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Pharmacotherapy 1 > 2 - Renal (Barker) > Flashcards

2 - Renal (Barker) Flashcards

1
Q

What kind of capillaries make up the glomerulus?

A

fenestrated

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2
Q

Besides endothelial cells and podocytes, and the parietal epithelium what other types of cells are in the glomerulus and what is their fxn?

A

mesangial cells: structure, growth, health of the glomerulus

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3
Q

What are the clinical manifestations of renal disease?

A 
acute kidney injury
CKD
HD and peritoneal dialysis
drug-induced kidney disease
nephritis
sodium and water homeostasis
ion homeostasis
acid-base disorder
tumors
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4
Q

How does renal disease present?

A 
azotemia
uremia
proteinuria
hematuria
altered naturesis (leading to HTN)
edema
circulatory congestion
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5
Q

What is azotemia?

A

biochemical abnormality in which an elevation of BUN and sCR levels, which is largely related to decr GFR

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6
Q

What is uremia?

A

excess of urea and other nitrogenous waste in the blood.

chara’d not only by failure of renal excretory fxn but also by a host of metabolic and endocrine alterations incident to renal damge

secondary GI, mneuomuscular, and CV involvement

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7
Q

Describe acute kidney disease/injury/failure.

A

abupt decr in GFR or CrCl

RIFLE: risk, injury, failure, lodd of kidney fxn, and end-stage kidney disease classifications

based on the anatomical area of jinury or malfunction: prerenal, intrinsic, postrenal

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8
Q

Describe CKD.

A

chronic renal insufficiency or progressive kidney disease.

Progressive loss of function occuring over several months to years and is characterized by the gradual replacement of normal kidney architecture with parenchymal fibrosis.

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9
Q

Describe peritoneal dialysis.

A

involves intallation of dialysate into the peritoneal cavity via a permanent peritoneal catheter.

the peritoneal membrane liens the highly vascularized abdominal viscera and acts as the semipermeable membrane across which diffusion and ultrafiltration occur.

Substances are removed from the blood across the peritoneum via diffusion and ultrafiltration.

Excess plasma water is removed via ultrafiltrated created by osmotic pressure generated by various dextrose or icodextrin concentrations.

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10
Q

Describe hemodialysis.

A

involves the perfusion of blood and dialysate on oposite sides of semipermeable membrane. substances are removed from the blodo by diffusion and convection. excess plasma water is removed via ultrafiltration.

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11
Q

Describe drug-induced kidney disease.

A

Drugs trigger acute damage to renal structures resulting in altered function.

Ex. NSAIDs, thiazide diuretics, ASA+APAP.

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12
Q

Describe glomerulonephritis (GN).

A

one of most common causes of CRF.

primary or secondary (SLE, HTN, DM, etc.)

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13
Q

What is the pathogenesis of glomerular disease?

A

immune rxn!

  1. antibody-associated injury
  2. cell-mediated
  3. other mechanisms
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14
Q

What are the types of antibody-mediated glomerular injury?

A
  1. immune complex deposition
  2. anti-glomerular basement membrane antibodies
  3. antibody against glomerular antigen (membranous nephropathy)
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15
Q

What is the postulated sequence of epithelial cell injury?

A

antibodies to epithelial cell antigens, toxins cytokines, or other factors cause injury and detachment of epithelial cells and protein leakage through defective GBM and filtration slits.

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16
Q

What are the three major glomerular syndromes?

A
  1. Nephrotic
  2. Nephritic
  3. Chronic Glomerulonephritis
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17
Q

What is the Nephrotic Syndrome?

A

protein leakage only

the glomeruli are leaky

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18
Q

What is the Nephritic Syndrome?

A

protein and RBC leakage.

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19
Q

What is Nephrosis?

A
  1. Nephropathy (any disease of the kidney)

2. Degeneration of renal tubular epithelial

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20
Q

What is Nephritis?

A

inflammation of the kidney

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21
Q

(What are some types of nephrotic syndrome?)

A
  • Minimal Change Disease (T Cell)
  • Membranous Nephropathy (Ab)
  • Focal Segmental Gomerulosclerosis (injur of visceral epithelial cells)
  • Membraneoproliferaitive Glomerulonephritis (Ab)
22
Q

What are Sx of Nephrotic Syndrome?

