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College Learning Series > Renal Physiology > Flashcards

Renal Physiology Flashcards

(49 cards)

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1
Q

Where does serum creatinine come from?

A
  1. Metabolism of creatine in skeletal muscle + dietary meat
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2
Q

Locations in nephron creatinine transferred?

A

Freely filtered accross glomeruli
Actively secreted proximal tubules,
Nil other transport

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3
Q

Average GFR/ day in humans?

A

180l/ day

(Or 125ml/ min)

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4
Q

Relation between Cr Cl and GFR?

A

Cr Cl estimates GFR,
exceeds true GFR by 10-20% due to active tubular secretion or creatinine
(excretion increased further as GFR decreasesv - up to 50% in ESRF)

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5
Q

Methods for estimating Cr Cl?

A

Equations
- Cockrauft Gault
- MDRD
- CKD-EPI (preferred these days)

Isotopic measurement (nuc med scan)

C-cystatin filtration (only done in research)

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6
Q

INTRA vs EXTRA cellular fluid %

A

ECF: 33%
ICF 66%

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7
Q

Main cation/ anion in ICF (IntraCellular fluid)?

A

cation: postassium
anion: phosphate

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8
Q

basic formula for estimating Serum osmolality?

A

2x Na + glucose + urea

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9
Q

Where are the important osmoreceptors located?

A

hypothalamus

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10
Q

Roles of ADH

A
  1. Maintain plasma osmolality (main role, V2 receptor)
  2. Volume regulator (V2, V1)
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11
Q

Mechanism of Tolvaptan

A

Blocks V2 receptors in distal nephron and collection duct
Prevents the binding of vasopressin, reduce expression of aquaporins

Reduces cyst formation in PCKD (??how)

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12
Q

Serum K and pH in SIADH

A

generally normal

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13
Q

Causes of SIADH

A

Ectopic secretion of ADH: SC Lung Cancer

CNS disorders

Drugs:
- chlorpropamide, carbamazepine ,SSRI, chemotherapy drugs, immunosuppression, ciprofloxacin, amiodarone, ecstasy

Any Recent Surgery

Pulmonary Disease

Hormone deficiency (pituitary, thyroid)

Idiopathic

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14
Q

Non-SIADH Causes of Euvolaemic Hypotonic Hyponatremia

A

Excessive water ingestion

Low dietary solute intake but high fluid intake
- Tea and toast diet or in alcoholics (Beer Potomania)

Advanced renal failure
(increase solute excretion but impaired water excretion despite normal levels of ADH)

Thiazides (Reduction in diluting ability of urine)

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15
Q

Hypovolemic hyponatremia causes

A

Excessive diuretics (High urine Na and chloride)

GI fluid losses such as diarrhea or sequestration of fluid in 3rd spaces
(Low urine Na)

GI losses due to vomiting
(High urine Na in severe metabolic alkalosis – Na excretion with loss of urinary bicarbonate , low urine chloride)

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16
Q

Hypertonic Hyponatraemia causes

A

Hyperglycemia -> increase serum osmolality -> water drawn from cells -> expands ECF and lowers serum Na concentration

IVIG infusion – hypertonic solution

Sorbitol or mannitol irrigation in urological or gynaecological procedures

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17
Q

Where in the nephron do various diuretics act?

A
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18
Q

Which diuretics increase/ decrease Ca reabsorption?

A

Furosemide/ loop diuretics decrease re-absorbtion: concern for nephrocalcinosis

Thiazides increase re-absorbtion: useful for kidney stone prevention

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19
Q

Transporter FUROSEMIDE effects, and where?

A

Na - K - 2Cl transporter
(descending loop of henle)

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20
Q

Transporter THIAZIDES effect, and where?

Study These Flashcards
A

Na-Cl transporter (DCT primarily)

21
Q

Genetic disorders affecting sodium chloride reabsorption in nephrons

Study These Flashcards
A

Bartter and Gitelman Syndromes

22
Q

What genetic expression are Bartter and Gitelman Syndromes?

Study These Flashcards
A

Autosomal Recessive

(multiple potential genetic abnormalities)

23
Q

Age groups for Bartter and Gitelman Syndromes

Study These Flashcards
A

Bartter - Babies

Gitelman - Grown ups

24
Q

Which diuretics do Bartter and Gitelman Syndromes mimic?

