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Therapeutics I - Spring 2017 > Overview of Renal Pathophys Lecture > Flashcards

Overview of Renal Pathophys Lecture Flashcards

1
Q

Azotemia definition

A

elevated BUN and Creatinine levels in blood usually due to decreased GFR

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2
Q

Uremia definition

A

excess urea and nitrogenous waste in blood = can be toxic! - can occur due to metabolic and endocrine alterations

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3
Q

Definition of Acute Kidney Disease

A

ABRUBT decrease in GFR or CrCl

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4
Q

How to classify Acute Chronic Kidney disease

A

RIFLE classification

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5
Q

what does RIFLE classification stand for

A 
Risk
Injury
Failure
Loss of Kidney Function
End-Stage Kidney Disease
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6
Q

Types of anatomical names for acute kidney injury/malfunction

A
  • pre-renal
  • intrinsic
  • post-renal
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7
Q

If the Acute chronic kidney disease is caused by a pre-renal malfunction - what does it mean?

A

decreased renal blood flow

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8
Q

If the Acute chronic kidney disease is caused by a intrinsic malfunction - what does it mean?

A

structure within kidney is damaged

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9
Q

If the Acute chronic kidney disease is caused by a post-renal malfunction - what does it mean?

A

obstruction within urine collection system

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10
Q

Definition of Chronic Kidney Disease

A

progressive loss of function - gradual replacement of normal kidney architecture with parenchymal fibrosis

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11
Q

4 possible disease states that can lead to chronic kidney disease

A

Diabetes Mellitus; Initial pathogenic injury; Hyperlipidemia; Systemic HTN

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12
Q

what is glomerulosclerosis

A

glomerulus is changing to fibrotic tissue (

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13
Q

what is the normal GFR level range

A

90 to 120 mL/min/1.73 m^2

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14
Q

Definition of Hemodialysis

A

perfusion of blood and dialysate on opposite sides of semipermeable membrane - remove substances from blood by diffusion = excess plasma water is removed via ultrafiltration

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15
Q

Peritoneal dialysis

A

permanent catheter - peritoneal membrane acts as semipermeable membrane - osmotic pressure is generated by various dextrose and icodextrin concentrations

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16
Q

What components can make up the osmotic pressure in peritoneal dialysis

A

dextrose; icodextrin

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17
Q

What is analgesic nephropathy

A

large doses of ASA and APAP can cause it

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18
Q

Nephritis = Glomerulonephritis = GN can be divided into what two groups

A

Primary and secondary

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19
Q

Secondary GN is associated with what?

A

systemic diseases - like SLE, HTN, diabetes

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20
Q

Pathogenesis of Glomerular Diseases = __________ reaction

A

immune

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21
Q

3 pathogenesis/immune reactions for glomerular diseases

A

1 - antibody - associated injury
2 - Cell mediated immune
3 - other mechanisms of glomerular injury

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22
Q

Nephrotic vs Nephritic Syndrome

A

Nephrotic - protein leakage only

Nephritic - protein AND RBC leakage

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23
Q

3 major types of Glomerular syndromes

A

nephrotic syndrome; nephritic syndrome; chronic glomerulonephritis

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24
Q

Common signs/symptoms of Nephrotic syndrome

A
  • proteinuria
  • hypoalbuminemia
  • edema
  • hyperlipidemia/lipiduria
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25
Q

Common signs/symptoms of Nephritic syndrome

A
  • hematuria
  • oliguria
  • azotemia
  • HTN
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26
Q

APKD:

inherited mutation of ________ gene _______ which gives rise to the protein ________

A

Dominant; PKD1 and PKD2; polycystein

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27
Q

Pathogenesis of APKD

A

Abnormal cysts formation in both kidneys; ultimately destroys intervening parenchyma; intermittent gross hematuria; HTN and urinary infection

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28
Q

Autosomal Recessive (______) Polycystic Kidney disease: Mutation in ______ which makes ______ (_______)

A

childhood; PKHD1; fibrocystin; polyductin

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29
Q

Clinical Features of Autosomal Recessive Polycystic Kidney Disease

A
  • serious at birth
  • young infants may die quickly from pulmonary or renal failure
  • Pts who survive infancy develop liver cirrhosis
30
Q 
Diuresis = ?
Natriuresis = ?
A 
D = increase in urine volume
N = increase in renal sodium excretion
31
Q

Possible Clinical uses for Diuretics

A
  • HTN
  • Edema
  • CHF
  • Kindey disease
  • hepatic cirrhosis
  • hypercalcemia
  • diabetes insipidus
32
Q

How do diuretics differ?