A

proteinuria
hypoalbuminemia
edema
hyperlipidemia and lipiduria

23
Q

What are Sx of Nephritic Syndrome?

A

hematuria
oliguria
azotemia
hypertension

24
Q

(What are some types of Nephritic Syndrome?)

A
  • acute proliferative glomerulonephritis (Ab)
  • Rapid Progressive Glomerulonephritis (?)
  • IgA Nephropathy (Berger Disease) (IgA)
25
Q

What are the pathways of infection leading to acute pyelonephritis?

A

-Hemotogenous infection results from bcteremic spread.

More common is ascending infx. which results from a combination of urinary bladder infx, vesicoureteral reflux, and intrarenal reflux.

26
Q

What are cysts?

A

abnormal membranous sac that forms in the structure. could be filled with gas, liquid, semisolid.

27
Q

What is the most common form of cystic renal diseas?

A

simple cysts

28
Q

What is the definition of autosomal dominant (adult) polycystic kidney disease (APKD)?

A

multiple expanding cysts of both kidneys that ultimately destroy the intervening parenchyma

29
Q

What is the pathogenesis of autosomal adult PDK?

A

inherited mutation of PKD1 or PKD2 gene in tubular cells

  • abnormal cyst formation in both kidneys
  • destroy interening parenchyma
  • intermittent gross hematuria
  • HTN and urinary infection–>fatal–>renal transplantation is necessary
30
Q

What is the pathogenesis of autosomal recessive (childhood) polycystic kidney disease?

A

autosomal recessive inhertiance

mutation in PKHD1–fibrocysin (polyductin)

31
Q

What are the clinical features of childhood PKD?

A

usual presents at birth

  • young infants die quickly from pulmonary or renal failure
  • survivors develop cirrhosis (congenital hepatic fibrosis)
32
Q

What is diuresis?

A

increase in urine volume

33
Q

What is natriuresis

A

increase in renal sodium excretion

34
Q

What are the clinical uses of diuretics?

A 
HTN,
edema, 
CHF, 
kidney disease, 
hepatic cirrhosis, hypercalcemia, 
diabetes insipidus
35
Q

What is the site of action of osmotic agents (mannitol)?

A

decrease water reabs in the PCT, loop, CD

36
Q

What is the site of action of loop agents (furosemide)?

A

ascending loop of Henl, decrease ions reabs

37
Q

What is the site of action of thiazides?

A

decrease NaCl reabsorption in the DCT

38
Q

What is the site of action of aldosterone antagonists?

A

decrease NaCl reabs in the collecting duct

39
Q

What is the site of action of ADH antagonists?

A

decrease water absorption in the collecting duct

40
Q

What is the site of action of adenosine (diuretic)?

A

glomerulerus
PCT
Collecting duct
thick ascending limb

41
Q

What are some examples of loop diuretics?

A

furosemide
bumetanide
ethacrynic acid

42
Q

What occurs in the thick ascnending limb of the nephron?

A

NaCl reabs!

also Ca, Mg, K reabs

43
Q

What are some examples of thiazides?

A

HCTZ

chlorthalidone

44
Q

What controls Ca2+ reabs in the PCT?

A

parathyroid hormone

45
Q

Describe the macula densa?

A

At intersection between glomerulus and DCT.

regulate blood pressure by sensing NaCl reabs.

the juxtaglomerular cells receive signal from the macula densa and release renin –> RAAS

46
Q

Where do potassium-sparing diuretics work?

A

CD

block sodium reabs, so no need to excrete K

47
Q

What are examples of K-sparing diuretics?

A

spironolactone
triamterene
amiloride

48
Q

How does potassium move in the collecting duct?

A

moves into the urine in exchange for Na reabs.

49
Q

Describe convective solute flow

A

solutes move with water along their concentration gradient

50
Q

How do ions/solutes movee across membrane?

A

convective solute flow
simple diffusion

mediated:
channel-mediated diffusion
carri-ermedicated difusion

active: ATP-medaited

secondary acive:
symport
antiport

51
Q

Drug targets for diuretics ae what kind of transporters?

A

active!

ATP, –>symport, –>antiport

Pharmacotherapy 1 (26 decks)

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