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MD > Renal > Flashcards

Renal Flashcards

1
Q

How do ACE inhibitors and NSAIDS impact glomerulus function?

A

ACE inhibitors stops the function of ANG2 which itself causes constriction of the efferent arteriole (-tensin the second one). Due to this, the efferent is dilated - allows blood to flow out quickly.

NSAIDS stop the dilation of the afferent arteriole by blocking prostaglandin action. They cause afferent vasoconstriction, limiting the flow of blood into the glomerulus.

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2
Q

Why might Hb be raised during hypovolemia?

A

Haemoconcentration

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3
Q

What does high sodium in the urine indicate?

A

Can be CKD, diuretics, crappy aldosterone activity

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4
Q

Which drug can reduce thirst response even in dehydration?

A

ACEi

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5
Q

Which 4 body mechanisms regulate GFR?

A
  • Autoregulation - macula densa and myogenic both act on afferent arteriole
  • RAAS - starts with renin release from granular cells
  • SNS
    -ANP/BNP
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6
Q

How does ADH work?

A

Increases number of aquaporins to resorb more water

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7
Q

How does aldosterone work?

A

Causes the body to resorb more sodium and subsequently secrete potassium - ENaCs in collecting duct

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8
Q

Name 3 causes of a pre-renal kidney issue?

A

All due to volume.
- hypovolemia - sepsis
- dehydration
- occlusion of arteries
- triple whammy drugs

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9
Q

What are the major cation and anion exchangers involved in acid/base homeostasis?

A

H+/K+
and
HCO3-/Cl-

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10
Q

What does percussive tenderness over the kidneys indicate?

A

Pyelonephritis

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11
Q

How does nephrotic syndrome cause edema?

A

Nephrotic syndrome is associated with mass proteinuria, peeing out albumin will lower oncotic pressure, allowing fluids to stay in the interstitium.

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12
Q

Compare potassium levels in an AKI vs CKD.

A

AKI will have whack potassium levels, too high in blood due to trying to counter acidosis.
CKD tends to have pretty normal potassium as the nephrons have adapted.

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13
Q

Why does CKD cause low bicarb?

A

Due to shitty nephrons unable to secrete H+, the blood is acidic and the bicarb is used to mop that up.
Bicarb is also made in the nephrons so if the nephrons are dying they cant make it.

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14
Q

How can you workout where urinary blood came from?

A

If from the kidneys - they will be deformed cos they’ve been through the wringer. Red cell casts.

If it’s from the bladder, they’ll be normal RBC.

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15
Q

Should ACEi be used in AKI and CKD?

A

AKI - NO - we need more filtration.
CKD - Yes, we want the nephrons to take it easy, take the pressure off them.

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16
Q

Should NSAIDS be used for AKI or CKD?

A

Neither, ever.

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17
Q

Describe the anatomy of the glomerulus?

A

Capillaries enter and the first layer is endothelial cells. Then the basement membrane, then the podocytes, then bowmans space.

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18
Q

Which structure of the glomerulus is usually damaged in nephrotic syndrome?

A

Podocytes

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19
Q

Brown casts in the urine usually indicate which condition?

A

Acute tubular necrosis

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20
Q

How does acute interstitial nephritis impact urine?

A

Without the functioning of the tubules, urine cannot be properly formed so it will be very dilute.
The glomerulus is spared.

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21
Q

What are the main causes of CKD?

A

HTN, T2D, Glomerulonephritis

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22
Q

Which structures are in front of the right kidney, which structures are below it?

A

In front - liver and duodenum.
Beneath - right colic flexure, small int.

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23
Q

Which structures are in front of the left kidney, which structures are below it?

A

In front - pancreas and left colic flexure
Beneath - descending colon and jujunum.

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24
Q

Describe the internal anatomy of the kidney?

A

Cortex on the outside, medulla on the inside forming pyramids, minor then major calyx.

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25
Q

Describe the origin and path of the arteries that supply the kidneys.

A

The renal arteries arise from the abdo aorta, the left one must go higher, the right must go longer and passes posterior to the IVC.

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26
Q

What are the 3 ureter stricture points?

A
  1. Uretopelvic junction
  2. Pelvic inlet at iliac bifurcation
  3. Entrance to bladder
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27
Q

Which 3 molecules should ideally never be in the urine?

A

BiCarbonate, glucose and albumin

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28
Q

Which cell type supports the glomerular capillary?

A

Mesangial cells

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29
Q

Frothy urine is typically due to what molecule?

A

Albumin

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30
Q

Which molecule is used to test glomerular function?

A

Creatinine

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31
Q

What is the oncotic pressure in the Bowman’s space?

A

Typically 0! There should not be any albumin in this space.

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32
Q

How does afferent arteriole dilation impact GFR and how?

A

Dilate = more blood coming in = more hydrostatic pressure = more filtration = higher GFR

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33
Q

Autoregulation can control GFR between which MAPs?

