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Renal > Renal > Flashcards

Renal Flashcards

1
Q

What type of hormone secretion do the kidneys do?

A

Endocrine

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2
Q

Where does bicarbonate regeneration occur?

A

In the proximal tubule@

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3
Q

If protein is in the urine which area of the kidney is diseased?

A

The proximal tubulue

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4
Q

What is the main hormone the kidneys secrete?

A

Erythropoeitin - release stimulated by hypoxia - used by athletes for doping.

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5
Q

What do the kidneys secrete the active form of?

A

Active vitamin D - 1, 25 dihydroxycholecalciferol
In kidney disease less vitamin D means low calcium absoprption, hence PTH secreted to release calcium from the bone but this causes (RENAL OSTEODYSTROPHY)

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6
Q

How do the kidneys control blood pressure?

A

Through renin secreted by the macula densa

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7
Q

Kidneys related to liver disease

A

In serious live failures an unknown signal cuts of blood supply to the liver, this causes hepatorenal failure!

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8
Q

Kidney disease and myeloma

A

Proteins deposited in the kidney can cause failure.

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9
Q

What do nitrates & leucocytes in the urine show

A

Infection

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10
Q

What will abdominal x-rays show?

A

Shows calcification but won’t show kidney stones unless they are calcified - use an US to see these

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11
Q

CT KUB

A

Shows calcification with an iodineg contrast

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12
Q

MRA

A

Shows blood supply to the kidneys

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13
Q

Vertebral levels of the kidneys

A

T12 - L3

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14
Q

What % of the glomerulus is in the cortex?

A

80% Glomerulus is the network of capillaries in the kidneys. 170L of blood passes through them a day. 1.5L of urine is produced!
Glomerulus is surrounded by the Bowmans capsule

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15
Q

Which parts of the kidney are in the cortex?

A

Proximal and distal convoluted tubulue, glomerulue, macula densa and juxtaglomerular apparatus and part of the collecting duct?

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16
Q

What part of the kidneys are in the medulla?

A

Loops of Henle and part of the collecting duct

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17
Q

Filtering in the Bowmans capsule

A

Fluid enters under high pressure
Fluid moves out due to high capillary hydrostatic pressure
Some fluid moves back into the capillary due to the oncotic pressure!

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18
Q

Reflux nephropathy

A

In Childhood, incompetent vesicoureteric junction. Some urine returns to bladder - risk of stagnation and infection! This can cause Pyelonephritis - injury and scarring of the kidneys leading to CKD
Child fails to meet developmental goals, milestones, family history often present!
Treat prophylactically with antibiotics

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19
Q

Haematuria

A

If over 45 suspect lesions and refer to urologist

If under 45 suspect glomerulonephritis (inflammation in the glomerulus) and refer to a renal physician!

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20
Q

Nephrotic syndrome

A

Proteinuria, hypoalbunaemia (causes oedema), hypercholesterolaemia

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21
Q

What happens to the podocytes in nephrotic syndrome?

A

They fuse, change charge, allow albumin to pass

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22
Q

Difference between nephrotic and nephritic syndromes?

A

Nephrotic means loss of protein

Nephritic means loss of blood

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23
Q

Nephritic syndrome

A

Haematuria, proteinuria, low urine volume, mild hypertension

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24
Q

Intersitial Nephritis

A

WBC enter the kidneys and can cause AKI. Can occur in people who have allergic reactions e.g. ibuprofen!

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25
Q

Where does reabsorption occur>

A

The loop of Henle

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26
Q

What affects the rate of filter across the glomerular basement membrane

A

Weight, charge, hydrostatic pressure

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27
Q

What releases creatinine?

A

Muscles - hence must require sex when estimating glomerular filtration rate as men have more muscle

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28
Q

How do kidneys control water

A

Kidneys produce concentrated urine in periods of low fluid intake. Do this by reabsorption of water due to establishing high conc. gradient in the medulla.

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29
Q

How much fluid loss through insensible?

A

500ml/24 hours

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30
Q

Proximal convoluted tubule

A

Recovers 70% of tubule! Reabsorbs Na, Cl, K, H20, HCO3. Bicarbonate reabsorption depends on carbonic anyhdrase!
Sodium exchanged for H+ to fuel the carbonic anhydrase, Carbonic anhydrase inhibitors act here!

