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Metabolic - Nephrology > Y2 Kidney Revision > Flashcards

Y2 Kidney Revision Flashcards

1
Q

What is atrial natriuretic peptide?

A

Secreted by the atria in repsonse to stretch

Decreases renin production and promotes sodium and water excretion

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2
Q

What does frothy urine idicate?

A

Protein in the urine

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3
Q

What does brown/red urine indicate?

A

Rhadbomyolysis - muscle break down

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4
Q

What would the presence of nitrites in the urine indicate?

A

Bacterial infection

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5
Q

Discuss autosomal dominant polycystic kidney disease

A

PKD1 (chromosome 16) mutation - affects people aged 30-40

PKD2 (chromosome 4) mutation - affects people 70+

PKD1 is more severe

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6
Q

What is the glomerulus?

A

Tuft of capillaries within Bowmanns capsule

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7
Q

What is the renal corpuscle?

A

Bowmans capsule + glomerulus

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8
Q

What is nephroptosis?

A

Kidney drop - often due to fat loss

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9
Q

What is hydronephrosis?

A

Swelling of the kidney due to urine buildup

Most commonly due to kidey stones

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10
Q

Discuss the two types of nephrons

A

1) Cortical: 85%
- Short loop, efferent supplies peritubular capillaries, renal corpuscle in the cortex
2) Juxtamedullary: 15%
- Long loop, efferent supplies vasa recta, renal corpuscle closer to medulla

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11
Q

What should glomerular filtration be?

A

90-120 ml/min

180L plasma/day

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12
Q

What are the cellular layers of the filtration membrane of the glomerulus?

A
  1. Fenestrated endothelium: blocks RBCs
  2. Glomerular basement membrane: blocks plasma proteins
  3. Podocytes: blocks macromolecules
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13
Q

What is renal clearance?

A

How quickly a substane is removed from the kidney and excreted in the urine

Clearance = concentration of substance in urine x flow rate/ concentration of substance in plasma

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14
Q

What should the clearance of createnine be?

A

140ml/min

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15
Q

What is inulin?

A

Used to measure GFR accurately - it is freely filtered and not absorbed

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16
Q

Discuss comparison of filtration of a substance to that of inulin

A

Cx (calculated clearance of substance)/ Clearance of inulin

= 1: substance is freely filtered

= <1: substance is absorbed

= >1: freely filtered and secreted

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17
Q

Where do the kidneys sit?

A

T12 - L3 vertebrae

Partially protected by ribs 11&12

Retroperitoneal

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18
Q

What are macula densa cells?

A

Chemoreceptors in the DCT

Detect NaCl

Low NaCl = low BP - macula densa cells cause afferent arteriole to dilate and increase the hydrostatic pressure in the glomerulus

MD cells cause granular cells to secrete renin

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19
Q

What are juxtaglomerular cells?

A

Secrete renin to increase Na reabsorption

Receive signals from macula densa cells

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20
Q

Discuss peritubular capillaries and the vasa recta

A

Peritubular capilaries surround DCT and PCT

Vasa recta surrounds the loop of Henle

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21
Q

What is mannitol?

A

Osmotic diuretic

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22
Q

What is acetazolemide?

A

Carbonic anhydrase inhibutor - diuretic

Reduces Na/H+ exchange so more Na in filtrate and more water loss

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23
Q

What is furosemide?

A

Loop diuretic

NKCC2 inhibitor

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24
Q

How do thiazide diuretics work?

A

Blocks Na/Cl transporter in the DCT and causes more potassium excretion because more Na reaches the collecting duct

In the collecting duct, Na is absorbed in exchange for the secretion of K+

*amiloride blocks this exchanger

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25
Q

Discuss K+ sparing diuretics

A

Amiloride: blocks Na+/ K+ exchanger in collecting duct - means less Na+ is absorbed and therefore less K+ is excreted

Spirololactone: blocks the aldosterone receptor, the activation of the aldosterone receptor normally causes more Na/K channels to be placed in the membrane

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26
Q

How does anti diuretic hormone work?

A

AKA vasopressin, secreted by posterior pituitary

  • Causes more AQP2 to be place in collecting duct membrane and promotes water uptake
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27
Q

Where is the majority of Na+ reabsorbed?

A

PCT

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28
Q

What is true of the thick ascending limb?

A

It is impermeable to water

Large simple squamous epithelial cells

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29
Q

Discuss countercurrent multiplication of the kidney

A

Descending limb: permeable to water, impermeable to ions

water flows into interstitium

Think ascending limb: impermeable to water, ions move into interstitium because of water loss from descending limb

  • Ultimately we lose water and ions to the interstitium and therefore end up with a more concentrated urine
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30
Q

What is the epithelia of the DCT?

