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Years 1+2 > S4C7 > Flashcards

S4C7 Flashcards

(61 cards)

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1
Q

What are the different types of proteinuria?

A 
Glomerular
Tubular
Overflow
Post-exercise
Post-prandial
Infection associated
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2
Q

What are the characteristics of glomerular proteinuria?

A

Most common form
90%
Feature of chronic kidney disease
Loss of albumin and higher molecular weight protein

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3
Q

What are the characteristics of tubular proteinuria?

A

Low molecular weight proteins

E.g. Β2-microglobulin

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4
Q

What are the characteristics of overflow proteinuria?

A

Increased production

Light chains in multiple myeloma

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5
Q

What are the characteristics of post-exercise proteinuria?

A

Transient benign

Can be up to 10g/day

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6
Q

What are the characteristics of post-prandial proteinuria?

A

Transient physiological proteinuria

Possibly through insulin action in podocytes

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7
Q

What are the characteristics of infection associated proteinuria?

A

Physiological response
Mediated by toll-receptors
Possibly involved in clearing pathogens from the circulation

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8
Q

What is the epidemiology of nephropathy?

A

2025: 300 million with diabetes
40% develop nephropathy
Genetic susceptibility
Most common cause of kidney failure worldwide

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9
Q

What are the stages of injury involved in nephropathy?

A 
Hyperfiltration
Microalbuminuria
Macroalbuminuria
Proteinuria
Declining renal function
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10
Q

What is the pathology of hyperfiltration?

A 
Glomerular
	GBM thickening
	Mesangial expansion
	Nodular sclerosis
	Advanced sclerosis
Tubulo-interstitial
Vascular
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11
Q

What can cause hyperfiltration?

A

Pregnancy
Diabetes
Autosomal-dominant polycystic kidney disease
Glomerulosclerosis

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12
Q

What are the goals for treating nephropathy?

A 
Glycaemic control
BP control
RAAS blockade ACEi/ARB
Lipid lowering
Reduce other CV risks
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13
Q

What are the 2 types of dialysis?

A

Peritoneal dialysis

Haemodialysis

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14
Q

What are the advantages of peritoneal dialysis?

A 
Immediate use reduces fluid overloads
No anticoagulation
Cheapest
Continuous
Least likely to cause fluid shifts and hypotension
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15
Q

What are the conditions of using heamodialysis and hemofiltration?

A 
Specialist nursing care
Tertiary units
Need for good central venous access
High and efficient solute clearance
Anticoagulation
Intermittent: not tolerated when haemodynamically unstable
Continuous: Hemofiltration
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16
Q

What are the key issues with transplantation?

A

Immunosuppression
Severe progressive complications
5 year survival rate SPK 70-80% (pancreas)

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17
Q

What is the physiology of beta cells?

A

pancreatic β-cells express GLUT2 glucose transporters, which permit rapid glucose uptake regardless of the extracellular sugar concentration

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18
Q

What is the effect of insulin on the liver, muscles, adipose tissue and blood?

A

Liver - Increased glucose uptake and glycogen synthesis
Muscle - Increased glucose uptake and glycogen synthesis
Adipose - Increased glucose uptake and storage as fat, decreased breakdown to fatty acids
Blood - glucose levels fall

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19
Q

What is associated with a 1% decreas in HbA1c

A

43% decrease in amputations or fatal peripheral blood vessel disease
37% decrease in micro-vascular complications
21% decrease in deaths related to diabetes
14% decrease in heart attack risk
12% decrease in stroke risk

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20
Q

What is the MOA for loop diuretics

A

inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle.
This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium.
Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron

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21
Q

What is the MOA for thiazide diuretics?

A

inhibit the active reabsorption of chloride in the ascending loop of Henle. (it may also do sodium)
These actions subsequently alter electrolyte transfer in the proximal tubule resulting in excretion of sodium, chloride, and water
also inhibits sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism.

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22
Q

What is the MOA for Potassium-sparing diuretics?

A

competitively inhibits aldosterone dependant sodium potassium exchange channels in the distal convoluted tubule. This action leads to increased sodium and water excretion, but more potassium retention. The increased excretion of water leads to diuretic and also antihypertensive effects.

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23
Q

What are the main points from the Human tissue act 2004?

A

Permits donation post mortem – opt-in
Allows family members to refuse if you have not registered on the Organ Donor Register (and occasionally even if you have)
Permits (some) live organ donation to be targeted to specific individuals
Makes paid donation illegal
Allow 12yo+ to make their own decisions

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24
Q

What point was ammended from the Human tissue act 2004 in the organ donation bill 2019?

