Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Years 1+2 > S4C7 > Flashcards

S4C7 Flashcards

1
Q

What are the different types of proteinuria?

A 
Glomerular
Tubular
Overflow
Post-exercise
Post-prandial
Infection associated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the characteristics of tubular proteinuria?

A

Low molecular weight proteins

E.g. Β2-microglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the characteristics of overflow proteinuria?

A

Increased production

Light chains in multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the characteristics of post-exercise proteinuria?

A

Transient benign

Can be up to 10g/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the characteristics of post-prandial proteinuria?

A

Transient physiological proteinuria

Possibly through insulin action in podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the stages of injury involved in nephropathy?

A 
Hyperfiltration
Microalbuminuria
Macroalbuminuria
Proteinuria
Declining renal function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pathology of hyperfiltration?

A 
Glomerular
	GBM thickening
	Mesangial expansion
	Nodular sclerosis
	Advanced sclerosis
Tubulo-interstitial
Vascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause hyperfiltration?

A

Pregnancy
Diabetes
Autosomal-dominant polycystic kidney disease
Glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the goals for treating nephropathy?

A 
Glycaemic control
BP control
RAAS blockade ACEi/ARB
Lipid lowering
Reduce other CV risks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 2 types of dialysis?

A

Peritoneal dialysis

Haemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the key issues with transplantation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 4 types of renal tubule acidosis?

A

Type 1 - Distal RTA
Type 2 - Proximal RTA
Type 3 - combination of types 1+2
Type 4 - Hyperkalaemia RTA (Hyperaldosteronism)

26
Q

What is the pathphysiology of Type 1 RTA?

A

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
Q

What is the pathphysiology of Type 2 RTA?

A

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
Q

What are the features of respiratory/metabolic acidosis?

A

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
Q

What are the features of respiratory/metabolic alkalosis?

A 
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
Q

What is NHE3?

A

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
Q

What is kNBCe1?

A

Electrogenic sodium bicarbonate cotransporter, a membrane transport potein found in the kidney.

32
Q

How is plasma pH regulated?

A

dominated by the HCO3- /CO2 buffering system

33
Q

How does the body balance acids and bases?

A

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
Q

How is H+ secreted? (overview)

A

Reabsorption of filtered HCO3-
Excretion of H+ as a titratable acid
Excretion of H+ and NH4+

35
Q

How is filtered HCO3- filtered?

A

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
Q

How is H+ excreted as a titratable acid?

A

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
Q

How is H+ secreted as NH4+?

A

NH4+ is synthesized by the kidney
Comes from glutamine metabolism
New HCO3- enters circulation and neutralizes acidity
NH3+ binds to H+

38
Q

What are carbonic anhydrases?

A 
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
Q

Where is HCO3- reabsorbed?

A

Mostly in PCT (80%)

40
Q

Where is NH4+ secreted?

A

Mostly PCT

41
Q

How is HCO3- reabsorbed in early PCT?

A

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
Q

How is HCO3- reabsorbed in the thick ascending limb and distal tubule?

A

H+ generated from CO2 and H20
Luminal CAIV less important
AE2 for HCO3- exit at the basolateral membrane

43
Q

How is HCO3- reabsorbed in α-intercalated cells of collecting tubule and duct cells

A

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
Q

What is the calculation for GFR?

A

GFR= filtration coefficient x (Glomerular capillary hydrostatic pressure - (Bowman’s capsule hydrostatic pressure + glomerular capillary oncotic pressue))

45
Q

What is blood flow to the kidneys like?

A 
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
Q

What are the 2 ways the kidney autoregulates pressure?

A

Myogenic - Vascular smooth muscle responds to stretch by vasoconstricting
Tubuloglomerular feedback - distal tubular flow regulates vasoconstriction

47
Q

What happens in the tubuloglomerular feedback?

A

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
Q

What is renal clearance? What is the equation?

A

Volume of plasma which is cleared of substance x per unit of time
([Urinary X] x Urine volume per unit time)/[Plasma X]

49
Q

What are the ranges for the PCR?

A

Protein:creatinine ratio
<20mg/mmol - normal
200mg/mmol - nephrotic range

50
Q

What are the ranges for the ACR?

A

Albumin:creatinine ratio
>3mg/mmol - microalbuminuria
>30mg/mmol - albuminuria

51
Q

How many people in the UK need long-term dialysis or transplantation?

A

~65,000

52
Q

How many people per month will reach ‘end stage kidney disease’ in UK?

A

600

53
Q

How is sodium secreted into the blood in the late PCT? (H+ mechanism)

A

Na+ brought into cell by NHE-3

K+ absorbed from the blood in exchange for Na+

54
Q

How is sodium secreted into the blood in the late DCT/ collecting duct? (H+ mechanism)

A

Na+ brought in by aldosterone

K+ absorbed from the blood in exchange for Na+

55
Q

What are the different carriers for glucose transport?

A 
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
Q

How is sodium secreted into the blood in the early PCT? (glucose mechanism)

A

Brought in with glucose by SGLT2
K+ absorbed from the blood in exchange for Na+
GLUT2 allows glucose to diffuse into the blood

57
Q

How is sodium secreted into the blood in the late PCT? (glucose mechanism)

A

Brought in with glucose by SGLT1
K+ absorbed from the blood in exchange for Na+
GLUT1 allows glucose to diffuse into the

58
Q

How is NH4+ secreted in the proximal tubule?

A

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
Q

How is NH4+ reabsorbed in the thick ascending loop?

A

Via ROMK2 channel, and NKCC1 accepts NH4+ in place of K+

Low NH3 permeability at apical membrane, so it leaves across basolateral membrane

60
Q

How is NH4+ re-secreted in collecting duct?

A 
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
Q

Describe the RAAS system.

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions