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Life Maintenance > Week 12 - Kidneys > Flashcards

Week 12 - Kidneys Flashcards

1
Q

Functions of the kidneys (4)

A

Control volume and composition of body fluids Get rid of waste Acid-base balance Endocrine functions - EPO, renin, vitamin D

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2
Q

Composition of glomerular fluid

A

Like plasma EXCEPT no cells and very little protein

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3
Q

Urine output indicating renal failure

A

Below 5mL a day (normal is 1.5L)

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4
Q

Importance/role of long loop of henle (in juxta-medullary nephron)

A

Concentrates / dilates urine Countercurrent created by movement of Na into interstitial space in ascending, corresponding movement of water in descending Vasa recta taking reabsorbed urea and H2O away

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5
Q

Outline reabsorption in PCT - how much is reabsorbed here? By what mechanisms do things move from lumen into cell? By what mechanisms do they move into the blood?

A

65-70% reabsorbed here Generally, passive transport INTO cell (Na/CL symport, H2O osmosis and diffusion of glucose and amino acids) INTO cell, and then Na moved into blood through Na/K ATP pump (K moves back into cell)

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6
Q

Role of thin descending loop of Henle

A

Very permeable to water 20% of filtered water reabsorbed here

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7
Q

Role of thin and thick ascending loop of Henle

A

Virtually impermeable to water, actively reabsorbs Na Site of action of loop diuretics

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8
Q

Describe countercurrent multiplication in loop of Henle

A

Salts pulled out from ascending loop, this creates a higher salt concentration in medulla which pulls water out of descending loop

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9
Q

Define hyperosmotic, hypoosmotic, isosmotic

A

Hyperosmotic - outside of cell is more concentrated than inside Hypoosmotic - outside of cell is less concentrated than inside Isoosmotic - outside / inside equal Takes into account both impermeable and impermeable solutes

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10
Q

Describe blood flow in vasa recta

A

Flow in Vr should be LOW - 5% of renal blood flow to minimise solute loss

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11
Q

Functions of DCT

A

Solute reabsorption (without water) High Na, K ATP-ase activity Very low H20 permeability Dilution of tubular fluid Role in acid-base balance

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12
Q

Cell types in collecting duct

A

Intercalated cells - acid base balance Principal cells - Na balance, ECF volume regulation

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13
Q

ADH stimulation and role

A

Released by posterior pituitary in response to changes in plasma osmolality Moves to kidney to stimulate aquaporin in collecting duct, which then pulls water out of collecting duct into blood

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14
Q

What is GFR?

A

How much filtrate is removed from blood each minute

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15
Q

What sets the GFR?

A

Intrinsic factors - autoregulation - vasoconstriction of afferent arteriole, feedback from DCT where it comes back around Extrinsic control - renal sympathetic vasoconstrictor nerve activity

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16
Q

Describe glomerular capillary pressure

A

Pressure within glomerular arterioles pushing filtrate out into capsule FAVOURING filatration

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17
Q

Describe the pressures opposing filtration in Bowman’s capsule

A

Hydrostatic in Bowman’s space Osmotic force of plasma proteins

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18
Q

Outline filtration in glomerulus (what prevents blood cells from getting through?)

A

Fenestrae (gaps) are about 50-100nm allow small things through to podocytes, blood is too big to fit Like sieve to smaller colander, some things can’t get through fenestrae, basement membrane filter and protein filter at filtration slits

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19
Q

Outline make-up and role of filtration slit pores

A

Made up of proteins (nephrin and podocin), role is filtration - they are narrow to block small things such as protein

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20
Q

What is nephrotic syndrome?

A

Loss of a lot of protein Podocytes disappear, not working properly - protein moves from blood through nephron into urine 3.5g/25hr Frothy urine Loss of protein from blood vessels, causes leaking / oedema around the body Albumin lost (key protein that is lost), liver tries to compensate by producing lipids Primary and secondary causes

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21
Q

Outline measurement of GFR

A

Use a substance that is freely filtered, not metabolised /absorbed / secreted INULIN Once at constant plasma concentration, measure how much is being excreted over time

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22
Q

Formula for GFR (ml/min)

A

Urine inulin concentration (mg/min) * Flow rate (ml/min) Divided by plasma inulin concentration (mg/ml) BE CAREFUL OF UNITS

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23
Q

What is renal clearance?

A

Volume of plasma that is completely cleared of the substance by the kidney per unit of time

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24
Q

Measuring renal clearance in clinical practice and what can give false reading? What may cause values to be off?

