Week 4 - Kidney Failure Flashcards

(32 cards)

1
Q

What are the 2 types of nephrons?

A

Cortical nephrons

Juxtamedullary nephrons

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2
Q

What is the funciton of the renal corpuscle and tubular system of nephron?

A

Renal corpuscle = site of initial blood filtration

Tubular system = controls concentration and content of urine

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3
Q

What are the blood supplies to the nephron?

A

Glomerulus capillary bed - in Bowman’s capsule - high hydrostatic pressure - FILTRATION

Peritubular capillary bed - aroudn tubular system - low hydrostatic pressure - REABSORPTION AND SECRETION

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4
Q

What is GFR?

A

Volume of fluid entering Bowman’s capsule per unit time

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5
Q

What does the glomerular filter look like?

A
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6
Q

What is the organisatino of golumerular capillary membrane?

A
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7
Q

What are the effects of afferent arteriole constriction, efferent arteriole constriction and hypoproteinaemia on GFR?

A

Afferent constriction = - GFR

Efferent constriction = + GFR

Hypoproteinaemia = + GFR

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8
Q

What are the benefits of using inulin to estimate GFR?

A
  • Freely filtered
  • Not reabsorbed, secreted or metabolised by kidney
  • No effect on renal function
  • Easily measured in urine
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9
Q

What is RPF?

A

Renal plasma flow = amount of plasma that perufses kidney per unit time

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10
Q

How do you derive renal bloodflow using RPF?

A

RBF = RPF / 1 - haematocrit

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11
Q

What is the filtration fraction?

What does high FF indicate?

A

The proportion of plasma that forms filtrate

+ FF = + colloid osmotic pressure in peritubular capillaries

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12
Q

What are the ways autoregulation alters GFR?

A

Myogenic - afferent arteriole contraction

Tubuloglomerular feedback - NaCl concentration in filtrate sensed by macula densa of JGA and singal produced, contractin afferent arterioles

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13
Q

What is the juxtaglomerular apparatus?

What is its role?

A

Macula densa + granular cells

Autoregulation and renin release

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14
Q

What effect do vasodilators and NSAIDs have on RBF and GFR?

A

Vasodilators = increase RBF and GFR (prostaglandins)

NSAIDs = block prostaglandin synthesis = + vasoconstriction and ischaemia = actue renal tubular necrosis

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15
Q

What is glycosuria?

What causes it?

A

When renal glucose threshold (RTG) is exceeded, glucose excreted in urine

  • Untreated diabetes
  • Hyperthyroidism
  • Pregnancy
  • Familial
  • Drugs
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16
Q

What happens in the proximal tubule?

A
  • Bulk reabsorption of filtered ions and solutes
  • Reabsorption of organic solutes, ions and water is coupled with sodium reabsorption
    • water permeability means so significant osmotic gradient
  • Tubular fluid = isosmotic with plasma
17
Q

How is sodium trnasported in proximal tube?

A

Readily enters epithelial cells across apical membrane

18
Q

How is bicarbonate transported in proximal tube?

A

Indirectly reabsorbed via carbonic anhydrase as apical membrane impermeable to bicarbonate

19
Q

How is water transported and reabsorbed in proximal tubes?

A

+ permeability

Occurs paracellularly across tight junctions and transcellularly via water channels on apical and basolateral membranes

Reabsorption:

  • Osmotic pressure gradient + low hydrostatic pressure = water passively moves down gradient
20
Q

How is sodium, chloride, potassium and water processed in thick ascending limb of loop of Henle?

A
  • Is impermeable to water
  • 1 Na+, 1 K+ and 2 Cl- enter cell via symporter protein in apical membrane
  • Cl- leaves via passive diffusion
  • Most K+ leaks back into lumen
  • Tubular lumen becomes + charged
  • Sodium enters cell via Na+/H+ antiporter
  • Sodium pumped out by sodium pump
  • Low sodium = electrochemical gradient = drives Na movement into cell
21
Q

What is the role of the thick ascending limb?

A
  • Reduces tubular fluid osmolality
  • Is diluting segment
  • Makes interstitial fluid of medulla hyperosmotic
    • role in creating medullary interstitium and regulating urine osmolality
22
Q

What are the effects of aldosterone in the late distal tube?

A
  • Enhances sodium reabsorption in principal cells
  • Enhances K+ secretion in principal cells
  • Enhances H+ secretion in intercalated cells
23
Q

What happens in hyperaldosteronism and hypoaldosteronism?

A

Hyper = + aldosterone, metabolic alkalosis, hypokalaemia, hypertension, oedema

  • DUE TO SODIUM AND WATER RETENTION

Hypo = type 4 renal tubular acidosis = hyperkalaemia

24
Q

What are the effects of ADH on inner medullary collecting duct?

A
    • urea permeability
  • Water diffuses out of tubule lumen, into medullary interstitium
  • Urea recycling occurs –> urea diffuses into ascending and descending limbs of loop of Henle
25
What happens to body during excess sodium and sodium defecit?
**_Excess:_** * - Weight gain * - Oedema * - Hypertension * - Nocturia **_Defecit:_** * - Weight loss * - Change in skin tugour * - Syncope * - Orthostatic hypotension
26
What happens during chronic kidney disease?
* Slow function loss overtime * Decreased ability to remove waste products * Treat with dialysis, transplant or supportive care * Clinically = \< 60 ml/min
27
How does chronic kidney failure present?
* Asymptomatic serum biochemical abnormaility * Asymptomatic proteinuria or haematuria * Hypertension * Oedema * Primary renal disease symptoms * Uraemia symptoms * Complications of CKD * Tiredness * Salt and water retention * Itching
28
How can you treat CKD?
* ACE inhibitors * Lifestyle change * Monitor BP, creatinine and GFR * Haemodialysis * Peritoneal dialysis
29
What is acute kidney injury?
* Rapid decline in kidney function * + serum creatinine conc. * Fall in urine output * Uraemia * Due to haemodynamic, septic, immunological, nephrotoxic or obstructive insults
30
What are causes of pre-renal AKI?
Intravascular volume depletion - cardiac output Systemic vasodilatation
31
What are the causes of intrinsic AKI?
Diseases or toxins damaging small renal vessels and glomeruli Acute tubular necrosis Miscallaneous renal diseases Toxins
32
What causes post-renal AKI?
Acute obstruction of urine flow