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Renal > Anatomy and Physiology of the kidney > Flashcards

Anatomy and Physiology of the kidney Flashcards

1
Q

Blood flow of the kidney

A

Artery goes into the kidney -> afferent arteriole goes into the Nephrone - renal corpuscle (Browman’s corpuscle + Glomerus) -> efferent arteriole -> down to the vasa recta (straight arteriole + straight venules) into the juxtamedullary nephron (MEDULLA)-> from venules of the vasa recta the blood leaves the kidney through the vein

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2
Q

Urine flow

A

Glomerus -> the filtrate is collected in the Browman’s capsule -> goes through the proximal convoluted tube -> descending loop of Henle (going down into the Medulla)-> thin and then thick ascending loop of Henle (up towards the cortex) -> goes through the distal convoluted tube -> urine goes into the collecting duct -> Ureter

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3
Q

Anatomy of the Renal Corpuscle

A

Renal Corpuscle
Podocytes on the capillary provide a barrier for molecules that should not leave the blood

Bowman’s capsule: collects the filtrate

Fenestra: little gaps on the capillary
basement membrane in between
Slit pores and foot processes in front of the urinary space

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4
Q

What is the predominant barrier molecules have to cross in order to get filtered in the kidney?

A

Basement membrane

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5
Q

Which molecules are likely to get filtered?

A

small hydrophilic molecules

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6
Q

Which molecules are not likely to get filtered?

A

large hydrophobic molecules
-drugs bound to albumin
-cells
-proteins

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7
Q

What is the Glomerular Filtration Rate (GFR)

A

The rate at which glomerular filtrate is formed (blood is filtered)

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8
Q

What determines the filtration rate (GFR)?

A

depends on
-the pressure in the glomerulus
-the blood flow to the glomerulus

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9
Q

Forces in the glomerulus

A

Glomerular blood pressure P(GC) 60mmHg - relatively high for a capillary BP

Fluid pressure in the Bowman’s space P(BS) - 15mmHg -> AGAINST

Osmotic force due to protein in plasma in the glomerular capillary O(GC) - 29 mmHG -> AGAINST

Net pressure: 60 - 15 - 29 = 16 mmHg towards the Bowman’s space

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10
Q

How does GFR change with change in glomerulus capillary (afferent, efferent)

A

-vasoconstriction of afferent capillary -> less blood flow -> decrease in GFR

-vasoconstriction of efferent capillary -> increase of pressure -> increase in GFR

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11
Q

What determines Renal clearance?

A

Filtration
Reabsorption
Secretion

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12
Q

Renal clearance equation

A

C = UV / P

Clearance (ml/min or ml/24h)
U: Urine concentration (mg/ml)
V: Urine volume (ml/min)
P: plasma concentration (mg/ml)

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13
Q

Which molecule is used to approximate GFR?

A

The clearance of creatinine

-> So it must be filtered and excreted but not secreted and not reabsorbed to be used for renal function calculations

-> In reality some are secreted in the proximal tubule

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14
Q

Which molecule is used to approximate renal plasma flow?

A

The clearance of PAH

we want to measure the plasma that is in the kidney and doesn’t leave the kidney
-> It is filtered and completely secreted, but NOT excreted, NOT reabsorbed

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15
Q

What is the difference between primary active transport and secondary active transport?

A

Primary active transport: uses ATP to go against the gradient

Secondary active transport: often uses Na+ to go against the gradient (low Na+ on the other side)
f.e. Glucose transport needs symport with Na+ to go against the gradient

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16
Q

Where does most of Reabsorption occur?

A

Proximal convoluted tube

17
Q

How does Glucose behave in the kidney with an increase in concentration?

A

-Filtration goes up - NO SATURATION
-Reabsorption goes - SATURATION bc the transporters (Na-Glucose-Cotransporter) are limited
-Excretion goes up - NO SATURATION -> Glycosuria (sign of diabetes)

18
Q

At which concentration does the Na-Glucose transporter start to get saturated?

A

200 mg/dl
200 mg/ 100ml

19
Q

Reabsorption of Na at the ascending limb
Which limp is permeable to H2O and Na+?

A

Descending limb: impermeable to Na+ and permeable to water

Ascending limb: permeable to Na+ due to NKCC transporter, impermeable to H2O due to tight junctions

20
Q

Consequences of blocking the NKCC transporter at the ascending limb

A

Na+ and K+ stays in the tubule -> water follows -> Excretion in the urine

Hypokalemia -> Patients using loop diuretics may have to supplement POTASSIUM

21
Q

Reabsorption of Na at the collecting duct

A

Na+ Reabsorption is regulated based on the body’s needs
-regulated with Aldosterone (gets into the cell and activates a transcription factor for the Na-K pump)

-Aldosterone upregulates the Na-K pump at the basolateral membrane -> more Na+ gets reabsorbed in the interstitial fluid

more K+ goes into the duct cells -> diffusion into the tubule (urine)

22
Q

How does Spirolactone affect Na and K?

A

Na+ stays in the tubule (urine), Na and water reabsorption decreased -> DIURETIC
K+ stays in the interstitial fluid (cells) -> K-sparing drug

23
Q

How is ADH release stimulated?

A

Renin -> Angiotensin II

24
Q

Where and how does Vasopressin (ADH) work?

A

in the distal convoluted + cortical and medullary collecting duct

-Vasopressin binds to Vasopressin receptors on the basolateral membrane of the collecting tube (or distal tube) -> activated adenylate cyclase -> conversion of ATP to cAMP -> more Aquaporins on the luminal membrane of the collecting tube -> water crosses from the tubular lumen (urine) into the cell -> crosses the cell into the interstitial fluid

-> Concentrated Urine

25
Q

What are the two roles of Vasopressin (or ADH)

A

-VASOPRESSIN: Binding on V1 receptors on smooth muscle cells: Vasoconstriction of smooth muscle cells (GI, respiratory, renal, eye, genital)

-ADH: Binding V2 receptors of the distal tubules: causing reabsorption of H2O via an increase in Aquaporins

26
Q

Where is Vasopressein produced?

A

-posterior pituitary gland (also oxytocin)
-it is a peptide
-administered IV, IM
-short half-life (15 min)

27
Q

What are the advantages of Desmopressin?

A

-a synthetic form of Vasopressin (short long-life)
-longer half-life
-more antidiuretic action (4000x) than vasoconstrictor -> more potent as antidiuretic
-administered IV, SC, intranasally, orally

28
Q

Vasopressin in Diabetes insipidus

A

-Treatment of pituitary (central cranial) diabetes -> insufficient ADH production from the pituitary gland

-Supplement ADH
-> Vasopressin (caution with patients cardiac conditions bc of vasoconstriction action) -> Desmopressin is the better option in those patients

-adverse effects: headache, nausea, abdominal cramps
-overdose: seizures, hyponatremia (ADH works too well -> the reabsorbed water is diluting the Na in the blood)

29
Q

What are the two forms of Diabetes insipidus

A

-Renal: enough ADH but it is not working on the kidney

-Pituitary: the pituitary is not secreting enough ADH

Renal (21 decks)

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