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Week 20: Vomiting and diarrhoea > general V+D > Flashcards

general V+D Flashcards

1
Q

Describe the pathophysiology of acute tubular necrosis

A
  • caused by ischaemic (hypotension) or nephrotoxic injury
  • results in death (or detachment from basement membrane) of tubular epithelial cells
  • presents as AKI and is one of the most common causes of AKI
  • reversible (supportive Rx)
  • muddy-brown casts in urine
  • hypoperfusion initiates cell injury (leads to cell death/necrosis)
  • decrease in GFR because of hypoperfusion and casts obstructing tubule lumen
  • renal IS; damage to tubule cells stimulate local secretion of pro-inflammatory cytokines which induces further necrosis
  • ischemia leads to reduced vasodilator release by tubular epithelium; further vasoconstriction and hypoperfusion
  • diagnostic features: hypotension, oligouria or anuria, tachycardia
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2
Q

define AKI

A

abrupt decline (over hours/days) in renal function defined as increased creatine or decrease in urine output

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3
Q

AKI can be classified as stage 1, 2 or 3. How is this defined?

A

defined by changes of patients baseline serum creatinine:

  1. increase of 1-1.9 x baseline
  2. increase of 2-2.9 x baseline
  3. increase of >3 x baseline (or need for dialysis)
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4
Q

who is at risk of AKI?

A 
elderly
CKD
diabetics
HF - poor CO
liver disease - hypotension
PVD - renal artery stenosis
patients already in hospital
inflammatory diseases
hypertension
surgery
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5
Q

what are the common triggers?

A 
hypotension
hypovolaemia
sepsis
deteriorating NEWS
surgery
contrast scans and angiography 
certain drugs (ACEi/ARB)
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6
Q

certain medication can make AKI worse. What are they?

A 
1. ACEi
2 ARB
3. NSAIDs
4. Metformin
5. Gentamicin
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7
Q

how could you assess a patients fluid status (hypovolemic or fluid overload)?

A
  • general appearance - e.g. mucous membranes, breathlessness, oedema, skin turgor
  • pulse and BP
  • JVP
  • chest sounds
  • peripheral oedema
  • weight changes
  • fluid balance chart
  • capillary refill
  • temperature of periphery

*(vital signs and general examination)

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8
Q

what vital signs are associated with increased risk of AKI?

A
  • NEWS>5
  • RR>20
  • BP<100mgHg
  • tachycardia>90
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9
Q

once AKI has been identified what is involved in the clinical care?

A
  1. supportive
  2. fluid balance
  3. appropriate drug therapy
  4. manage the underlying presenting complaint
  5. find the precipitant cause (pre- renal, renal or post-renal)
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10
Q

at what point should someone with AKI be referred?

A

stage 3 AKI or stage 2 non-responded, high K+ or any evidence of fluid overload

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11
Q

what are the indications that a patient may need fluid resuscitation and how would you initiate treatment?

A
  • sytolic BP <100mmHg
  • HR >90
  • capillary refill >2s (or periphery cold to touch)
  • RR >20breaths per min
  • NEWS >5

Treatment:

  • identify cause and respond
  • give a fluid bolus of 500ml of crystalloid (containing sodium 130-154mmol) over less than 15mins
  • reassess
  • if pt still needs fluid allow up to 2L before seeking expert help (seek immediate help if pt shows signs of shock)
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12
Q

what cannula would be used if you wanted to get fluids into your pt asap?

A

14G red 3.5min

22G blue 22min; 20G pink 15min;18G green 10min; 16G grey 6min

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13
Q

what are the causes of AKI?