A

80 and 180

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34
Q

Describe the mechanisms of autoregulation in the kidneys.

A

Myogenic - local contraction of the afferent arteriole in response to stretch. Will constrict afferent arteriole.

Tubuloglomerular feedback - Macula Densa cells sitting at the distal tubule (next to afferent arteriole) - detect increase GFR/pressure and cause vasoconstriction of afferent arteriole.

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35
Q

What is the major buffer in the ECF and intracellularly?

A

ECF - bicarb
Intracellular - phosphate

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36
Q

Define volatile acids and fixed acids.

A

Volatile acids - can be turned into gas and breathed out - eg. bicarb binding to H+ allows for carbon dioxide to be made and breathed out

Fixed acids - cannot be turned into a gas and must be excreted

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37
Q

Which organ system controls short term pH control and which does long term pH control?

A

Short term - respiratory
Long term - Kidneys

38
Q

List the areas of the nephron and what key molecules are involved in each area.

A
  1. Glomerulus
  2. Proximal tubule - does pretty much everything. Key is taking in bicarb and pushing out H+. Na/H transporter.
  3. Descending Loop - H20 absorbed.
  4. Ascending loop - Na/K/Cl transporter
  5. Distal tube - Na/Cl transporter - ENaCs
  6. Collecting Duct - as above
39
Q

How is bicarb recycled?

A

Bicarb filtered by the glomerulus will bind to H+ secreted into the proximal tubule, making CO2 and water, the CO2 will enter the cell and carbonic anhydrase will use it and water to remake bicarb and hydrogen (just as it was on outside), but this time the H+ will be secreted into the lumen and the bicarb will be sent into the blood for re-use.
Very clever system.

40
Q

Metabolism of which amino acid allows for new bicarb to be made?

A

Glutamine

41
Q

Which transporter allows glucose to be reabsorbed in the proximal tubule?

A

SGLT - Sodium/Glucose Transporter

42
Q

What are the 3 ways renin can be released?

A
  • Granulocytes detect low stretch in afferent arteriole
  • Macula Densa detects low salts in the nephron
  • SNS activation - carotid stretch receptors
43
Q

Renin is largely released to combat what?

A

Low BP

44
Q

What are the 5 effects of ANG2?

A
  • systemic vasoconstriction especially the efferent arteriole
  • upregulates Na/H transport in proximal tube
  • promotes ADH creation
  • aldosterone release
  • SNS activated leading to more vasoconstriction, more renin and more CO.
45
Q

What is the function of the ANP?

A

Atrial Naturetic Peptide works against RAAS to piss out sodium (and therefore water).
It reduces ENaC activity and dilates the afferent arteriole.

46
Q

Which parts of the nephron are in the medulla of the kidney?

A

Loop and collecting duct.

47
Q

Why do the distal tubule and collecting duct have variable abilities to absorb water?

A

Depends on the presence of hormones

48
Q

Which area of the nephron cannot absorb water

A

Ascending loop

49
Q

What is the maximum urine osmolarity and what does it correspond to?

A

About 1200 mOsm, corresponds to maximum medullary osmolarity.

50
Q

Where are the body’s osmoreceptors and how do they function?

A

In the hypothalamus.
If the ECF osmolarity falls, water will leave the ECF and enter the cells.
If the ECF osmolarity rises, water will leave the cells.

51
Q

What hormone is KEY to concentrating urine?

A

ADH (vasopressin)

52
Q

Which molecule promotes ADH production in the hypothalamus?

A

ANG2

53
Q

How to tell the proximal and distal collecting tubules apart on histo?

A

Proximal has brush border, distal does not.

54
Q

Mnemonic for nephrotic syndrome.

A

PALE
P - proteinuria
A - albumin (low)
L - LDL high
E - Edema

55
Q

Compare the timeframe of post-streptococcal glomerulonephritis and IgA nephropathy

A

IgA - days after illness
Post Strep - weeks after illness

56
Q

What is Acute Tubular Necrosis and describe the histology.

A

Ischaemia kills tubular epithelium. Occurs due to hypoperfusion. Lumens are blocked on histo - totally full of crap. REVERSIBLE.

57
Q

What causes acute interstitial nephritis?

A

Inflam of kidney insterstitium, often due to allergy to antibiotics.

58
Q

Describe pylonephritis on histo?

A

Pure purple focal spots scattered around tissue (bacteria)

59
Q

What is the most important risk factor for kidney cancers?

A

Tobacco, then HTN, obesity etc

60
Q

List the 3 renal cancers I must know for adults, their prognosis and how they appear on histo.

A
  1. Clear Cell Renal Cell Carcinoma - worst
    - clear cytoplasm due to glycogen
  2. Papillary renal cell carcinoma - middle
    - papillary appearance
  3. Chromophobe - least
    - similar to CCRCC but cytoplasm has sort of pink veins or dots inside - not totally clear.
61
Q

Which factor on histology of renal cancers is associated with poor prognosis?