A

differ by site of action

33
Q

Most of water is reabsorbed where?

A

proximal tubule

34
Q

Examples of loop diuretics

A

furosemide; bumetanide; ethacrynic acid

35
Q

Examples of potassium sparing diuretics

A

spironolactone; triamterene; amiloride

36
Q

Examples of thiazides

A

HCTZ; Chlorthalidone

37
Q

What does the macula densa do and how?

A

monitors BP - done by looking at the amount of NaCl being reabsorbed

38
Q

What happens in the proximal convoluted tubule

A

Water, NaCl and HCO3 reabsorbed

39
Q

Loop of Henle: Descending limb is _________ to water vs ascending limb is ________ to water

A

permeable; impermeable

40
Q

Thick ascending limb is also known as “___________” because it pulls _____ back into the body

A

diluting segment; ions

41
Q

What gets reabsorbed in the ascending loop of henle?

A

NaCl; Ca2+; Mg2+

42
Q

The macula densa is near what portion of the tubules

A

distal convoluted

43
Q

ADH affects what part of the nephron

A

collecting duct

44
Q

Loop diuretics affect what of the nephron

A

ascending loop

45
Q

Aldosterone is a ___________ which acts on the __________ to keep what?

A

mineralcorticoid; collecting duct; NaCl and therefore water

46
Q

PASSIVE transport options for ions/solutes

A
  • Convective solute flow (dragged with water)
  • simple diffusion
  • channel-mediated
  • carrier- mediated/facilitated diffusion/uniport
47
Q

Is uniport passive or active transport?

A

passive

48
Q

is symport passive or active transport?

A

active

49
Q

is antiport passive or active transport?

A

active

50
Q

primary active or secondary active transport?

ATP - mediated transport

A

primary

51
Q

primary active or secondary active transport?

symport

A

secondary

52
Q

primary active or secondary active transport? antiport

A

secondary

53
Q

symport aka ________

A

co-transport

54
Q

antiport aka

A

counter transport

55
Q

what are active transport ways to move ions/solutes

A

ATP mediated transport, symport, antiport

56
Q

Types of Antibody mediated glomerular injury

A
  • circulating - immune complex deposition
  • Anti - GBM antibody
  • antibody against glomerular antigen
57
Q

what is Anti-GBM antibody glomerular injury

A

an antibody will bind to the Glomerular Basement Membrane and cause damage to the membrane - autoimmune issue

58
Q

what is immune complex deposition glomerular injury

A

a complex (antibody AND antigen) will bind to membrane and cause breakdown of the membrane

59
Q

If the _________ are damaged/detached then protein leakage through defective GBM and filtration slits will occur

A

podocyte foots

60
Q

Common agents that will cause an ascending infection

A

E.Coli, proteus, enterbacter

61
Q

Combination of what things can lead to an ASCENDING INFECTION to cause acute pyelonephritis/renal infection

A

Urinary bladder infection; vesicoureteral reflux; intrarenal reflux

62
Q

What two infections can lead to acute pyelonephritis

A

hematogenous infection and ascending infection

63
Q

Pathogenesis Autosomal/Adult PKD

Hypertension and Urinary infection –> Ultimately fatal –> ________ is necessary.

A

Renal transplantation

64
Q

what notable parts of the nephron are in the cortex

A

proximal (straight and convoluted) tubule, distal convoluted tubule; collecting tubule

65
Q

what notable parts of the nephron are in the medulla

A

descending limb; ascending limb; collecting duct

66
Q

Where does the diuretic work?:

Osmotic agents

A

proximal convoluted tube; descending limb; collecting duct

67
Q

Where does the diuretic work?:

Acetazolamide - an Carbonic anhydrase inhibitor

A

proximal convoluted tubule

68
Q

Where does the diuretic work?:

Loop agents

A

ascending limb

69
Q

Where does the diuretic work?:

Thiazides

A

Distal convoluted tubule

70
Q

Where does the diuretic work?:

Adenosine

A

glomerulus; proximal convoluted; thick ascending; collecting duct

Therapeutics I - Spring 2017 (17 decks)

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