A

pre-renal:

  • reduced blood flow (hypotension, cardiac failure
  • dehydration/hypovolaemia (burns, haemorrhage, v+d, diuretics) reduced ECV
  • infection
  • damage to kidney that is reversible
  • heptorenal syndrome
  • vasoactive drugs (NSAIDs and immunosuppressants)
  • ask- about vomiting or diarrhoea, infection, heart failure, ACEi/ ARB

renal:

  • glomerulonephritis (systemic lupus, erythmatosis or post strep infection PSGN)
  • vasculitis (lupus)
  • interstitual nephritis (allergic reactions and infection)
  • acute tubular injury (nephrotoxins, rhabdomyolysis, proloned pre-renal AKI)
  • complex
  • ask-about drugs, contrast medium, myeloma, rhabdomyolysis, glomerular disease

post-renal:

  • kidney stones
  • prostatic hypertrophy
  • retroperitoneal fibrosis
  • ask-lower urinary tract symptoms, obstruction, pelvic symptoms
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14
Q

name some functions of the kidney?

A
  • regulation of ECF volume and BP
  • regulation of osmolality
  • maintenance of ion balance
  • regulation of pH
  • excretion of waste
  • production of hormones
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15
Q

what are the 2 different types of nephrons based on location?

A
  1. superficial (high in cortex)
  2. juxtamedullary (tubules go down into medulla)

*the arterial supply to the Loop of Henle of superficial nephrons is fed from juxtamedullary vasa recta

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16
Q

describe the main processes that occur in the nephron (5steps)

A
  1. filtration by glomerulus (under pressure, fluid is regressed from capillaries)
  2. OBLIGATORY reabsorption (Na+, Cl-, K+, glucose, amino acids, urea, bicarbonate and water) and secretion (creatinine, drugs and H+) by proximal tubule
  3. generation of osmotic gradient by LOH (descending limb= reabsorbtion of water; thick ascending limb reabsorbtion of Na+, Cl-, HCO3-, Ca2+, Mg2+ and K+)
  4. REGULATED reabsorption (Na+, Cl-, K+, Ca2+, Mg+ and bicarbonate) and secretion (H+, K+) by distal tubule
  5. regulation of water uptake by collecting ducts (reabsorbtion of Na+, Cl-, urea and water)
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17
Q

define renal re absorption and secretion

A

reabsorption - movement of water and solutes from the nephron tubule back into circulation

secretion - movement of solutes and water from the circulation into the nephron tubule

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18
Q

describe the function of the juxtaglomerular apparatus

A

composed of distal convoluted tubule and the glomerular afferent arteriole. main function is to regulate blood pressure and the filtration rate:

  • macula densa cells sense Na+ concentration in the DCT (decrease in Na+ causes (1) decrease in resistance to blood flow in the afferent arterioles, which raises glomerular hydrostatic pressure and helps return the GFR (2) increases renin release from granular cells. increase in Na+ causes relaease of adenosine that inhibits the renin system)
  • renin increases blood pressure via RAAS
  • extraglomerular mesangeal cell function unclear
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19
Q

what is the function of (a) podocytes and (b) mesangeal cells?

A

a) support capillaries of glomerulus and prevent blood pressure from expanding and bursting capillaries. prevent large molecule (e.g. albumin) filtration
b) scaffolding of glomerulus. contractile cells that can contract and relax to alter filtration rate

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20
Q

filtrate has to cross a triple barrier which allows free passage of solutes only up to ~60kDa (-vely charged molecules are filtered less easily than +ve - BM is -vely charged). what makes up this barrier?

A
  1. endothelial lining of the capillaries
  2. basement membrane of the capillaries
  3. foot processes of epithelial cells (podocytes)
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21
Q

what are the starling forces favouring and opposing movement into tubules?

A

favouring = HP of 55mmHg

opposing = HP of -15mmHg, OP = -30mmHG

*net filtration = 10mmHg

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22
Q

what are the 2 autoreglation mechanisms (intrinsic factors) of glomerular filtration?