A

Cuboidal cells, no microvilli

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31
Q

Discuss the transporters of the DCT

A
  1. Basolateral Na/K exchanger - Na absorbed into blood and K secreted
  2. Apical Na/Cl co-transporter
  3. Apical Ca2+ transporter

*Ca2+ and Mg+ reabsorption is thought to occur passively

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32
Q

Discuss HCO3- reabsorption in the kidney

A

PCT: Na is absorbed in exchange for H+ secretion

H+ and HCO3- combine in lumen to form carbonic acid

Carbonic acid then converts into water and CO2

CO2 enters the cell from the lumen and combines with water to become H+ and HCO3-

HCO3- can then be absorbed along with Na+

DCT: same as above but HCO3- reabsorption requires Cl- instead of Na+

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33
Q

Where does most acid-base balance occur?

A

PCT

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34
Q

What is the role of type B intercalated cells?

A

Express a chloride-bicarbonate exchanger, pendrin, at their apical membrane and express H+-ATPase at their basolateral membrane

Essentially they secrete HCO3- and reabsorb H+

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35
Q

What is the role of type a intercalated cells?

A

Acid secretion - damage to these cells causes distal renal tubular acidosis

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36
Q

What are the renal tubule buffers?

A

Phosphate (HPO4-) + H+ = H2PO4

Glutamine breakdown = Ammonia (NH3) + H+ = NH4 (ammonium)

*stop the urine being too acidic

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37
Q

What could cause metabolic acidosis?

A
  • Diabetes: ketone bodies
  • Too much protein in diet
  • Diarrhoea
  • Antifreeze
  • Aspirin
38
Q

What could cause metabolic alkalosis?

A
  • Vomiting
  • Too many rennies
  • Too much fruit
  • Thiazide and loop diuretics - K+ and H+ loss
  • Loss of function of type B intercalated cells (spit out bases)
  • Hyperfunction of type A intercalated cells (spit out acid)
39
Q

Where is arterial blood usually taken from for blood gases?

A

Radial

40
Q

What is the normal level of HCO3-?

A

22-26mEq

41
Q

What is the normal range of CO2?

A

34-45mmHg

42
Q

What is the key intracellular and plasma buffer?

A

Hb - forms HHb when combined with H+

43
Q

Discuss buffering in the body

A
  • 52% of the buffering capacity is in cells
  • 5% is in RBCs
  • 43% of the buffering capacity is in the extracellular space
  • of which 40% by bicarbonate buffer, 1% by proteins and 1% by phosphate buffer system
44
Q

What could cause a respiratory alkalosis?

A

Depression of respiratory centres by narcotics

  • Restrictive lung disease
  • Paralysis of respiratory muscles
45
Q

Where are the majoirty of drug components secreted in the kidney?

A

PCT

46
Q

Discuss the role of urine pH in drug excretion

A

Acidic urine: alklaine drug more readily ionised and therefore more easily excreted

Alkaline urine: acidic drug more easily excreted

47
Q

What would be given in the case of an aspirin overdose?

A

Sodium bicarbonate - makes urine more alkaline and promotes loss of salicylic acid (aspirin metabolite)

48
Q

Which drug has a 25x increased half life in renal failure?

A

Aminoglycosides (30s inhibitors)

  • Can also cause ototoxicity
49
Q

Which diuretics are associated with gout

A

Thiazides - promote uptake of urea

50
Q

What does nosocomial mean?

A

Originating in hospital

51
Q

What is the most common UTI causing bacteria?

A

E.Coli UPEC

*E.Coli 0157 causes intestinal disease

52
Q

What pathogen rarely causes UTIs?

A

M.Tuberculosis

53
Q

Discuss E.Coli UPEC

A

Uropathogenic E.Coli

  • Type 1 fimbriae bind to mannose residues on host cells
  • Type P frimbriae adhere to urinary tract cells and prevent phagocytosis
54
Q

What are the risks of UTIs in pregnancy?

A
  • Low birth weight
  • Prematurity
55
Q

What is pyelonephritis?

A

Kidney inflammation usually due to infection

56
Q

Uncomplicated vs. Complicated UTI

A

Uncomplicated: not pregnant, no evidence of kidney spread, normal urinary system, normal pathogen

Complicated: opposite of above

57
Q

Name a commonly used antibacterial for UTIs

A

Trimethoprim: stops DHF - THF, prevents folate production and inhibits DNA

58
Q

What is nitrofurantoin?

A

Used to treat UTIs

Inhibits the synthesis of DNA, RNA, protein and cell wall synthesis

  • ineffective for kidney infection
  • highly stable against resistant bacteria due to number of MOA
59
Q

How would UTIs be treated in children?

A

Lower: amoxicillin, trimethoprim

Upper: Co-amoxiclav (combination consisting of amoxicillin, a β-lactam antibiotic, and potassium clavulanate, a β-lactamase inhibitor)

60
Q

Which drugs are commonly used for pyelonephritis?

A

Co-amoxiclav and ciproflaxin

Sometimes trimethoprim

61
Q

How is chronic kidney disease defined?

A

Structural damage

GFR <60mL/min/1.73m2 for 3 months

62
Q

How is acute kidney disease defined?

A

Creatinine >26mmol/L

Urine <0.5mL/Kg/day

63
Q

Discuss causes of renal failure

A

Pre renal: HF, hypovolemia

Renal: Tubular necrosis, trauma, sepsis

Post renal: bladder obstuction, stones

64
Q

Discuss stages of kidney disease

A

Per GFR

Stage 1 >90

Stage 2 <90

Stage 3 <60

Stage 4 <30

Stage 5 <15 or dialysis

65
Q

What is nephrotic syndrome?

