Exam 2 (renal, ANS) Flashcards
(121 cards)
1
Q
What part of the kidney are the nephrons found?
A
The cortex–outer edge
2
Q
What order does urine move through the parts of the kidney?
A
Cortex –> Calyx –> Renal pelvis –> ureter
3
Q
Where does filtration of blood/formation of urine first occur?
A
Bowman’s capsule
4
Q
What are the major functions of the kidney?
A
Filter out waste and toxins
Control ion concentrations
Control Blood pressure
5
Q
What are fenestrae?
A
Holes in the endothelium of the kidney that allow things to be filtered out of the blood
6
Q
What happens if the basement membrane of the kidney breaks down?
A
Protein or blood is released into the urine
7
Q
What does a mesingeal cell do?
A
Maintain structure and growth of a kidney
8
Q
What is azotemia?
A
Increased BUN and creatinine related to decreased GFR
9
Q
What is uremia?
A
An excess of urea and other nitrogenous waste in the blood; toxic
10
Q
What causes uremia?
A
Failure of renal excretion from (usually) a secondary condition–GI, neuromuscular, or cardiovascular
11
Q
What is proteinuria?
A
Protein in the urine
12
Q
What is albuminuria?
A
Protein in the urine–specifically albumin
13
Q
What is hematuria?
A
Blood in the urine; can be gross (visible to the eye) or microscopic
14
Q
What is naturesis?
A
Sodium excretion
15
Q
What can altered naturesis cause?
A
Hypertension
16
Q
What is circulatory congestion?
A
Build up of plasma volume from decreased renal function
17
Q
What is the major characteristic of acute kidney disease/failure/injury?
A
Abrupt decrease in GFR and creatinine clearance
18
Q
What does creatinine clearance measure?
A
How well the kidneys are clearing substances from the blood
19
Q
How is acute kidney disease classified?
A
RIFLE
Risk, Injury, Failure, Loss of function, End-stage kidney disease
20
Q
How are the causes of acute kidney disease classified?
A
- Prerenal (low blood flow to the kidneys)
- Intrinsic (structure within the kidney damaged–nephron)
- Postrenal (obstruction in urine collection system)
21
Q
What are some possible causes of acute kidney disease/injury/failure?
A
Vascular damage
Drugs
Dehydration
Infection
22
Q
Where does acute kidney failure occur?
A
Many different levels
23
Q
Where does chronic kidney disease occur?
A
Damage to the glomerulus
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)
25
What causes Chronic Kidney disease?
Damage to the glomerulus, usually from another disease (DM, HTN, hyperlipidemia) that changes blood
26
What is glomerulosclerosis?
The process of glomeruli turning into fibrotic tissue
27
What is hemodialysis?
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)
28
What is Peritoneal dialysis?
A tube is put into the peritoneal cavity, fills it with fluid, draws out ions and water, and drains it from the body
29
What is the semipermeable membrane in peritoneal dialysis?
The peritoneal membrane that lines the vascularized bdominal viscera
30
What particles are in peritoneal dialysis solution to draw plasma water out?
Dextrose or icodextrin
31
What drugs cause drug-induced kidney disease?
Antibiotics
NSAIDs
Thiazide diuretics
Analgesics (aspirin and APAP together)
32
What is analgesic nephropathy
Inflammatory reaction to aspirin/APAP in high or combined doses that causes damage to renal structure
33
What causes glomerular diseases?
Immune reactions!
34
What are the 3 types of immune reactions that can cause glomerular diseases?
1. Antibody-associated injury
2. Cell-mediated injury
3. Other mechanisms of glomerular injury..
35
What is chronic glomerulonephritis? (GN)
One of the most common causes of renal failure
36
What are the two classifications of GN?
Primary or secondary (often from systemic diseases like SLE, HTN, DM)
37
How does complex deposition cause glomerular injury?
Antibody + antigen complexes deposit in the membrane of the kidneys, causes it to break down
38
What are anti-GBM antibodies?
Antibodies against specific antigens on the glomerular membrane
39
What can anti-GBM antibodies cause?
The immune system to attack the GBM, which causes damage to the membrane
40
How can T cells cause glomerulonephritis?
