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semester 2 2019 > 265 - renal disorders > Flashcards

265 - renal disorders Flashcards

1
Q

what is the vasa recta?

A

network or blood vessels surrounding the nephron tubules which allow the urine to become concentrated

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2
Q

describe the blood vessel structure of the glomerulus

A

about 50 capillaries, with arterioles on either side of the capillaries (smooth muscle of arteriole allows for vasoconstriction to regulate glomerular blood pressure

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3
Q

which ion concentrations do the kidneys regulate?

A 
Na+
Cl-
K+
Ca2+
HPO4(2-)  (hydrogen phosphate)
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4
Q

how do the kidneys regulate blood pH?

A

excrete H+ in urine and retain HCO3- to reduce acidosis

excrete HCO3- and retain H+ to reduce alkalosis

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5
Q

what is venous blood pH?

A

7.32 - 7.42

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6
Q

how do the kidneys regulate blood pressure?

A

through increasing or decreasing secretion of water according to ADH/aldosterone present

through secretion of renin

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7
Q

which hormones do the kidneys produce?

A

calcitriol

erythropoietin

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8
Q

what is the normal osmolarity of blood, as regulated by the kidneys?

A

about 275-299 mOsm/L

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9
Q

what are some of the wastes removed from the body by the kidneys?

A 
ammonia
urea
bilirubin
creatinine
uric acid 
toxins/chemicals from the diet
drugs
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10
Q

what percentage of cardiac output do the kidneys receive?

A

about 20-25%

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11
Q

why is anaemia associated with acute renal failure?

A

lack of production of EPO (can now by supplemented artificially)

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12
Q

how do the kidneys help to regulate blood glucose levels

A

gluconeogenesis (secondary to the liver) in the renal cortex

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13
Q

describe renal blood flow

A

Blood enters renal artery → branches out into afferent arterioles (one per nephron) → glomerulus (capillary network)→ efferent arterioles→form peritubular capillaries → VASA RECTA (surrounds Nephron loop (of Henle) → blood exits kidneys via renal vein.

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14
Q

describe the regulation of renal blood flow

A
  1. autoregulation - stretch (myogenic effect) from increased flow → constriction of the afferent arterioles → ↓blood flow
  2. regulation by the SNS
  3. RAAS
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15
Q

where is angiotensinogen produced?

A

the liver

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16
Q

what is renin?

A

an enzyme

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17
Q

effects of angiotensin II?

A

vasoconstriction

release of aldosterone from the adrenal cortex → ↑ reabsorption of Na+ and H2O follows passively

release of antidiuretic hormone (ADH) from posterior pituitary gland → ↑reabsorption of H2O and ↑vasoconstriction

↑ thirst

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18
Q

what triggers RAAS?

A

decreased renal flow causes release of renin

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19
Q

which meds will affect kidney function?

A

NSAIDs e.g. large doses of aspirin, ibuprofen

some antibiotics e.g. gentamycin, vancomycin

alcohol

some blood pressure medications

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20
Q

about how much filtrate is produced each day?

how much (very roughly) per minute?

A

180L/day

120 ml/min

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21
Q

why do proteinuria and haematuria occur in inflammation/infection?

A

inflammation causes the pores in the glomerular capillaries to enlarge and this allows protein and blood into the urine

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22
Q

what are the processes/functions of the nephron that allow for urine production?

A

glomerular filtration

tubular reabsorption

tubular secretion

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23
Q

renal function tests?

A

creatinine clearance - estimates GFR - 24hr urine collection + bloodtest

Blood Urea Nitrogen (BUN) - rough estimate of GFR

Cystatin C - a protein produced in most cells which gets filtered but reabsorbed - good marker of renal function

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24
Q

what is transport maximum (Tmax)?

A

the limit to which the amount of a solute (e.g. glucose) can be reabsorbed from the filtrate into the blood. When exceeded the solute appears in the urine

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25
Q

what is renal threshold?

A

the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine

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26
Q

describe Tmax and renal threshold using glucose as an example

A

Tmax for glucose is roughly 10mmo/L. If blood glucose is < 10mmol/L all the filtered glucose will be returned to the blood → no glucose in the urine.

if blood glucose is > than 10mmol/L then the renal threshold is exceeded and not all glucose can be returned to the blood → glucose in the urine (glycosuria)

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27
Q

difference between urethritis, cystitis and pyelonephritis?

A

urethritis – inflammation of the urethra
cystitis – inflammation of the bladder
pyelonephritis – inflammation of the ureters/renal pelvis

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28
Q

why are UTIs so common in hospital?

what percentage of nosocomial infections do they represent?

A

largely due to use of IDCs

about 40% of nosocomial infections

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29
Q

main organisms involved in UTIs?