A

Deemed consent
The person concerned is to be deemed, for the purposes of …(transplantation).. to have consented to the activity unless a person who stood in a qualifying relationship to the person concerned immediately before death provides information that would lead a reasonable person to conclude that the person concerned would not have consented

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25
What are the 4 types of renal tubule acidosis?
Type 1 - Distal RTA Type 2 - Proximal RTA Type 3 - combination of types 1+2 Type 4 - Hyperkalaemia RTA (Hyperaldosteronism)
26
What is the pathphysiology of Type 1 RTA?
Distal RTA Defective H+ excretion by distal segment of nephron Inability to acidify urine – serious systemic consequences (Metabolic acidosis) May be incomplete (compensatory mechanisms of proximal tubule) But treatable by HCO3- supplementation Several transporter mutations - mainly affecting the α-intercalated cells: kAE1, V-type H+-ATPase, CAII
27
What is the pathphysiology of Type 2 RTA?
Proximal RTA Rare autosomal-recessive disease Impaired HCO3- reabsorption in proximal tubule Severe metabolic acidosis Not treatable by HCO3- supplementation (80% of bicarbonate is reabsorbed in PCT) Attributed to mutations in kNBCe1 Ocular abnormalities too because of kNBCe1 and pNBCe1 expression there too
28
What are the features of respiratory/metabolic acidosis?
Increased PCO2 (resp.) or decreased [HCO3-] (metab.) both directly stimulate increased H+ secretion and increased NH4+ synthesis by proximal tubule chronic leads to increased expression of NHE3 and kNBCe1
29
What are the features of respiratory/metabolic alkalosis?
``` Decreased PCO2 (resp.) or Increased [HCO3-] (metab.) both directly stimulate decreased H+ secretion and decreased NH4+ synthesis by proximal tubule chronic leads to more β-intercalated cells (HCO3- secreting) in collecting tubule ```
30
What is NHE3?
NHE3 is a sodium-hydrogen exchanger | For absorption in the intestine and renal proximal tubule, where it accounts for the majority of total Na absorbed
31
What is kNBCe1?
Electrogenic sodium bicarbonate cotransporter, a membrane transport potein found in the kidney.
32
How is plasma pH regulated?
dominated by the HCO3- /CO2 buffering system
33
How does the body balance acids and bases?
15000 mmol CO2 produced per day Potential acid - secreted by lungs so not a problem Metabolism produces ~40 mmol H+ per day Non-volatile acids - sulphuric, phosphoric, organic acids ~30 mmol H+ net uptake by the GI tract Kidneys have to: Excrete ~ 70 mmol H+ per day pH=1.3 without buffering Reabsorb all the filtered HCO3- (Equivalent to ~4000 mmol H+ per day)
34
How is H+ secreted? (overview)
Reabsorption of filtered HCO3- Excretion of H+ as a titratable acid Excretion of H+ and NH4+
35
How is filtered HCO3- filtered?
H+ secretion at apical membrane reclaims HCO3- as CO2 + H2O HCO3- extruded at basolateral membrane Involves carbonic anhydrases II and IV Net transfer of HCO3- from lumen to blood
36
How is H+ excreted as a titratable acid?
H+ and HCO3- generated from CO2 + H2O Secreted H+ is mostly buffered by filtered phosphate - Also creatinine, urate etc New HCO3- enters circulation and neutralizes acidity
37
How is H+ secreted as NH4+?
NH4+ is synthesized by the kidney Comes from glutamine metabolism New HCO3- enters circulation and neutralizes acidity NH3+ binds to H+
38
What are carbonic anhydrases?
``` Zn- containing enzymes 16 isoforms Catalyse the reactions Two important isoforms CAII - soluble cytoplasmic CAIV - Extracellular, linked to the membrane (by a GPI anchor) ```
39
Where is HCO3- reabsorbed?
Mostly in PCT (80%)
40
Where is NH4+ secreted?
Mostly PCT
41
How is HCO3- reabsorbed in early PCT?
NHE3 is dominant in proximal tubule Large capacity but limited gradient generation (pH 6-ish in the lumen) Vacuolar-type H+ATPase can generate a bigger gradient (pH 4-5 - More important later in the tubule where lumen is more acidic) 1:3 stoichiometry of kNBCe1 make it electrogenic - This allows HCO3- efflux from the cell because of extra drive from membrane potential NOTE: Unusual to have Na+ leaving the cell on a cotransporter
42