They can attach to mesangial cells and release a variety of substances--protease, growth factors, eicosanoids, nitric oxide
41
How can epithelial cell injury cause glomerulonephritis?
The epithelial cells are injured and detach from the basement membrane, causing protein leakage through defective GBM and filtration slits
42
What is nephrotic syndrome?
Protein leakage only; caused by leaky glomeruli
43
What is nephritic syndrome?
Protein and RBC leakage; collection of signs associated with disorders affecting the kidneys, specifically glomerular disorders
44
What is nephrosis?
Nephropathy (any disease of the kidney)
| Degeneration of renal tubular epithelium
45
What is nephritis?
Inflammation of the kidney
46
What usually causes glomerular disease?
The immune system
47
What is associated with nephritic syndrome?
Hematuria, oliguria (sugar in urine), azotemia, HTN
48
What is associated with Nephrotic syndrome?
Hypoalbuminemia, proteinuria, hyperlipidemia
49
What can cause nephrotic syndrome?
Infections
Toxins
DM
50
Do nephritic and nephrotic syndrome have different causes?
Yes
51
What are the three cystic disease of the kidney?
Simple Cysts
APKD (acute polycystic kidney disease)
ARPKD
52
What is APKD?
Multiple expanding cysts of both kidneys that destroy the intervening parenchyma (functional part of kidney)
53
What causes APKD?
Mutation in PKD1 or PKD2 gene in renal tubular cells that makes a mutated polycstine 1/2, which disrupts tissue structure
54
How do you treat APKD?
Renal transplant
55
What are some complications with APKD?
Hematuria, hypertension, urinary infection
56
What is autosomal recessive polycystic kidney disease?
Mutation in PKHD1 (fibrocystin) that fails to maintain normal structure of the kidney
57
What determines the severity of ARPKD?
The type of mutation that the patient has--different mutations can cause the disease
58
What are the clinical features of ARPKD?
Present from birth
Young infants die quickly from pulmonary/renal failure
Patients who survive develop liver cirrhosis
59
What is diuresis?
An increase in urine volume
60
What is natriuresis?
An increase in renal sodium excretion
61
What are some uses of diuretics?
hypertension, renal failure, edema, CHF, diabetes insipidus, hypercalcemia, hepatic cirrhosis
62
In the context of the kidney, what does it mean to excrete something?
Move it from the body/blood into the urine
63
In the context of the kidney, what does it mean to reabsorb something?
Bring it from the urine back into the body
64
What are the major functions of the proximal tubule?
```
Bicarbonate reabsorption
Water reabsorption (60%)
NaCl reabsorption (40%)
```
65
What are the major functions of the descending loop of henle?
Water excretion
66
What are the major functions of the thick ascending Loop of Henle?
Dilute the urine--reabsorb ions (K, NaCl-33%, Mg, Cl, Ca) but not water
67
What are the major functions of the distal convoluted tubule?
```
NaCl reabsorption (10%)
Ca reabsorption (controlled by PTH)
```
68
What are the major functions of the macula densa?
Detect NaCl concentration to signal control of blood pressure
69
What are the major functions of the collecting duct?
NaCl reabsorption (5%)
Water reabsorption
K and H excretion
70
Where does potassium wasting occur?
The collecting duct
71
Where do thiazides act?
Distal convoluted tubule
72
Where do loop diuretics act?
Thick ascending limb of the Loop of Henle
73
Where do potassium-sparing diuretics act?
Collecting duct
74
Where does carbonic anhydrase act?
Proximal tubule
75
What are thiazide diuretic examples?
Hydrochlorothiazide and chlorthalidone
76
What are loop diuretic examples?
Furosemide
Bumetanide
Ethacrynic acid
77
What are potassium-sparing diuretic examples?
Spironolactone
Triamterene
Amiloride
78
What are carbonic anhydrase inhibitors?
Acetazolamide
79
What does aldosterone do?
NaCl reabsorption (for water reabsorption) in the collecting dut
80
How do thiazides work?
Block the NaCl transport system
81
What is convection?