A

E. coli mostly, also staph et al.

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30
Q

about how long does it take for a catheter to become colonised?

A

about 48 hrs, therefor IDCs should be avoided and removed ASAP

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31
Q

risk factors for UTIs?

A

urinary stasis

foreign bodies ie. stones, catheters

anatomical factors: congenital defects, fistulas

compromised immune (ageing, DM, HIV)

functional disorders (constipation)

other factors - pregnancy, menopause, poor hygiene, habitual delay of urination, spermicide/diaphragm use

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32
Q

what can cause urinary stasis?

A

intrinsic obstruction - stone, tumour of urinary tract,
urethral stricture, BPH (benign prostatic hyperplasia)

extrinsic obstruction (tumour, fibrosis compressing urinary tract)

urinary retention

renal impairment

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33
Q

pathophysiology of UTI?

A

introduction of organisms into a normally sterile bladder

NB: lower urethra colonized by perineal organisms which are flushed out with urine flow.

34
Q

UTI signs and symptoms?

A

burning/stinging when passing urine - dysuria

urgency with small volumes passed each time and incontinence (dribbling) of urine after voiding

ascending infections can cause severe pain

35
Q

why is urinary incontinence associated with UTI?

A

indicates dysfunction or urinary sphincters, less ability to keep out pathogens

36
Q

potential consequences of untreated UTI?

A

bacteraemia (organisms in blood)

sepsis (bacterial toxins in blood)

death from septic shock

37
Q

which bacteria cause nitrites in the urine?

A

gram -ve only

38
Q

management of UTIs?

A

Ural from chemist alkalinises urine to relieve burning on voiding

antibiotics should match the infective organism

adequate fluid intake

antipyretics & analgesia – care in patients with renal dysfunction

39
Q

diagnosis of UTIs?

A

urinalysis - nitrites/proteins/blood

MSU and urine cultures

40
Q

which AB commonly used to treat UTIs is contraindicated in people with renal failure? why?

A

co-trimoxazole as it increases serum potassium

41
Q

nursing management of UTIs?

A

recognise risk factors

teach preventative measures: emptying the bladder regularly and completely & wiping from front to back

drinking adequate amount of liquid (1.5-2L/day depending on renal and cardiac function)

avoid unnecessary catheterisation and early removal of indwelling catheters

42
Q

what is acute kidney injury also known as?

A

acute renal failure (old name for it)

43
Q

why is acute kidney injury potential fatal?

A

inability to excrete ions leads to electrolyte imbalances (hyperkalaemia can mean cardiac arrest)

44
Q

common causes of AKI?

A

low fluid volume

nephrotoxic drugs e.g. vancomycin, gentamicin, NSAIDs

45
Q

common causes of low fluid volume?

A 
dehydration, 
haemorrhage, 
diuretics, 
vomiting, 
diarrhoea, 
heart failure, 
sepsis
46
Q

pathophysiology of AKI?

A

RAAS → constriction of renal arterioles → ↓GFR

low fluid volume → blood diverted from kidneys to maintain heart and brain circulation

47
Q

assessment for AKI?

A

signs of dehydration: dry mucous membranes, hypotension, oliguria

urinalysis is normal or near normal

48
Q

AKI classifications?

A

prerenal- develops outside the kidneys

intrarenal –develops in the kidneys

postrenal –develops in ureters, bladder or urethra

49
Q

causes of prerenal AKI?

A

sudden or severe drop in BP:

hypovolaemia
sepsis
burns
fluid losses
dehydration

or flow obstruction to the kidneys due to:

atherosclerosis
ischemia

50
Q

causes of intrarenal AKI?

A

direct damage to kidney

inflammation or infection of the kidney including pyelonephritis or glomerulonephritis

toxins/drugs

autoimmune diseases such as lupus

51
Q

causes of postrenal AKI?

A

obstruction of urine flow due to enlarged prostate, stones, tumour, injury, benign prostatic hyperplasia

52
Q

what is pyelonephritis?

A

ascending bacterial infection from bladder to kidneys (renal pelvis)

53
Q

signs and symptoms of pyelonephritis?

A 
fever
back pain 
signs of UTI
nausea and vomiting 
haematuria
pyuria
WBCs and bacteria in urine
54
Q

what is glomerulonephritis?

A

Inflammation of the glomeruli in the nephrons due to diabetes, genetics, following streptococcal infection or viral infections e.g. hepatitis A or C

55
Q

signs and symptoms of glomerulonephritis?

A 
haematuria 
proteinuria 
hypertension
fluid retention 
oedema
56
Q

difference between chronic kidney disease and acute kidney injury?

