Renal: Renal Disease Flashcards

1
Q

What is the definition for AKI?

A

Abrupt decline in renal function
Clinically manifesting as a reversible acute increase in nitrogen waste products—measured by blood urea nitrogen (BUN) and serum creatinine levels over the course of hours to weeks.

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2
Q

What is NFP?

A

Net filtration= total pressure that promotes filtration. Determined by Starling forces. Increase in renal arterial pa/RBF increases GFR.

NFP = Glomerular blood hydrostatic pressure (45) – [capsular hydrostatic pressure (15) + blood colloid osmotic pressure (30)] = 10

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3
Q

What happens if GFR is too high or too low?

A

If GFR is too high substances that are needed cannot be reabsorbed quickly enough and are lost in the urine

If the GFR is too low then everything is reabsorbed including wastes that are normally disposed of- urea, K+ all raised

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4
Q

Describe the effects of angiotensin converting enzyme inhibitors and ang II receptor blockers on glomerular filtration.

A

Inhibit ACE to reduce levels of Angiotensin II
Decreases arteriolar resistance + vasoconstriction. This decreases BP, hyperfiltration and intraglomerular pa.
Decreasing vasoconstriction is good bc too much vasoconstriction reduces glomerular flow and GFR
Also reduces potassium excretion in the kidneys
But, too much vasodilation= drop in renal perfusion pa and subsequent decrease in glomerular filtration.

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5
Q

What are the clinical manifestations/ outcomes of AKI?

A

Rapid decline in GFR means hay a rise in urea and creatinine
Leading to loss of normal water and solute homeostasis
Metabolic acidosis develops as a result of impaired acid excretion
REVERSIBLE

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6
Q

What are the indications for dialysis/renal replacement therapy?

A

Hyperkalaemia: leads to arrhythmias- complete heart block. Wide QRS complex carries risk of ventricular fibrillation
Pulmonary oedema- fluid retention
Acidaemia
Symptomatic uraemia (urea>60)- uraemic frost. Confusion, seizures. Pericarditis. Uraemic flap (hands like C02 retention)

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7
Q

What are the phases of AKI?

A

Onset: Kidney injury occurs
Oliguric (anuric): urine output decreases from renal tubular damage. Kidney can’t excrete water
Polyuric phase: GFR increase as kidneys try to heal and urine output increases but tubular scarring occurs. Solute diuresis (sodium wasting) from the delivery of a high load of solute through the nephron.
Recovery: Tubular oedema resolves and renal function improves

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8
Q

the 3 causes for AKI can be pre renal, renal and post renal. What is meant by pre renal?

A

PRE-RENAL- issue before you enter the kidney
Hypovolaemia
– Haemorrhage
– Diarrhoea/vomiting
↓Perfusion
– Septic shock
– Cardiac failure
Drugs
– ACEi, NSAIDs

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9
Q

the 3 causes for AKI can be pre renal, renal and post renal. What is meant by renal?

A

INTRINSIC RENAL DISEASE- problem lies within kidneys

Glomerular
Vascular
Tubular
Interstitial

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10
Q

the 3 causes for AKI can be pre renal, renal and post renal. What is meant by post renal?

A

POST-RENAL (after the kidneys)

Sudden obstruction of urine flow causing
Hydronephrosis, Hydroureter (stretching of ureters, back pressure) due to:
- Kidney Stones
- Bladder tumour
-Enlarged prostate (men)

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11
Q

Draw a diagram to explain the types of renal causes of AKI

A
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12
Q

Describe types of vascular kidney disease

A
  • Hypertensive nephrosclerosis: Hyalinosis, fibro intimal thickening, tubular atrophy, ischaemic shrunken glomeruli
  • Renal artery stenosis
  • Atheroemboli
  • Vasculitis- can affect blood vessels dentro el nephron
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13
Q

Describe types of tubuluointerstitial kidney disease

A

•Acute tubular injury
•Acute tubulointerstitial nephritis. Causes can be:
Infectious eg tb
Non-infectious
Allergic- NSAIDs, antibiotics
•Chronic tubulointerstitial nephritis

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14
Q

Describe glomerular disease and what you would see in a urine sample

A

Often Vasculitis or glomerulitis

A urine dip tendra protein. Hay que quantify this via a urine albumin creatinine ratio, then a urine protein creatinine ratio

Fresh urine sample under the microscope can have a red cell cast or a glomerular dysmorphic erythrocyte. Dysmorphic erythrocyte means the blood has passed through the glomerulus

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15
Q

What is the 1st principle of glomerular disease?

A

1: NEPHROTIC SYNDROME. This must inc: Oedema. Heavy Proteinuria (>3.5g/day). Hypoalbuminuria= low albumin (<30g/L)
Symptoms: frothy urine, hypercoagulability, hypercholesterolaemia. Causes:
Minimal change disease
Membranous, or diabetic nephropathy
Focal segmental glomerulosclerosis

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16
Q

What is the 2nd and 3rd principle of glomerular disease?

A

2: NEPHRITIC DISEASE is the abrupt onset of:
Haematuria
Proteinuria
Decreased GFR (raised creatinine, oedema, hypertension)
Classical cause: post-streptococcal GN

3rd principle: Isolated proteinuria/haematuria

17
Q

What is the 4th principle of glomerular disease?

A

Rapidly progressive GN

  • Like nephritic syndrome but weeks/months. Main causes:
  • Anti-glomerular basement membrane (Goodpasture) disease
  • Small vessel anti-neutrophil cytoplasm antibody (ANCA) +ive vasculitis
18
Q

How do you treat kidney disease

A

Treatment of underlying condition- pre, renal, post.
Good bp control and reducing proteinuria prevents progression
Treat endocrine issues:
Ca2+, PO4, vit D, PTH: using PO4 binders, alfacalcidol
Anaemia: using iv iron, erythropoietin

End Stage KD: Dialysis, transplant, conservative management- almost palliative

19
Q

What is Chronic kidney disease (CKD)?

A

Kidney damage over long term (>3 months)

urinary albumin excretion of ≥30 mg/day or equivalent OR

decreased kidney function (defined as [eGFR] <60 mL/min/1.73 m2) for ≥3 months

20
Q

What are symptoms of CKD?

A

CKD patients are initially asymptomatic. However symptoms w advanced renal failure inc:

  • volume overload
  • hyperkalemia
  • metabolic acidosis
  • hypertension
  • Anemia
  • mineral and bone disorders (MBDs)

•The onset of ESKD results in a constellation of symptoms referred to as uremia

21
Q

How do you treat and manage CKD?

A

Treatment of reversible causes of renal failure (think about pre, renal, post)
•Decreased renal perfusion
•Drugs (NSAIDs, contrast)
•Urinary tract obstruction

Preventing or slowing the progression of renal disease
•ACEi/ARB BP < 130/80, stopping smoking
•Protein reduction- less strain to not filter proteins
•Glycaemic control- sugars can cause fibrosis of your interstitial.
•Treatment of chronic metabolic acidosis

22
Q

complications of renal failure?

A
  • •Volume overload
  • •Hyperkalaemia
  • •Mineral and bone disorders
  • •Hypertension
  • •Anaemia- changes erythropiotin
  • •Dyslipidaemia
  • •Uraemic bleeding
  • •Pericarditis
  • •Thyroid dysfunction –low freeT3