A

Inulin is a lot of work, creatinine is natural proxy (released from skeletal muscle) Be careful of people on trimethoprim (antibiotic) which is competitive inhibitor of creatinine secretion Blood test

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25
Q

eGFR - values and drawbacks

A

CKD-EPI MDRD 24 hour urine (best but time consuming and difficult to control)

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26
Q

Describe filtration, reabsorption and excretion of glucose

A

Glucose is readily filtered, but then is completely reabsorbed from PCT should not be excreted at all unless overload

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27
Q

Glucose transport in tubule

A

Glucose carried against its concentration gradient via Sodium / glucose co-transporter (symport called SGLT2) and then into blood through GLUT2

28
Q

Why can’t you inhibit SGLT1 in patients with diabetes?

A

Also in gut, to absorb sugar

29
Q

Normal clearance values from glucose, inulin and PAH - and why?

A

Glucose - 0ml/min (completely reabsorbed) Inulin - 124ml/min (nor reabsorbed, not secreted) PAH - 625ml/min (completely secreted)

30
Q

Functions of kidney (7)

A

Excrete waste substances Acid base balance Vit D activation Blood pressure control RBC production Regulate water balance Regulates ECF minerals

31
Q

Drawbacks of using eGFR

A

Studies to develop equation largely in white populations, not always useful eGFR should only be used in steady state - change in creatinine more useful

32
Q

Outline pre- intra- and post-renal

A

Pre-renal - Issue with blood getting to kidney Intra-kidney- Issue within kidney Post-renal - obstruction

33
Q

Outline pre-renal causes of AKI

A

Hypovolaemia (from haemorrhage, diarrhoea/vomiting) Drop in perfusion (septic shock, cardiac failure) Drugs - ACE / ARBs / NSAIDs

34
Q

Outline the impact of ACE/ARB and NSAIDs on kidney function

A

Afferent (NASIDs) and efferent (ACE/ARB) Pressure DOWN Issue in patients with renal artery stenosis or reduced kidney function

35
Q

How do you quantify proteinuria?

A

Urine albumin:creatinine ratio (albumin most common to leak but both tests can be used interchangeably) Urine protein:creatinine ratio

36
Q

What are red cell casts and what do they mean?

A

Evidence of glomerular bleeding

37
Q

How can you tell if blood is coming from glomerulus or lower down?

A

If glomerular, may see red cell casts in the blood and/or destroyed/damaged blood cells in urine

38
Q

Difference between primary and secondary glomerular disease

A

Primary - Direct glomerular disease Secondary - Systemic disease

39
Q

Nephrotic syndrome vs. Nephritic syndrome

A

Nephrotic - heavy proteinuria caused by breakdown of podoctyes (associated with oedema) Nephritic (days) - blood in urine caused by breakdown of fenestrations in capillary (usually inflammation related)

40
Q

Outline rapidly progressive GN

A

Like nephritic syndrome but over weeks/small number of months Often how renal impairment in vasculitis present, Goodpastures

41
Q

Chronic kidney disease - first investigation, what might you see

A

Ultrasound, small kidneys

42
Q

Describe acute tubular injury

A

Affects part or all of tubular system Most common in PCT Ischaemic or toxic - Sepsis, drugs Loss of brush border, epithelium broken down with remnants in lumen

43
Q

What can cause acute allergic interstitial nephritis?

A

antibiotics (methacylin), PPIs, NSAIDs can cause acute renal failure about 2 weeks post drug exposure

44
Q

Outline management of acute kidney injury (7)

A

Correct and pre-renal factors or relieve obstruction May need to treat renal factors (stop nephrotoxic drugs) Maintain fluid/electrolyte balance Nutrition Gastric protection Care with drugs / dosing Watch for and address sepsis

45
Q

What are 3 urgent indications for haemodialysis and/or haemofiltration?

A

hyperkalaemia Volume overload (too much fluid has been given, kedneys aren’t working well enough to clear it out) Evidence of end organ damage (pericarditis, encephalopahy, neuropathy, myopathy)

46
Q

Outline RRT - role and indications

A

Transplant- DBD, DCD, Living Dialysis - haemodialysis and peritoneal dialysis

47
Q

Stages of chronic kidney disease

A

1 Kidney damage (GFR >90mL/min) 2 Mild GFR (GFR 60-89mL/min) 3a/b Moderate GFR (GFR 30-44 and 45-59mL/min) 4 Severe GFR (GFR 15-29mL/min) 5 Kidney Failure (GFR <15 or dialysis)

48
Q

What are the common causes of chronic kidney disease?