Study These Flashcards
A

Bartter - loop diuretic
(also high prostaglandin production -> stimulates renin)

Gitelman - thiazide

25
Stimulation of renin release?
• hypotension (baroreceptors, granular cells sense) • volume depletion (macula sends cells detect Na levels) • increased sympathetic activity
26
Receptors that detect change in ECF volume:
• Baroreceptors or stretch receptors in the wall of the afferent arteriole • Cardiac and arterial receptors • Cells of macula densa in early distal tubule –stimulated by decrease in chloride
27
Where is angiotensinogen produced?
mainly by liver but also: brain, large arteries, kidney, adrenal glands and adipose tissues
28
Effects on angiotensin II in kidneys On binding Angiotensin type 1 receptor
vasoconstriction of efferent and afferent arterioles - decreased blood flow - increased glomerular pressure Inflammatory mediator (pro inflammatory) Proliferation vascular smooth muscle cells aldosterone release/ sodium retention
29
Systemic effects of aldosterone
• Activation of inflammatory cascade and production of proinflammatory cytokines • Contributes to insulin resistance • Promote cardiac fibrosis • potentially involved in metabolic syndrome
30
Effect of aldosterone in Kidneys
• Increases number epithelial sodium channels in distal tubule -> Na and water reabsorption -> increase blood pressure -> K secretion and low K levels
31
Causes of primary hyperaldosteronism
• Bilateral hyperplasia of adrenals • Unilateral adenomas (Conn`s syndrome) • Very rarely, unilateral hyperplasia, adrenocortical carcinomas (tumour > 4cm) or ectopic tumours
32
When to suspect Conn`s syndrome
• Hypokalemia and HTN –classic presentation (30% cases) Screen if: • Poorly controlled hypertension • Younger patients • Family hx
33
Tests for primary hyperaldosteronism
• Early morning renin/aldosterone ratio • CT scan of the adrenals abnormal • Oral salt load test • Adrenal vein sampling • Spironolactone has to be ceased prior
34
Factors that increase K uptake into cells
• Insulin • Aldosterone • Catecholamines, growth hormones • Increase in pH in ECF –alkalosis
35
Hyperkalaemia and acidosis
High plasma K levels -> entry of K into cells + hydrogen ion moving out -> acidosis of plasma + intracellular alkalosis
36
Where is bicarb reabsorbed in Kidneys?
85-90% on PCT (Na-H exchange) 10% CT (H ATPase, H-K ATPase)
37
Where is H+ excreted in kidneys
mostly in CT (H ATPase, H-K ATPase)
38
What buffers H+ in urine
ammonia, phosphate
39
Causes for NAGMA
Loss of bicarbonate • Severe diarrhea • Using ileum to replace a bladder- sodium bicarbonate losses • Renal failure – due to accumulation of anions such as sulfate and phosphate • Proximal type 2 RTA Impaired renal acid excretion • Moderate Renal impairment • Distal (type 1) RTA and type 4 RTA
40
hyper/ hypokalaemic RTAs
Hypokalemic • Classic distal Type 1 –defects in distal hydrogen ion excretion • Proximal Type 2 –reduce capacity to reclaim filtered bicarbonate Hyperkalemic • Type 4- hypoaldosteronism
41
Pathophys of Type 1 RTA
impaired H+ excretion by H-ATPase Causes: autoimmune diseases: Sjogren`s syndrome, Rheumatoid arthritis, hypercalciuria as a primary defect
42
Which RTA is associated with renal stones?
Type 1 (Calcium phosphate stones)
43
Pathophys of CaPO4 stones in Type 1 RTA
• Metabolic acidosis release calcium phosphate from bones to buffer the retained acid • Reduction of tubular absorption of Ca and phosphate > increase urinary levels • High urine pH precipitates calcium phosphate • High urine pH also reduces citrate excretion (normal citrate forms a soluble complex with Calcium)
44
Treatment for Type 1 RTA?
Bicarb tablets
45
Synonyms for type 1 RTA
Distal RTA Classic RTA
46
Pathophys of type 2 RTA?
Reduced reabsorbtion of HCO3 Causes: - monoclonal gammopathies(myeloma), - Fanconi`s syndrome, - drugs, - isolated
47
Treatment for TYpe 2 RTA?
Bicarb - much harder than type 1, will lead to K wasting
48
Pathophys of Type 4 RTA?
Hyperkalaemia/ hypoaldosteronism Causes: • Hyporeninemic hypoaldosteronism (NSAIDs/ calcineurin use, chronic interstitial nephritis or DM nephropathy, acute GN) • Treatment with Angiotensin II inhibitors, k sparing diuretics • Heparin – toxic effect on adrenal zona glomerulosa cells • Primary adrenal insufficiency/Addison`s
49
Treatment of type 4 RTA
• Treat underlying disorder • Fludrocortisone (caution required as can lead to fluid retention)

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