsiness/paresthesia

85
Q

Acetazolamide Contraindications

A

Sulfa allergies

Hepatic cirrhosis

86
Q

Loop diuretics mechanism

A

Inhibits the Na/K/Cl symporter
Decreases reabsorption of Mg/Ca
Increases renal blood flow

87
Q

Loop diuretics clinical uses

A
  • Edema/pulmonary edema
  • Hypercalcemia
  • Acute renal failure
  • Hyperkalemia
  • Anion overdose
88
Q

Loop diuretics toxicities

A 
Hypomagnesemia
Hypokalemic Metabolic alkalosis
Dehydration
Ototoxicity (ethacrynic acid)
Hyperuricemia
89
Q

Loop diuretics contraindications

A

Sulfa allergies (not ethacrynic acid)

90
Q

Ethacrynic acid

A

Loop diuretic–without sulfur

91
Q

Furosemide

A

Loop diuretic

92
Q

Bumetanide

A

Loop diuretic

93
Q

Thiazide mechanism

A

Inhibits the Na/Cl symporter

Increases Ca reabsorption by decreasing the NA in the cells lining the lumen

94
Q

Thiazide Clinical uses

A
  • Hypertension
  • CHF
  • Nephrogenic diabetes insipidus
  • Nephrolithiasis (kidney stones) from hypercalciuria
95
Q

Thiazide toxicities

A 
Hyperuricemia
Hypokalemic metabolic acidosis
Impaired carb intolerance
Hyperlipidemia
Hyponatremia
96
Q

Thiazide contraindications

A

Sulfa allergens

Caution: DM

97
Q

Amiloride class

A

Potassium sparing diuretic

98
Q

Amiloride mechanism

A

Blocks Na+ channel in collecting duct, which blocks Na_ reabsorption
No K+ excretion
Decreased H+ excretion

99
Q

Amiloride Clinical uses

A

Adjunctive treatment with thiazide for CHF or hypertension

100
Q

Amiloride toxicities

A

Hyperkalemia

Hyperchloremic metabolic acidosis

101
Q

Amiloride Contraindications

A

K+ supplements

ACE Inhibitors

102
Q

Triamterene class

A

Potassium sparing diuretic

103
Q

Triamterene clinical uses

A

Edema w/ CHF
Hepatic cirrhosis
nephrotic syndrome
hyperaldosteronism

104
Q

Triamterene toxicities

A

Hyperkalemia

hyperchloremic metabolic acidosis

105
Q

Contraindications

A

Kidney stones
K+ supplementation
ACE Inhibitors

106
Q

Mannitol mechanism

A

Sugar in the extracellular space, stays in the lumen to draw water in and keep it there without losing any Na+

107
Q

Mannitol clinical uses

A

Increase urine volume

Decrease intraocular/intracranial pressure

108
Q

Mannitol toxicity

A

Extracellular volume expansion
Dehydration
Hypernatremia

109
Q

Spironolactone drug type

A

Aldosterone antagonist

110
Q

Spironolactone mechanism

A

Antagonizes aldosterone (which is in charge of increasing Na reabsorption in the collecting duct)
Potassium sparing
Inhibits 5-alpha reductase

111
Q

Spironolactone clinical uses

A

Hypertension or CHF
Mineralocorticoid excess
Aldosteronism

112
Q

Spironolactone toxicities

A 
Hyperkalemia
Hyperchloremic metabolic acidosis
Gynecomastia
Impotence
BPH
113
Q

Spironolactone contraindications

A

K+ supplementation
ACE Inhibitors
Chronic renal insufficiency

114
Q

Inspra mechanism

A

Antagonzies aldosterone
POtassium sparing
Antagonist of mineralocorticoid receptor in kidney, heart, blood vessels, and brain

115
Q

Inspra Clinical uses

A

Hypertension

116
Q

Inspra toxicitites

A

Hyperkalemia

Hypertriglyceridemia

117
Q

Inspra contraindications

A 
K+ supplementation
ACE Inhibitors
K+ sparing diuretics
Chronic renal insufficiency
Diabetes with microalbuminuria
CYP450 3A4 inhibitors
118
Q

Demeclocycline drug type

A

Anti-ADH

119
Q

Demeclocycline mechanism

A

ADH antagonist

Similar to lithium salts

120
Q

Demeclocycline toxicity

A

Nephrogenic diabetes insipidus

Renal failure

121
Q

Demeclocycline clinical uses

A

SIADH

elevated ADH

Therapeutics I (9 decks)

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