A

Lots - Autoimmune disease (SLE, vasculitis), diabetes,

49
Q

Risk factors for CVD in CKD

A

Inflammation Oxidative stress Anaemia calcification - many others PLUS all normal risk factors

50
Q

Describe autosomal dominant polycystic kidney disease

A

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys. It is the most common inherited disorder of the kidneys. Symptoms usually develop between the ages of 30 and 40, but they can begin earlier, even in childhood. The most common symptoms are pain in the back and the sides and headaches. Other symptoms include liver and pancreatic cysts, urinary tract infections, abnormal heart valves, high blood pressure, kidney stones, brain aneurysms, and diverticulosis. About 90 percent of all cases of polycystic kidney disease (PKD) are inherited in an autosomal dominant fashion. ADPKD is caused by mutations in the PKD1 and PKD2 gene. Although there is no cure for ADPKD, treatment can ease symptoms and prolong life.[1]

51
Q

General management of chronic renal failure (2)

A

Slow progression Treat symptoms and complications Early treatment of diabetes BP control (under 130/80) ACE/ARB SGLT inhibitor /endothelin A antagonist Healthy lifestyle

52
Q

Uraemia

A

Syndrome produced by retention of urea, creatinine

53
Q

Complications of chronic renal failure

A

Na/H2O retention - glomerular disease Na/H2O loss - Tubulointerstitial disease Retention of potassium Problems with Ca+, phosphate, vit D Lack of erythropoetin

54
Q

Renal anaemia and correction

A

People with interstitial kidney damage often get renal anaemia Treat with erythropoietin to 100-120

55
Q

What is nephritic syndrome?

A

Loss of a lot of blood Immune complex recruits white cells, start breaking down endothelium (which allows red blood cells, white cells AND protein through) Blood in the urine, low urine output High blood pressure Inflammation (this is the key difference between nephrotic and nephritic) - this is likely to cause sediment in the urine

56
Q

Describe the health as functional capacity model Class associations, indicators

A

Health is a functional concept - ie you have health because you don’t have disease or health despite disease May be associated with working class Ability to fulfil social.work roles, health as coping

57
Q

Describe the disease candidacy model

A

Explores lay explanations of relative risk (candidacy) of disease - constructed from appearance of a person, circumstances surrounding around event Can either support or challenge the biomedical reality

58
Q

Describe the 5 potential triggers that drive people to seek medical care

A

Interpersonal crisis Perceived interference with work Perceived interference with social / leisure People insist you have to go Symptoms persist beyond arbitrary time limit

59
Q

What are the aims of body fluid homeostasis? (4)

A

Blood volume Blood pressure Tonicity Composition of plasma / interstitial fluid

60
Q

Types of fluid depletion (2)

A

Loss of isotonic fluid (salt and water) Loss of water

61
Q

Acute Kidney injury stages

A

1 Serum creatinine increases 26 with 48hr OR 1.5-1.9 fold from baseline, urine output less than .5ml/kg/hr for 6h 2 SCr increase 2-2.9 fold from baseline, UO less than o.5ml/kg/hr for 12h 3 SCr increase more than 3fold from baseline or above 354 or on RRT, UO less than 0.3ml/kg/hr for 24h or anuria for 12h

62
Q

What are the 3 mechanisms that help correct body pH?

A

Intra- and extra-cellular buffering Respiratory adjustment of ECF PCO2 Renal adjustment of ECF [HCO3-]

63
Q

How does the kidney sense extracellular acid-base levels?

A

Molecules (such as GPR4, Erb1/2, sAC) scan epithelial cell enviroment

64
Q

How does the respiratory system know to adjust pH? Where?

A

Chemosensitive area in medulla regulates respiration Monitors [H+] of plasma via CSF INDIRECTLY (Co2 crosses BBB and can be sensed)

65
Q

Describe mixed acid-base disorder

A

Seriously ill patients may present with two primary disorders - one causing alkalosis and one acidosis. They can either cause additive issues OR can cancel each other out

66
Q

Cause of acute tubular necrosis, Cytology visible under microscope

A

Caused by injury to tubular endothelial cells (whether toxic or ischaemic). May cause cell death or detachment from basement membrane. Sloughing of epithelial cells, casts in urine, flattened remaining epithelial cells

Life Maintenance (6 decks)

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