A

CKD is decrease in function that happens over three months; acute happens in less than three months

acute is usually reversible

57
Q

most common form of acute kidney injury?

A

intrarenal AKI

58
Q

four main causes of intrarenal AKI?

A

acute glomerular nephritis

acute tubular nephritis

acute interstitial nephritis

vascular causes - vasoconstriction, endothelial dysfunction, increased adhesion of inflammatory cells

59
Q

what percentage of intrarenal AKI is caused by acute tubular nephritis?
what are the most common causes of acute tubular nephritis?

A

about 50%

cause is usually ischemic (from prolonged hypotension) or nephrotoxic (from an agent that is toxic to the tubular cells)

60
Q

you need to remember that prerenal, intrarenal and postrenal AKI are heavily interrelated -

A

especially that prerenal and postrenal AKI will often then cause intrarenal AKI

61
Q

two main changes that cause decreased GFR?

A

vascular changes (particularly in the afferent arteriole)

tubular change including damaged cells, necrotic bodies causing obstruction

62
Q

characteristics of AKI?

A

functional changes:

decreased GFR

decreased urine output

increased nitrogenous wastes present in blood (urea, creatinine)

and structural changes:

cell death

loss of adhesion to intrinsic renal cells

63
Q

what is acute interstitial nephritis mostly due to?

A

allergy or infection

64
Q

examples of nephrotoxic drugs?

A

aminoglycosides (gentamicin, tobramicin), vancomycin, NSAIDS

65
Q

what are the four phases of AKI, and their duration?

A

onset phase - hours to days
oliguric phase - 8 - 14 days
diuretic phase - 7 - 14 days
recovery phase - several months to a year

66
Q

describe the first phase of AKI?

A

onset phase:

renal blood flow 50% of normal

tissue perfusion 50% of normal

urine output <0.5ml/kg/hr

67
Q

describe the second phase of AKI?

A

oliguric phase:

urine output <400 ml/day (can be as low as 100ml/day)

increases in blood urea nitrogen (BUN) and creatinine

electrolyte disturbances, acidosis, fluid overload

68
Q

describe the third phase of AKI?

A

diuretic phase:

occurs when cause of AKI corrected

renal tubule scarring and oedema

increased GFR

daily urine output > 400ml

possible electrolyte depletion from excretion of more water and osmotic effects of high BUN

69
Q

describe the fourth phase of AKI?

A

recovery phase:

decreased oedema

normalisation of fluid and electrolyte balance

return of GFR to 70% - 80% of normal

70
Q

what happens if there is no recovery phase in AKI?

A

leads to CKD

71
Q

what are the electrolyte imbalances associated with the oliguria phase of AKI?

A

↑ K+, ↓ Na+, H+ and metabolic acidosis due to kidneys unable to excrete ions

72
Q

clinical manifestations of oliguria phase of AKI?

A

fluid retention, oedema

kussmaul’s respirations as a result of metabolic acidosis

neurological disorders (fatigue, poor concentration, seizures, coma) due to neurotoxic effects of nitrogenous wastes

if Na+ < 135mmol/L → cerebral oedema

73
Q

describe urine output in the diuretic phase of AKI?

A

daily urine output > 400ml as distinct from oliguric phase

1 to 3L urine/day, but may be > 5L

74
Q

management of AKI?

A

Prerenal:
• Correction of fluid volume deficit
• Improve cardiac function with inotropic agents
• Correct hypotension

Intrarenal:
• Correct cause e.g. antibiotics for infection Postrenal:
• Correct cause of the obstruction

Postrenal:
• Correct cause of the obstruction

75
Q

nursing management of AKI?

A
  1. Monitor blood electrolyte levels
  2. Daily weight (fluid load)
  3. Monitor urine output
  4. Strict fluid balance record
  5. Restriction of sodium and potassium intake
  6. Fluid restriction – based on patients clinical condition
  7. Health education for the person and family
76
Q

define CKD?

A

progressive and irreversible loss of kidney function

either the presence of kidney damage, or a decreased GFR < 60 mL/min/1.73 m2 for longer than 3 months

77
Q

main causes of CKD?

A

hypertension (20%),

diabetes and metabolic syndrome (30%)

glomerulonephritis (25%)

78
Q

main systemic effects of CKD?

A

increased blood volume (can lead to CCF)

uremia, azotemia - CNS abnormalities, GIT upset

hyperkalaemia - disrhythmias/cardiac arrest

anaemia

hypocalcaemia leading to bone disease

blood clotting disorders

increased infections

79
Q

what is azotemia?

A

increased nitrogenous wastes in blood

80
Q

what is uraemia?

A

increased urea in blood

semester 2 2019 (16 decks)

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