A
  1. myogenic mechanism: stretch activated ion channels in arterioles .
    - afferent arteriole: constriction reduces filtration P and GFR falls. Dilation increases P and GFR increases
    - efferent arteriole: constriction causes P to back up within the capillary increasing GFR. dilation allows blood to easily escape the capillary and P falls = GFR fall
  2. tubuloglomerular feedback: in conditions of high filtrate flow - increase of Na+ concentrations within the DCT. ions monitored by the macula densa cells which send signals (adenosine) to afferent arteriole causing it to constrict. lower filtration rate to normal limits (prostoglandins cause arteriole to relax)
23
Q

what are the extrinsic hormonal factors affecting renal blood flow and GFR?

A

decreased afferent blood flow - vasoconstriction:

  • SNS; norepinephrine
  • circulating epinephrine
  • angiotensin II (also constics efferent arteriole)

increased afferent blood flow - vasdodilation:

  • renal prostoglandins
  • atrial natriuretic peptide
24
Q

give an example of active and secondary active transport in the kidney tubules

A

active: Na+/K= pump transports Na+ from tubular epithelium through basolateral membrane (created concentration gradient, therefore sodium can diffuse from lumen into tubular cells)

secondary active: SGLT (sodium glucose co-transporter) transports glucose along with sodiums gradient from lumen into tubular cells

25
Q

where does the following take place?

a) 5% of filtered load of sodium absorbed
b) 20% of filtered water and 25% of filtered sodium, chloride and potassium reabsorbed
c) 65% of filtered load of sodium and water reabsorbed
d) impermeable to water
e) absorbed less than 10% of filtered water and sodium
f) only permeable to water
g) urine becomes more dilute

A

a) early DCT
b) ascending LOH
c) PCT
d) ascending LOH and early DCT and collecting duct (unless ADH is present)
e) collecting ducts
f) descending LOH
g) DCT and CD

26
Q

what are the different classes of diuretics and where do thy have affect?

A

Loop diuretics:
- furosemide, ethacrynic acid and bumetanide
- inhibit transport of Na+. 2Cl- and K
+ in thick ascending limb of LOH
- cannot reabsorbe Na+ therefore lost in urine with water (water follows salt)

Thiazide diuretics:
- inbibit Na+/Cl- co-transport in early DCT

aldosterone antagonsist:

  • spironolactone and eplerenone
  • leads to high K+ in serum and increased sodium excretion (affects Na+/K+ pump) in principal cells of late DCT

Na+ channel blockers:

  • amiloride and triamterene
  • block sodium entry into principal cells of late DCT. therefore, remain in tubular lumen
27
Q

what are the 2 cell types of the late DCT?

A

principal cells: absorb water and sodium

intercalated cells: absorb K+ and secrete H+

28
Q

how does aldosterone, angiotensin II and ADH hormones regulate tubular reabsorbtion?

A

aldosterone:

  • acts on the collecting tubule and ducts
  • increases NaCl and water reabsorbtion and K+ secretion
  • increases blood pressure and vol

angiotensin II:

  • acts on PCT, thick ascending LOH, DCT and CT
  • increases NaCl and water reabsorbtion. increases H+secretion
  • acts during heamorrage
  • stimulates aldosterone release

ADH:

  • acts on DCT and coleecting tubule and duct
  • increases water reabsorbtion
29
Q

describe the changes in the osmolarity of fluid as it travels through the nephron

A

-normal Osm of ECF as it enters the kidney = 300mOsm/L
(- increases to 600mOsm/L is LOH)
- reduced to 100mOsm/L by entry into DCT
- additional rabsorbtion of NACl in the DCT and collecting ducts reduces the Osm further (about 70 mOsm/L)
- if ADH present the tubule is impermeable to water and fluid is as low as 50mOsm/L

30
Q

what mechanism actively generates a concentration gradient being greater the deeper into the medulla you go?

A

counter-current mechanism of the Loop of Henle

31
Q

the ability to excrete urine that is more concentrated than plasma is essential for survival. why is this and what is needed for this to happen?