How is HCO3- reabsorbed in the thick ascending limb and distal tubule?
H+ generated from CO2 and H20 Luminal CAIV less important AE2 for HCO3- exit at the basolateral membrane
43
How is HCO3- reabsorbed in α-intercalated cells of collecting tubule and duct cells
kAE1 has shorter N-terminus than eAE1 Main site of V-type H+-ATPase activity Uses H+,K+-ATPase as well (mainly to reabsorb K+) V-type H+-ATPase in apical membrane of α-intercalated cells absent from principal cells
44
What is the calculation for GFR?
GFR= filtration coefficient x (Glomerular capillary hydrostatic pressure - (Bowman's capsule hydrostatic pressure + glomerular capillary oncotic pressue))
45
What is blood flow to the kidneys like?
``` Cardiac output = 5L/min Kidneys receive 20% (1L/min) RBF 10-50 times greater than other organs RBF exceeds O2 requirements of kidneys RBF not regulated metabolically ```
46
What are the 2 ways the kidney autoregulates pressure?
Myogenic - Vascular smooth muscle responds to stretch by vasoconstricting Tubuloglomerular feedback - distal tubular flow regulates vasoconstriction
47
What happens in the tubuloglomerular feedback?
Increased arterial pressure increases glomerular pressure and plasma flow. This increases GFR and PCT-DCT flow. The macula densa sense this and cause afferent arteriole constriction by Ca2+ Also stimulates granules contained renin to be released for juxtaglomerular cells This increases preglomerular resistance
48
What is renal clearance? What is the equation?
Volume of plasma which is cleared of substance x per unit of time ([Urinary X] x Urine volume per unit time)/[Plasma X]
49
What are the ranges for the PCR?
Protein:creatinine ratio <20mg/mmol - normal 200mg/mmol - nephrotic range
50
What are the ranges for the ACR?
Albumin:creatinine ratio >3mg/mmol - microalbuminuria >30mg/mmol - albuminuria
51
How many people in the UK need long-term dialysis or transplantation?
~65,000
52
How many people per month will reach 'end stage kidney disease' in UK?
600
53
How is sodium secreted into the blood in the late PCT? (H+ mechanism)
Na+ brought into cell by NHE-3 | K+ absorbed from the blood in exchange for Na+
54
How is sodium secreted into the blood in the late DCT/ collecting duct? (H+ mechanism)
Na+ brought in by aldosterone | K+ absorbed from the blood in exchange for Na+
55
What are the different carriers for glucose transport?
``` Solute carrier family SLC5 (Sodium-linked co-transporter) SGLT1 - 1 glucose: 2 Na SGLT2 - 1 glucose: 1 Na GLUT gene family - facilitated diffusion GLUT1 GLUT2 ```
56
How is sodium secreted into the blood in the early PCT? (glucose mechanism)
Brought in with glucose by SGLT2 K+ absorbed from the blood in exchange for Na+ GLUT2 allows glucose to diffuse into the blood
57
How is sodium secreted into the blood in the late PCT? (glucose mechanism)
Brought in with glucose by SGLT1 K+ absorbed from the blood in exchange for Na+ GLUT1 allows glucose to diffuse into the
58
How is NH4+ secreted in the proximal tubule?
NH4+ produced by glutamine metabolism. This splits to make NH3 and H+ This also makes new HCO3- which is secreted into the interstitial space with Na+ Na+ is brought into the cell, in exchange for H+ which is pumped into the tubule lumen NH3 binds with H+ to make NH4+ in the lumen.
59
How is NH4+ reabsorbed in the thick ascending loop?
Via ROMK2 channel, and NKCC1 accepts NH4+ in place of K+ | Low NH3 permeability at apical membrane, so it leaves across basolateral membrane
60
How is NH4+ re-secreted in collecting duct?
``` Most crosses epithelium as NH3 Some NH4+ is carried in by Na+K+ATPase NH4+ splits to H+ and NH3 NH3 crosses epithelium into lumen H+ is transported across Bind together to create NH4+ ```
61
Describe the RAAS system.
Liver produces Angiotensiongen Kidney produced renin which converts this to ANG1 ACE (produced in lungs) converts this the ANG11 This stimulates the pituitary gland to produces ADH which binds to V2 receptor on kidneys Also stimulates Adrenal gland to release aldosterone which causes the collecting ducts to retain water increasing BP.

Years 1+2 (21 decks)

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