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31
Q

Ascending Limb of Henle

A

Absorbs Na, 2Cl and K via one pump and H20. Furosemide blocks this pump. Hence can develop hypo of these ions.

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32
Q

Cortical collecting duct

A

Aldosterone acts here, causes Na absorption (with H20 and Cl) in exchange for K+
Also absorption of Na via its own channel. Thiazides block this.

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33
Q

Spirinalactone

A

An aldosterone antagonist. Hence inhibits uptake of Na in the cortical collecting duct. Potassium is retained causing hyperkalaemia.

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34
Q

Medullary Collecting Duct

A

ADH acts here to increase water absorption - aquaporinis inserts to increase the absorption
Diabetes insipidness - central failure to secrete ADH or peripheral resistance to ADH - causes hypovolaemia, polyuria, hyponatraemia!

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35
Q

Pre renal AKI

A

Often vascular problems, if prolonged bp leads to intrinsic kidney disease!

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36
Q

Urine output in intrinsic kidney disase

A

Maintained or decreased. Increased creating!

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37
Q

AKI Staging

A

1) 1.5 to 1.9 fold increase in creatinine or less than 0.5ml urine per kg for 6 hours
2) 2 to 2.9 fold increase or less than 0.5ml urine per kg for 12 hours
3) 3+ increase or less than 0.3ml urine per kg for 24 hours

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38
Q

Causes if pre-renal kidney disease.

A

Sepsis, hypotension, hypovolaemia, MI, diuretics causing hypovolaemia and ACEi causing hypovolaemia. All vascular issues
C

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39
Q

Causes of intrinsic kidney disease!

A

Acute tubular injury, sepsis and hypotension, nephrotoxins, NSAIDS, Controst, Rhabdomyolosis (from muscle breakdown), myeloma, snakebites, vasculitis, and glomeruneprhtitis

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40
Q

Post Renal

A

Kidney stones, prostatic hypertrophy, obstructions, intrabdominal hypertension etc.

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41
Q

Presentation of AKI

A

Poor fluid intake, excessive fluid loss, drug history of nephrotoxins or contrast, kidney stones, lone pain, haematuria etc.
Rash - showing vasculitis or interstitial nephritis
Join swelling in vasculitis

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42
Q

Hyperkalaemia

A

Addition of PT wave and then P wave disappears. Give calcium gluconate to protect. Also give glucose and insulin, insulin pushes K+ into cells to give you more time

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43
Q

Uraemia complications

A

Pericarditis and encephalopathy (confusion)

44
Q

Complications of AKI

A

hyperkalaemia, academia (due to poor HC03 regeneration), pulmonary oedema and uraemia!

45
Q

How to prevent risk factors of AKI

A

Sepsis
Toxins
Optimise bp
Prevent harm

46
Q

Treating ANCA Vasculitis

A

Immunosuppressants and plasma exchange

47
Q

When to give renal replacement therapy

A

If AKI is progressive, K+ unresponsive to treatment, sever acidosis (less than 7.1) and uraemiac complications occur

48
Q

CKD

A

Reduced kidney functions for more than 3 months, reversal unlikely

49
Q

Causes of CKD

A

Diabetes, glomerular disease, ADCKD, renal vascular disease (hypertensions and atherosclerosis), AKI, Intersitial disease (e.g. allergic reaction to a drug)

50
Q

Diabetes and CKD

A

Most common cause of ESKD, 20% get this nephropathy! Other features are retinopathy, neuropathy and proteinuria!. Due to change to vasculature and damage to the basement membrane. Also sclerotic deposits

51
Q

Presentation of Nephrotic

A

Swollen ankles (due to hypoalbunaemia), proteinuria and hypocholesterolaemia

52
Q

Nephritic presentation

A

throat infection, swollen ankles, often in children! Deposition of material causes the loss of the capillary loop.

53
Q

RPGN

A

Join pain, fever, red eyes. Often thought to be a UTI. Acute nephritis and AKI

54
Q

ADPKD

A

Hypertension, berry aneurysm
85% due to mutation in PKD1 gene on chromome 16 - coges for polycystin 1 a membrane glycoprotein for cell - cell interactions
15% due to PKD2 on chromosome 4 - codes for polycystin 2 a calcium ion channel. PKD2 causes slower progression to CKD

55
Q

ADPKD - PKD1

A

85% due to mutation in PKD1 gene on chromome 16 - coges for polycystin 1 a membrane glycoprotein for cell - cell interactions

56
Q

ADPKD - PKD2

A

15% due to PKD2 on chromosome 4 - codes for polycystin 2 a calcium ion channel. PKD2 causes slower progression to CKD

57
Q

Classification of CKD

A

1) GFR over 90
2) 60-89
3A) 45-69
3B) 30-44
4) 15-29
5) LLess than 15 - start dialysis

58
Q

CKD Complications

A

Anaemia, platelet abnormalities, skin problems, GI tract problems, endocrine abnormalities, polyneuropathy, CVS and CNS effects, renal problems and renal osteodystrophies!

59
Q

Pruiritis

A

Accumulationof phosphate

60
Q

How to distinguish between AKI and CKD

A

Low calcium and high phosphate in CKD

Small shrunken kidneys shown in US in CKD

61
Q

Management of CKD

A

BP Control
GLuid balance
rEPO for anaemia
It D for bone problems. - e.g. calcimmetics to inhibit parathyroid secretion
Give sodium bicarbonate to replace bicarbonate not lost in kidneys
Avoid foods with potassium and phosphate or give phosphate binders with food to reduce absorption

62
Q

How do kidneys regulate pH

A

H+ secretion and HCO3- regeneration

Also NH3 converted no NH4+ so lose an extra H+

63
Q

Increased risk of acid base abnormalities in

A

CKD when eGFR is less than 30, liver disease and lunch disease

64
Q

Approaches to acid/base

A

1) Traditional - SChwarts - Barterr - uses Bronsted Lowry. H+ concentration is a function of the ratio between PC02 and serum bicarbonate. Used Anion gap to classify disturbances
2) Alternative steward approach. Based on principle HC03 doesn’t affect pH

65
Q

Severe acidaemia

A

Damage to cardiac function and vascular tone

66
Q

Severe alkalemia

A

Irrigation of cardiac muscle and skeletal muscle

67
Q

Anion gap

A

Unmeasured anions - unmeasure cations

=[NA+] - ([HCo3] + [CL])

68
Q

High anion gap

A

Acidosis

69
Q

Low anion gap

A

Aklalosis

70
Q

Causes of metabolic acidosis

A

Can be high anion gap or normal anion gap

71
Q

High anion gap acidosis

A 
Methanol - drug
Uraemia
Diabetes - ketacidosis
Paraldeyhyde
Alcohol
Lactate - liver failure, metformin, hypoxia
Ethylene glycol - drug
Salicylate (aspirin) - drug
72
Q

Ethylene glycol

A

Metabolism creates toxic glycolate. Causes high anion gap acidosis. Calcium oxidate crystals in urine suggest ethylene toxicity. If difference between measured and calculate is greater than 25 suspect toxicity.
Calculated = 2 x [na] + glucose + urea
Give alcohol infusion to stop formation as it inhibits alcogol dehydrogenase, also fomepizole inhibits it or dialysis

73
Q

Normal Anion Gap Acidosis

A

1) GI HCO3 loss
2) Renal HCO3 loss - e.g. acetazolamide (carbonic anyhdrase inhibitor) and renal tubular acidosis
2) infusion of 0.9% Saline

74
Q

What causes the afferent arteriole to dilate?

A

Prostaglandins

75
Q

Aldosterone stimulates?

A

Na+ absorption and K+ excretion

76
Q

ACEi

A

Inhibits vasoconstrictive effect of AT2 on efferent arteriole
Side effects - hypotension (Don’t use for AKI), hyperkalaemia as inhibits aldosterone and can develop cough due to bradykinin build up

77
Q

ATR Blockers

A

Valsartan and Ibrestan

78
Q

Loop Diuretics

A

Inhibit the na/2cl/k pump in the ascending loop of henle
Furesomide
Use for CKD, nephritic syndrome, hypertension, cardiac failrue
Can cause hypovolaemia, and hypokalaemia (but use with a potassium sparing one e.g. amolaride)

79
Q

Thiazides

A

Inhibit Na uptake in cortical collecting tube
Use for CKD, nephrotic syndrome, hypertension, cardiac failaure etc
Side effect: Hypovolaemia

80
Q

Spirinolactone

A

Inhibits Aldosterone. Hence Na not reabsorbed and K+ retained also H20 Not observed
Uses: Cardiac failure with an ACEi and liver cirrhosis to prevent ascites.
Risk of hyperkalaemia

81
Q

Amiloride

A

Blocks Na+ Absorption for K+

Use in tandem with a good diuretic

82
Q

CKD Drugs

A

Anti-hypetensive, diuretics, sodium bicarbonate and statins

83
Q

Vitamin D Analogues

A

E.g. alpha calcidol - activated in the liver to increase calcium and phosphate absorption for the gut. Can cause hypercalcaemia and hyperphosphataemia!

84
Q

Kidneys and phosphate

A

Kidneys control phosphate levels, in kidney disease can’t excrete phosphate so it builds up!

85
Q

How to replace Epo

A

SC Injection when GFR is less than 15.

Side effects are hypertension and pure red apalasia (due to antibodies)

86
Q

Prostaglandins

A

Prostaglandins cause dilation of the afferent arteriole. NSAIDS inhibit this dilation, hence don’t give otherwise reduces blood flow to kidneys further!

87
Q

What happens in sepsis

A

Capillaries become leaky, potassium can leak out

88
Q

Where are Na and K+ predominantly

A

Na+ extracellular, K+ intracellular and most of fluid is intracellular

89
Q

Replacement fluids

A

Can use Dextrose or NaCl or combination. Need to determine losses, give large amounts fluid via a central vein

90
Q

Resuscitation fluids

A

aims to restore circulating fluids as hypovolaemia causes hypotension can cause AKI. Can give NaCL 0.9%, Hartmans - but contains potassium so don’t use in hyperkalaemia and also contains lactate to make into HCO3
Or give blood, O- in an emeergency. Give clotting factors too once 4 litres of blood given

91
Q

IV Fluids Crystalloids

A

Saline and dextrose

Balanced crystalloids: Hartmanns and Ringers

92
Q

Colloids

A

No longer used as no significant advantages

93
Q

Crystalloids

A

Water to which solute added. Low sodium fluid and it disperses intracellular and extracellular. Na pumped extracellular causing fluids to disseminate to the extracellular comparment

94
Q

Colloids

A

Contain large proteins, can’t cross capillary walls so stay in the capillaries hence increase intravascular volume. Can be synthetic e.g. gelatine but large volumes without free water can cause a hypertonic state

95
Q

SEPSIS 6 Management

As sepsis can result in vasodilation, leaky capillaries and shock and multigrain failure

A

Blood culture and septic screen
Urine output, U&E and urine culture
Fluid resuscitation (generally 500ml over 15mins)
Antibitoics IV
Lactate (high in ischaemia) and Hb measurements
Oxygen to correct hypoxia

96
Q

ADPKD

A 
Berry aneurysm in 10-15%
50% Need RRT by the age of 60
Lower bp to slow progression
Cysts produce erythropoietin hence anaemia less common
Decline in function is linear!
97
Q

Symptoms of ADPKD

A

Metabolic acidosis, hyperkalaemia, Low Calcium and High Phospahte, high PTH, anaemia, high creatine, decline in kidney function

98
Q

Medications for ADPKD

A

Caclium acetate to bind phosphate and prevent absorption
Alfacalcidol to treat hyperparathyroidism
Anti-hypertensives

99
Q

Dialysis in the young and increase death rate x100 why?

A

As caclium deposition occurs in bessels!

100
Q

Haemodilaysis

A

create a fistula to create a large vein! semi permeable membrane and negative pressure.
Fistula preferred choice as lower rate of infection then central venous catheters

101
Q

Central venous catheters

A

CVCs inserted in emergencies, 400mls a minute of blood goes throguh the machine

102
Q

Pertioneal Dialysis

A

Fluid put into the peritoneum, capillary endothelium acts as the semi permeable membrane. Glucose added to fluid to control water loss

103
Q

Why you can’t give HD

A

Vascular access issues, severe haemodynamic instability and inadequate bp?

104
Q

Why you can’t give PD

A

Environment, already had complicated abdominal surgery or incapactiy to carry out exchanges

105
Q

HD Advantages and disadvantages

A

Less protein loss, shorter treatment times, less individual responsibility, high efficient, can start immediately

Disadvantages: access problems, bleeding risk due to anticoagulation and infections

106
Q

PD advantages and disadvantages

A

Home based, preserves renal function, less fluid restriction, less biochemical perturbation, no anti-coagulation

Disadvantages: hernias and peritonitis, membrane failure as peritoneum exposed to high osmalartiy of dialysis fluid
Protein loss!

Renal (2 decks)

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