A

Protein loss due to dysfunction of podocytes

Causes frothy urine and oedema

Adults: Focal segmental glomerulosclerosis

In children: most common cause is minimal change disease - so called because the damage is so small it cant be seen using a microscope

66
Q

What are the consequences of nephrotic syndrome?

A
  • Oedema
  • Hypoalbuminemia
  • Proteinuria
  • Hyperlipidemia
  • Hypercoaguability
67
Q

What is Berger’s disease?

A

Nephritic disease: IgA neuropathy

  • Hematuria (gross, frank, microscopic)
  • Oedema in hands and feet
  • Cola- or tea-colored urine
68
Q

What is nephritic syndrome?

A

Immune cmplexes build up and elecit an immune response that damages the filtration membrane

  • Loss of RBCs
  • Proteinuria
  • Oliguria
  • Hypertension

Henloch-Schonlein and Goodpasture’s

69
Q

What is Goodpasture’s syndrome?

A

Immune system attacks the basement membrane in kidney and allows blood through into the urine

70
Q

What is the first sign of kidney damage?

A

Oliguria

71
Q

What is used to treat BPH?

A

Finasteride - 5a reductase inhibitor, prevents DHT production from testosterone

72
Q

What is tamulosin?

A

Alpha 1a blocker, relaxes muscle fibres in prostate and bladder neck and allows for easier micturition

73
Q

Discuss renal cell cancer

A
  • Clear cell (most common - treated with surgical resection) AKA renal adenocarcinoma
  • Papillary types 1&2
  • Chromophobe (similar appearance to clear cell but cells are larger)
  • Oncocytic
  • Collecting duct: rare, seen in young adults, aggressive
74
Q

Discuss bladder cancer

A
  • Transitional cell (most common)
  • SCC
  • Adenocarcinoma
  • 7th most common in UK
75
Q

What is the blood supply to the bladder?

A

Superior and inferior vesical arteries, which arise directly or indirectly from the internal iliac artery

76
Q

Which nerve supplies the external urethral sphincter?

A

Pundendal

77
Q

Discuss micturition

A

Pelvic nerve: parasympathetic, ACh release, causes contraction of detrusor muscle

Pudendal nerve: parasympathetic, ACh release, contraction of external urethral sphincter

Hypogastric nerve: sympathetic, noradrenaline release, relaxes detrusor and contracts internal spincter

78
Q

What is the difference between nicotinic and muscarinic receptors?

A

Both are ACh receptors

Nicotinic: ionotropic

All are excitatory

Muscarinic: GPCRs

79
Q

Discuss the three layers of the bladder

A

Outer: adventitial connective tissue

Middle: smooth muscle detrusor)

Inner: Transitional epithelium

80
Q

What is acute urinary retention?

A

Painful inability to void with relief following catheterisation

>800mL

81
Q

Discuss drug interactions with spironolactone

A

ACE inhibitors: dangerous hyperkalemia because ACE inhibitors also increase potassium retention - Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors can cause retention of potassium

Aspirin: defecreases spironolactone effectiveness

82
Q

Which drugs increase GFR?

A

Afferent dilators: Atrial natriuretic peptide, prostaglandins

Efferent constrictors: angiotensin II and ANP (by blocking affect of noradrenaline)

83
Q

How do NSAIDs affect the kidney?

A

Contrict the afferent arteriole and therefore reduce GFR

84
Q

Why are ACEi and ARB contraindicated in renal artery stenosis?

A

Renal artery stenosis = GFR low

ACEi and ARB = dilate efferent arteriole and decrease GFR even further

85
Q

What would be the result of a dilated efferent arteriole?

A

GFR would decrease because blood can easily flow out via the efferent

86
Q

What would happen to the GFR if the efferent arteriole was constricted?

A

GFR would increase

87
Q

What are the consequences of renal artery stenosis?

A

Stenosis causes hypoperfusion of kidney

Kidney senses low BP and release renin

Renin causes increase BP systemically but this can’t get past the renal stenosis and thus more renin is released etc etc

Causes hypertension

88
Q

What affect does noradrenaline have on GFR?

A

Increases GFR by constricting the efferent arteriole

89
Q

Discuss causes of nephritic syndrome in adults and children

A

Children: Haemolytic uraemic syndrome

Henloch-Scholein purpura

Post-streptococcal GN

Adults: Goodpasture’s, ANCA associated vasculitis, lupus (SLE)

90
Q

What is ANCA associated vasculitis?

A

(ANCA)-associated vasculitis (AAV) is a group of diseases (granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis and microscopic polyangiitis), characterized by destruction and inflammation of small vessels

91
Q

Discuss various causes of nephritic disease

A

Immune complex trapping: Systemic lupus erythematosus

In situ antigen: Goodpasture’s - circulating anti-glomerular basement membrane antibody

Post infectious: bacterial antigen sits in the membrane

Metabolic - Nephrology (18 decks)

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