A
  • to allow conservation of water especially when water intake is limited
  • needs to be high concentration of ADH (make collecting ducts permeable to water) and a gradient to pull the water out (high osmolarity in the medullary interstitial fluid)
32
Q

how can urea contribute to the osmolarity of the medullary interstitial gradient when the kidney needs to form maximally concentrated urine in dehydration?

A
  • urea becomes increasingly concentrated through the tubules as more and more water is reabsorbed
  • is even further increased in the presence of ADH
  • the high conc causes it to diffuse out of the medullary collecting ducts into the medullary interstitial fluid (facilitated by urea transporters- can be activated by ADH)
  • allows you to drag out last remnants of water
  • re-enters the LOH to re-circulate process
  • in full hydration, water loss is faster than urea re-circulation
33
Q

what conditions cause an increase or decrease in ADH secretion from pituitary?

A

increase:

  • increase in plasma osmorality
  • decrease in blood volume
  • decrease in blood pressure
  • nausea
  • hypoxia
  • drugs e.g. morphine, nicotine

decrease:

  • decrease in plasma osmolarity
  • increase in blood volume
  • increase in BP
  • drugs e.g. alcohol, clonidine (anti-hypertensive), haloperidol (dopamine blocker)
34
Q

what is GFR?

A

•Proportional to the number of functioning glomeruli present – reflects ‘function’ of the kidney
•Volume of plasma filtered/unit of time =120mL/m (varies depending on age, weight, race, sex etc)
-use eGFR to consider variable factors

35
Q

name 1 value and 1 limitation of testing (a) creatinine levels, (b) urea levels and (c) eGFR to assess renal function?

A

a) value:- freely filtered and not reabsorbed
limitations: - can temporally rise in dehydration

b) value:- exogenously acquired from protein intake
limitation: - up to 50% is reabsorbed in PCT

c) value:- since GFR declines with age and has other variable factors, needs to be standardised
limitation: - Cockcroft-Gault formula weight it a surrogate for muscle mass and MDcalc is less acurate if near normal GFR (under estimate)

36
Q

How does renal blood flow affect GFR?

A

-due to the hydraulic pressure in the glomerulus based on afferent and efferent dilation/constriction

37
Q

what drugs can affect GFR and how?

A

ACEi (inhibit AT-II production) and ARB (block AT-II receptors):

  • dilate efferent arteriole > afferent
  • reduce intraglomerular pressure

NSAIDs:

  • inhibit prostoglandin synthesis
  • reduce intraglomerular pressire
  • drop GFR

*allow 30% creatinine rise and 25% GFR drop before renal problem identified in pt’s on these drugs (blood test before initiating drug and check 1-2wks after)

38
Q

what imaging investigations can be used to identify renal function?

A

•MAG3
- look at perfusion and effective renal plasma flow

•Cr-EDTA/Tc-DTPA
-measure renal or plasma clearance

•DMSA
- assess renal morphology, structure and function

39
Q

what additional Ix can assess renal function?

A
  • urinanalysis (blood, bilirubin, ketones, glucose, protein, nitrites, leukocytes, pH, specific gravity)
  • ACR or PCR ratio
  • haemoglobin (EPO)
40
Q

why might you prescribe ACEi in nephropathy?

A

diabetic patient

  • protein in urine = nephropathy
  • give ACEi to take load off vessels to decrease GFR
41
Q

what are the complications of AKI?

A

uraemia:

  • toxic
  • anorexia, nausea, confusion, fatigue, oedema (cant get rid)

hyperglycemia:

  • life threatening
  • K >5.5
  • cardiac arrhythmia

pulmonary oedema:

  • life threatening
  • (in anuria, need dialysis)
  • give diuretic (Heart>kidney)

(uraemic) pericarditis:
- life threatening
- cardiac tamponade + death

infection:

  • life threatening (sepsis)
  • catheter
42
Q

how would you manage hyperkalemia?