A

Sarcomatid/rhabdomatid differentiation

62
Q

What is the childhood kidney cancer I need to know?

A

Nephroblastoma

63
Q

What cell type is the epithelium of the ureters and bladder, what special cell do they have?

A

Urothelium, has umbrella cells

64
Q

What is the most common cause of haematuria

A

UTI is most common by far.

65
Q

what finding is diagnostic of pyelonephritis?

A

White cell casts in urine

66
Q

Mnemonic for causes of haematuria?

A

TINIPIGS
Trauma, Infection, Neoplasia, Inflammation, Periods, Iatrogenic, Genetic (Polycystic Kidney disease), Stones

67
Q

What is the best way to check for urinary system cancer and what is a potential problem with this test?

A

Urine cytology.
Low sensitivity, high specificity.

68
Q

What are the four progressions of urinary cancers?

A

Low grade papillary urothelial carcinoma (cells maintain polarity), high grade, carcinoma in situ, invasive carcinoma.

69
Q

What does it mean if squamous epithelium is present in urine sample?

A

Poor collection

70
Q

How much bacterial growth is significant for a supra-pubic aspirate of urine?

A

Any. That site should be sterile.

71
Q

what does low urea indicate in urine, what about high urea?

A

Low urea - low protein = malabsorption, shit diet or dud liver.
High urea - high protein - lots of protein in gut can be a bleed

72
Q

Name 3 causes of pre-renal, renal and post renal disease.

A

Pre: Hypovolemia (MAP below 70), haemorrhage, hypoalbuminemia, renal artery stenosis, drugs.

renal: glomerulonephrtiis, acute interstitial nephritis, acute tubular necrosis.

Post- renal = obstructions. cancer, stones, clots.

73
Q

What is the best measurement for fluid balance?

A

Daily body weight

74
Q

What does CKD do to nephrons, what is the end result of poorly treated CKD?

A

Causes them to hypertrophy, eventual glomeurlosclerosis.
End stage renal disease.

75
Q

How does CKD impact bone health?

A

Crap nephrons cant activate vitamin D so calcium absorption is inhibited.
More importantly, bad nephrons can’t secrete phosphate, which mops up the calcium, causing hypocalcemia, which will activate bone degradation.
RENAL OSTEODYSTROPHY

76
Q

List the 3 classes of diuretics, their sites of action and their targets.

A
  1. Loop diuretic - Frusemide for Chronic Kidney Failure - most powerful. target the Na/K/Cl channels of the ascending loop.
    Side effect: hypokalemia, due to potassium trying to bring in heaps of the Na left in the lumen from the channel’s inhibition.
  2. Thiazide diuretics - for HTN - act on the distal tubule. Inhibit Na/Cl channels.
    Side effects: hypokalemia, also GOUT risk as they increase plasma uric acid.
  3. Potassium sparing diuretics - shittest but spare potassium.
    eg. spironalactone - aldosterone receptor antagonist.
    Sides: hyperkalemia - works well to couple with Loop diuretic.
77
Q

name an osmotic diuretic

A

mannitol - good for ICP

78
Q

What is pyuria?

A

Neutrophils in the urine

79
Q

How can puffy eyelids be related to the kidneys?

A

Peri-orbital edema can be due to hypoalbuminemia.

80
Q

What type of immune hypersensitivity is glomerulonephritis?

A

Type III

81
Q

What is a possible complication of post-streptococcal glomerulonephritis?

A

Rapidly progressing glomerulonephritis

82
Q

How does E.coli ascend the urinary tract?

A

uses fimbriae and adhesins, and pili to scale. It can switch off its flagellin to survive the TLR5 of the bladder and then switch it on again to climb to the kidney.

83
Q

What causes sterile pyuria?

A

WBC in urine but no organism growth. Often a chronic infection like TB.

84
Q

Order of the renal hilum?

A

Anterior: Vein
then artery
Posterior: renal Pelvis

85
Q

What is the function of renin?

A

It turns angiotensinogen into ANG1

86
Q

What glomerulus layer is impacted in nephritic haematuria? What about nephrotic?

A

Blood + protein (nephritic) = basement membrane

Just protein (nephrotic) = podocytes

87
Q

Name 3 functions of aldosterone

A

Ups ENaCs on luminal surface and ups Na/K ATPase on basal surface
Also vasoconstricts

88
Q

Which muscle is immediately posterior to kidneys?

A

Quadratus lumborum

89
Q

Are drugs carried by proteins filtered in the glomerulus?

A

Glomerular filtration relies on the ‘leaky glomerulus’. But carried drugs cannot be filtered this way and must be secreted.

90
Q

Which kidney is higher?

A

Left is higher as liver limits right kidney

MD (15 decks)

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