Solute moves across membrane with the solvent; moving down concentration gradient
82
Acetazolamide mechanism
Carbonic anhydrase inhibitor--inhibits bicarbonate reabsorption, H+ excretion, Na+ reabsorption
83
Acetazolamide clinical uses
Acute mountain sickness
Metabolic alkalosis
Urinary alkalinization
Glaucoma
84
Acetazolamide Toxicities
Hyperchloremic metabolic acidosis
Renal stones
Renal potassium wasting
Drowsiness/paresthesia
85
Acetazolamide Contraindications
Sulfa allergies
| Hepatic cirrhosis
86
Loop diuretics mechanism
Inhibits the Na/K/Cl symporter
Decreases reabsorption of Mg/Ca
Increases renal blood flow
87
Loop diuretics clinical uses
- Edema/pulmonary edema
- Hypercalcemia
- Acute renal failure
- Hyperkalemia
- Anion overdose
88
Loop diuretics toxicities
```
Hypomagnesemia
Hypokalemic Metabolic alkalosis
Dehydration
Ototoxicity (ethacrynic acid)
Hyperuricemia
```
89
Loop diuretics contraindications
Sulfa allergies (not ethacrynic acid)
90
Ethacrynic acid
Loop diuretic--without sulfur
91
Furosemide
Loop diuretic
92
Bumetanide
Loop diuretic
93
Thiazide mechanism
Inhibits the Na/Cl symporter
| Increases Ca reabsorption by decreasing the NA in the cells lining the lumen
94
Thiazide Clinical uses
- Hypertension
- CHF
- Nephrogenic diabetes insipidus
- Nephrolithiasis (kidney stones) from hypercalciuria
95
Thiazide toxicities
```
Hyperuricemia
Hypokalemic metabolic acidosis
Impaired carb intolerance
Hyperlipidemia
Hyponatremia
```
96
Thiazide contraindications
Sulfa allergens
| Caution: DM
97
Amiloride class
Potassium sparing diuretic
98
Amiloride mechanism
Blocks Na+ channel in collecting duct, which blocks Na_ reabsorption
No K+ excretion
Decreased H+ excretion
99
Amiloride Clinical uses
Adjunctive treatment with thiazide for CHF or hypertension
100
Amiloride toxicities
Hyperkalemia
| Hyperchloremic metabolic acidosis
101
Amiloride Contraindications
K+ supplements
| ACE Inhibitors
102
Triamterene class
Potassium sparing diuretic
103
Triamterene clinical uses
Edema w/ CHF
Hepatic cirrhosis
nephrotic syndrome
hyperaldosteronism
104
Triamterene toxicities
Hyperkalemia
| hyperchloremic metabolic acidosis
105
Contraindications
Kidney stones
K+ supplementation
ACE Inhibitors
106
Mannitol mechanism
Sugar in the extracellular space, stays in the lumen to draw water in and keep it there without losing any Na+
107
Mannitol clinical uses
Increase urine volume
| Decrease intraocular/intracranial pressure
108
Mannitol toxicity
Extracellular volume expansion
Dehydration
Hypernatremia
109
Spironolactone drug type
Aldosterone antagonist
110
Spironolactone mechanism
Antagonizes aldosterone (which is in charge of increasing Na reabsorption in the collecting duct)
Potassium sparing
Inhibits 5-alpha reductase
111
Spironolactone clinical uses
Hypertension or CHF
Mineralocorticoid excess
Aldosteronism
112
Spironolactone toxicities
```
Hyperkalemia
Hyperchloremic metabolic acidosis
Gynecomastia
Impotence
BPH
```
113
Spironolactone contraindications
K+ supplementation
ACE Inhibitors
Chronic renal insufficiency
114
Inspra mechanism
Antagonzies aldosterone
POtassium sparing
Antagonist of mineralocorticoid receptor in kidney, heart, blood vessels, and brain
115
Inspra Clinical uses
Hypertension
116
Inspra toxicitites
Hyperkalemia
| Hypertriglyceridemia
117
Inspra contraindications
```
K+ supplementation
ACE Inhibitors
K+ sparing diuretics
Chronic renal insufficiency
Diabetes with microalbuminuria
CYP450 3A4 inhibitors
```
118
Demeclocycline drug type
Anti-ADH
119
Demeclocycline mechanism
ADH antagonist
| Similar to lithium salts
120
Demeclocycline toxicity
Nephrogenic diabetes insipidus
| Renal failure
121
Demeclocycline clinical uses
SIADH
| elevated ADH
