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NUR370 Pathophysiology and Pharmacology > Renal Disorders > Flashcards

Renal Disorders Flashcards

1
Q

How are glucose and insulin used to treat hyperkalemia associated with AKI?

A

when insulin transports glucose into cells, it carries potassium with it

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2
Q

Most common causes of CKD

A

Diabetes (35%)
High blood pressure (30%)
Glomerulonephritis (12%)

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3
Q

Functions of the kidney

A
  1. waste management
  2. drug and peptide hormone elimination
  3. maintenance of fluid and electrolyte balance
  4. regulation of acid-base balance
  5. endocrine functions
  6. regulation of extracellular fluid balance and BP
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4
Q

Hormones associated with kidneys

A

a. Renin - RAAS
b. Aldosterone - reabsorption at distal tubule
c. ADH - reabsorption at collecting tubule
d. activate vitamin D - stimulate Ca and phosphate absorption in intestine
e. erythropoietin formation - bone marrow

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5
Q

What goes on in the Glomerulus/Bowman’s Capsule

A

Filtration

  • water, NaCl, glucose, amino acids, urea
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6
Q

What goes on in proximal convoluted tubule?

A

Reabsorption

  • NaCl, water, urea, bicarbonate, glucose, others
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7
Q

What goes on in Loop of Henle?

A

Concentrate urin

reabsorb water (descending loop)
reabsorb sodium (ascending loop)
urea secretion (thin segment)
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8
Q

What goes on in distal convoluted tubule and collecting tubule?

A

distal tubule: acid-base balance

collecting tubule: electrolyte/fluid balance

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9
Q

How much fluid does the kidney filter per day?

A

180L/day

120mL/min

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10
Q

Causes of Pre-renal AKI

A

reduction in blood flow to kidney

a. hypovolemia
b. decreased CO
c. thrombo-embolic obstruction of renal vasculature

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11
Q

Causes of intra-renal AKI

A

damage to structures within kidney

a. acute tubular necrosis
b. glomerular, tubular or interstitial damage

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12
Q

Causes of post-renal AKI

A

obstruction in the urinary tract BELOW kidney

a. renal calculi (kidney stones)
b. clots in ureters/urethra
c. tumours

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13
Q

Kidneys receive how many percent of CO?

A

20-25%

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14
Q

Acute Tubular Necrosis (ATN)

A

death of tubular epithelial cells, damage to tubules

caused by nephrotoxic drugs, severe hemolytic reactions or muscle trauma

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15
Q

Glomerulonephritis

A

inflammation of the glomeruli caused by an IMMUNE RESPONSE

antigen-antibody complex trapped in glomerulus, causing large molecules to enter filtrate

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16
Q

Manifestations of glomerulonephritis

A

hematuria
proteinuria
hypertension
edema

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17
Q

Pyelonephritis

A

inflammation of kidney pelvis and parenchyma from infection

  • can descend from bloodstream or ascend from UTI
  • causing fibrosis formation
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18
Q

Manifestations of pyelonephritis

A 
Fever
abdo pain
dysuria (pain when urinating)
cloudy urine
polyuria/urgency
urinary odour
19
Q

Nephrotic syndrome

A

urinary excretion of >3g of protein/day, edema, hypoalbuminemia

(SEVERE)

20
Q

Nephritic syndrome

A

nephron inflammation characterized by hematuria and RBC casts, SOME proteinuria and edema

  • less severe as nephrotic
21
Q

Manifestations of Nephrotic syndrome

A

edema (face, eyes, leg, ankle)
foamy urine (protein)
weight gain

22
Q

Azotemia

A

nephrotoxicity that involves excess nitrogen compounds (urea, creatinine, nitrogen-rich compounds)

  • elevated BUN and creatinine
  • uremic frost

can occur in all types of AKI

23
Q

Uremia

A

high levels of urea in blood
(more severe than azotemia)

TERMINAL clinical manifestation of kidney failure

CrCl <10-20mL/min

24
Q

Acute uremic symptoms

A
  1. fluid/electrolyte balance dysregulation
  2. increase metabolic wastes (metabolic acidosis)
  3. uremic waste affecting GI tract
  4. decreased platelet adhesiveness and immune response
  5. metabolic waste on skin
  6. decreased EPO secretion (anemia)
25
Q

AKI management

A

a. Discontinue all nephrotoxic agents when possible
b. Ensure volume status and perfusion pressure (plasma expanders or diuretics)
c. Consider functional hemodynamic monitoring
d. Monitor serum creatinine and urine output
e. Avoid hyperglycemia
f. dialysis (if none else works)

26
Q

CKD Management

A

a. Management of protein intake
b. Supplemental vitamin D
c. Maintenance of sodium and fluid
d. Restriction of potassium (prevent hyperkalemia)
e. Maintenance of adequate caloric intake
f. Management of dyslipidemias
e. Erythropoietin as needed
f. ACE inhibitors or receptor blockers
g. Dialysis
h. Renal transplantation

27
Q

Increase in the following is usually indicative of kidney disease

A
  • BUN
  • serum creatinine
  • serum potassium
28
Q

Decrease in the following is usually indicative of kidney disease

A
  • GFR
  • creatinine clearance
  • drug excretion
29
Q

Sudden causes of uremia

A

trauma, shock, toxins, acute glomerulonephritis, sepsis

30
Q

What components are needed to calculate CrCl using Cockroft Gault?

A

age
BW in kg
SCr in μmol/L

31
Q

What causes hyperkalemia in kidney disease?

A

a. kidney dysfunction causing inability to excrete K+
b. K+ move out of cells (metabolic acidosis)
c. ACEIs
d. excessive K+ intake

32
Q

Sever hyperkalemia

A

K+ >= 7.0mmol/L

K+ = 6.0-6.9mmol/L with ECG changes

33
Q

What is the most appropriate treatment when hyperkalemia is accompanied by ECG changes?

A

calcium gluconate to stablize cardiac membrane

34
Q

Interventions to shift K+ into cells

A

a. insulin plus glucose (most effective! rapid acting)
b. sodium bicarbonate
c. inhaled salbutamol

35
Q

Interventions to remove K+ from body

A

a. sodium polystyrene - binds K+ in gut to increase GI excretion
b. hemodialysis
c. diuresis

36
Q

4 Key Therapeutic Strategies in management of diabetes and CKD

A
  1. manage hyperlipidemia
  2. control HTN
  3. maintain optimal glycemic control
  4. minimize proteinuria
37
Q

Causes of malnutrition in CKD

A
  1. decreased oral intake
  2. protein/vitamin loss from dialysis
  3. low serum albumin
38
Q

What drugs should be used to manage HTN in CKD?

A

ACEIs, ARBs, CCBs

Loop diuretics when CrCl <25ml/min

39
Q

What intervention is used to treat anemia in CKD?

A

blood transfusion

erythropoiesis stimulating agents

possibly iron supplements

40
Q

What is the target Hgb when administering ESA for anemia? What is the concern?

A

Hgb: 100-110 g/L

above target could increase risk of CV event

41
Q

What causes hypocalcemia in kidney disease?

A

a. increased phosphate bind to calcium causing calcium decrease
b. decreased activation of vit D causing decreased calcium absorption
c. decreased calcium stimulates PTH secretion (causing body to take calcium from bone)

42
Q

pharmacokinetic alterations in renal impairment

A
  • decreased absorption
  • decreased blood levels
  • increased free fraction (protein binding)
  • increased drug half life
43
Q

Drug dosing adjustment is based on

A
  • creatinine clearance

- if >50% of drug is renally eliminated

NUR370 Pathophysiology and Pharmacology (20 decks)

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