A

1st:
- IV Ca2+
- effective within 3mins
- reduces depolarisation effect of an elevated K on cardiac myocytes
- only lasts 30-60 mins so need to repeat dose!!
- stabilised K+, still need to get rid

2nd:

  • insulin-dextrose
  • causes intracellular accumulation of K+
  • effect in 5mins, peak 60min
  • lasts 2 hours and then get a rebound when it starts to leak out again
  • salbutamol can increase the efficacy of Na+/K+ transporter internalising the K+ (but 40% pts are unresponsive)
  • stabilised K+, still need to get rid (1+2 are holding measures)

3rd:

  • need to flush K+ out
  • via fluid resuscitation
  • reestablishes filtration of K+
  • dialysis if anuric
43
Q

what are the key clinical signs of aki?

A
  • reduced GFR
  • increased creatinine
  • oliguria
  • Hypernatremia
  • oedema
44
Q

what are the key clinical signs of acute tubular necrosis?

A
  • decreased GFR
  • hyponatremia (increase Na+ in tubule is detected by MD cells –> adenosine –> decrease renin –> vasoconstriction afferent arteriole –> hypertention)
  • oligourea
  • muddy brown casts in urine
  • hyperkalemia
  • metabolic acidosis
  • Azotemia
45
Q

what are the clinical signs of nephrotic syndrome?

A
  • proteinurea!!!! - (frothy coca-cola urine)
  • hypoalbuminemia
  • hyperlipidemia
  • oedema
46
Q

what are the clinical signs of nephritic syndrome?

A
  • proteinurea
  • haematuria
  • oliguria
  • hypertension
  • inflammation
  • WBCs in urine
47
Q

what are some of the possible effects of kidney disease on drug activity?

A
  • Reduced renal excretion/ prolonged half-life ->Drug metabolites build up -> toxicity
  • Sensitivity to some drugs increased even if elimination is unimpaired (e.g. opioids being more readily available to cross the BBB)
  • Increase risk of adverse drug effects
  • Some drugs are not effective with reduced renal function
  • Drug-induced renal disorders are more common in pt’s with CKD
48
Q

What are the 3 approaches to altering drug maintenance doses in pt’s with RI, depending on the desired goal of therapy

A
  1. standard dose given but at extended intervals
  2. or a reduced dose is given at usual intervals
  3. or a combination of reduced dose and extended intervals
49
Q

Vancomycin, gentamicin, digoxin and lithium are high renal clearance drugs with narrow therapeutic windows. What actions are recommended when prescribing these drugs in aki patient?

A

Dose reduction and extended dose intervals

*drugs with narrow T.window require the greatest care in use

50
Q

The Sick Day Rule cards have been produced to aid patients in understanding which medicines they should stop taking temporarily during illness which can result in dehydration (e.g. vomiting, diarrhoea and fever). what are the 5 drugs?

A
  1. ACEi
  2. ARB
  3. diuretics
  4. NSAIDs
  5. Metaformin

*potentially nephrotoxic drugs

51
Q

You suspect a manifestation of sepsis in one of your patients and want to urgently start treatment. You know that you need to be cautious about doses because of their renal impairment. What do you do?

A
  • Initial/loading dose is usually not reduced
  • ½ life of drug usually prolonged in renal disease, therefore, longer to get to steady state (usually takes 4-5 ½ life’s to get to SS)
  • Once reached target therapeutic serum drug concentration then reduce maintenance dose or introduce intermitted treatment
52
Q

What drug affect occurs as a result of hepatic shunting?

A
  • Reduce 1st pass extraction of the liver
  • High hepatic clearance such as morphine, propranolol –> increased risk of adverse effects as bioavailability increases
53
Q

describe the health implications of Heamolytic uremic syndrome

A
  • common in children
  • typically follows acute diarrhoeal illness
  • related to epidemic gastroenteritis caused by E.coli
  • notifiable disease

Week 20: Vomiting and diarrhoea (1 decks)

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