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semester 2 2019 > 265 - renal disorders > Flashcards

265 - renal disorders Flashcards

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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
what is renal threshold?
the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine
26
describe Tmax and renal threshold using glucose as an example
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)
27
difference between urethritis, cystitis and pyelonephritis?
urethritis – inflammation of the urethra cystitis – inflammation of the bladder pyelonephritis – inflammation of the ureters/renal pelvis
28
why are UTIs so common in hospital? | what percentage of nosocomial infections do they represent?
largely due to use of IDCs about 40% of nosocomial infections
29
main organisms involved in UTIs?
E. coli mostly, also staph et al.
30
about how long does it take for a catheter to become colonised?
about 48 hrs, therefor IDCs should be avoided and removed ASAP
31
risk factors for UTIs?
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
32
what can cause urinary stasis?
intrinsic obstruction - stone, tumour of urinary tract, urethral stricture, BPH (benign prostatic hyperplasia) extrinsic obstruction (tumour, fibrosis compressing urinary tract) urinary retention renal impairment
33
pathophysiology of UTI?
introduction of organisms into a normally sterile bladder NB: lower urethra colonized by perineal organisms which are flushed out with urine flow.
34
UTI signs and symptoms?
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
why is urinary incontinence associated with UTI?
indicates dysfunction or urinary sphincters, less ability to keep out pathogens
36
potential consequences of untreated UTI?
bacteraemia (organisms in blood) sepsis (bacterial toxins in blood) death from septic shock
37
which bacteria cause nitrites in the urine?
gram -ve only
38
management of UTIs?
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
diagnosis of UTIs?
urinalysis - nitrites/proteins/blood MSU and urine cultures
40
which AB commonly used to treat UTIs is contraindicated in people with renal failure? why?
co-trimoxazole as it increases serum potassium
41
nursing management of UTIs?
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
what is acute kidney injury also known as?
acute renal failure (old name for it)
43
why is acute kidney injury potential fatal?
inability to excrete ions leads to electrolyte imbalances (hyperkalaemia can mean cardiac arrest)
44
common causes of AKI?
low fluid volume nephrotoxic drugs e.g. vancomycin, gentamicin, NSAIDs
45
common causes of low fluid volume?
``` dehydration, haemorrhage, diuretics, vomiting, diarrhoea, heart failure, sepsis ```
46
pathophysiology of AKI?
RAAS → constriction of renal arterioles → ↓GFR low fluid volume → blood diverted from kidneys to maintain heart and brain circulation
47
assessment for AKI?
signs of dehydration: dry mucous membranes, hypotension, oliguria urinalysis is normal or near normal
48
AKI classifications?
prerenal- develops outside the kidneys intrarenal –develops in the kidneys postrenal –develops in ureters, bladder or urethra
49
causes of prerenal AKI?
sudden or severe drop in BP: ``` hypovolaemia sepsis burns fluid losses dehydration ``` or flow obstruction to the kidneys due to: atherosclerosis ischemia
50
causes of intrarenal AKI?
direct damage to kidney inflammation or infection of the kidney including pyelonephritis or glomerulonephritis toxins/drugs autoimmune diseases such as lupus
51
causes of postrenal AKI?
obstruction of urine flow due to enlarged prostate, stones, tumour, injury, benign prostatic hyperplasia
52
what is pyelonephritis?
ascending bacterial infection from bladder to kidneys (renal pelvis)
53
signs and symptoms of pyelonephritis?
``` fever back pain signs of UTI nausea and vomiting haematuria pyuria WBCs and bacteria in urine ```
54
what is glomerulonephritis?
Inflammation of the glomeruli in the nephrons due to diabetes, genetics, following streptococcal infection or viral infections e.g. hepatitis A or C
55
signs and symptoms of glomerulonephritis?
``` haematuria proteinuria hypertension fluid retention oedema ```
56
difference between chronic kidney disease and acute kidney injury?
CKD is decrease in function that happens over three months; acute happens in less than three months acute is usually reversible
57
most common form of acute kidney injury?
intrarenal AKI
58
four main causes of intrarenal AKI?
acute glomerular nephritis acute tubular nephritis acute interstitial nephritis vascular causes - vasoconstriction, endothelial dysfunction, increased adhesion of inflammatory cells
59
what percentage of intrarenal AKI is caused by acute tubular nephritis? what are the most common causes of acute tubular nephritis?
about 50% cause is usually ischemic (from prolonged hypotension) or nephrotoxic (from an agent that is toxic to the tubular cells)
60
you need to remember that prerenal, intrarenal and postrenal AKI are heavily interrelated -
especially that prerenal and postrenal AKI will often then cause intrarenal AKI
61
two main changes that cause decreased GFR?
vascular changes (particularly in the afferent arteriole) tubular change including damaged cells, necrotic bodies causing obstruction
62
characteristics of AKI?
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
what is acute interstitial nephritis mostly due to?
allergy or infection
64
examples of nephrotoxic drugs?
aminoglycosides (gentamicin, tobramicin), vancomycin, NSAIDS
65
what are the four phases of AKI, and their duration?
onset phase - hours to days oliguric phase - 8 - 14 days diuretic phase - 7 - 14 days recovery phase - several months to a year
66
describe the first phase of AKI?
onset phase: renal blood flow 50% of normal tissue perfusion 50% of normal urine output <0.5ml/kg/hr
67
describe the second phase of AKI?
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
describe the third phase of AKI?
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
describe the fourth phase of AKI?
recovery phase: decreased oedema normalisation of fluid and electrolyte balance return of GFR to 70% - 80% of normal
70
what happens if there is no recovery phase in AKI?
leads to CKD
71
what are the electrolyte imbalances associated with the oliguria phase of AKI?
↑ K+, ↓ Na+, H+ and metabolic acidosis due to kidneys unable to excrete ions
72
clinical manifestations of oliguria phase of AKI?
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
describe urine output in the diuretic phase of AKI?
daily urine output > 400ml as distinct from oliguric phase 1 to 3L urine/day, but may be > 5L
74
management of AKI?
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
nursing management of AKI?
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
define CKD?
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
main causes of CKD?
hypertension (20%), diabetes and metabolic syndrome (30%) glomerulonephritis (25%)
78
main systemic effects of CKD?
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
what is azotemia?
increased nitrogenous wastes in blood
80
what is uraemia?
increased urea in blood

semester 2 2019 (16 decks)

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