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gu / gyn & renal > B&B Renal: Anatomy & Physiology > Flashcards

B&B Renal: Anatomy & Physiology Flashcards

1
Q

Germ layer of origin

Kidney Development

A

Mesoderm

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2
Q

Pronephros

Kidney Development

A
  • 1st embryonic renal structure
  • Forms & degenerates by week 4 of gestation
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3
Q

Mesonephros

Kidney Development

A
  • 2nd embryonic renal strucutre
  • Acts as interim kidney during 1st trimester
  • Contributes to vas deferens in males
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4
Q

Metanephros

Kidney Development

A
  • 3rd embryonic renal structure
  • Forms permanent kidney
  • Appears during 5th week gestation
  • Develops into kidney through weeks 32-26
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5
Q

Kidney Formation

A

2 key structures
1. Ureteric bud
2. Metanephric mesenchyme

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6
Q

Ureteric bud

Kidney Formation

A
  • Outgrowth of mesonephric (Wolffian) duct
  • Forms ureter, renal pelvis & calyces, collecting ducts
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7
Q

Metanephric mesenchyme

Kidney formation

A
  • Mesoderm tissue around ureteric bud
  • Interacts with ureteric bud to form glomerulus through distal tubule of nephron
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8
Q

Most common renal malignancy in young children

A

Wilm’s tumor

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9
Q

Abnormal proliferation of metanephric mesenchyme
* Produces embryonic glomerular structures
* Associated with WT1 mutations
* WT1 is expressed in metanephric mesenchyme

Pathophysiology

A

Wilms’ tumor

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10
Q

Absence of one or both kidneys at birth
* Unilateral: remaining kidney compensates
* Hypertrophy
* Hyperfiltration
* Risk of FSGS
* Risk of renal failure after decades
* Bilateral:
* Oligohydramnios
* Potter’s syndrome

FSGS: focal segmental glomerular sclerosis

A

Renal Agenesis

Congenital Anomaly

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11
Q

Renal Agenesis

Pathophysiology

A
  • Ureteric bud fails to develop
  • Lack of signals to mesenchyme to trigger differentiation
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12
Q

Renal dysplasia resulting in replacement of kidney with cysts
* No / little functioning renal tissue
* Usually unilateral

A

Multicystic Dysplastic Kidney

Congenital Anomaly

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13
Q

Multicystic Dysplastic Kidney

Pathophysiology

A

Abnormal ureteric bud-mesenchyme interaction

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14
Q
  • Common cause of single kidney obstruction
  • Narrowing in proximal ureter at UPJ
  • Often detected in utero
  • Can be treated surgical after birth
A

Ureteropelvic junction (UPJ) obstruction

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15
Q

UPJ obstruction

Complications

A
  • Hydronephrosis
  • Poor urinary flow –> kidney stones, UTIs
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16
Q

Duplex Collecting System

Duplicated Ureter

A
  • Occurs when 2 ureteric buds form on right / left side or if a ureteric bud bifurcares during development
  • Results in formation of upper / lower kidneys
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17
Q

Duplicated Ureter

Complications

A
  • May lead to poor urinary flow; UTIs
  • Hydronephrosis
  • Associated with vesicoureteral reflux
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18
Q
  • Backward urine flow from bladder to kidneys
  • Leads to recurrent UTIs
A

Vesicoureteral reflux

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19
Q

Abnormal closure of UVJ
* Occurs in children
* Associated with duplex ureters

UVJ = ureterovesical junction; where ureter inserts into bladder

A

Primary vesicoureteral reflux

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20
Q

Retrograde flow of urine due to high bladder pressure
* Associated with posterior urethral valves

A

Secondary vesicoureteral reflux

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21
Q

Retrograde flow of urine due to high bladder pressure
* Associated with posterior urethral valves

A

Secondary vesicoureteral reflux

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22
Q

Loss of fetal cushioning to external forces resulting from decreased / absent amniotic fluid
* External compression of fetus: abnormal face / limb formation
* Alteration in lung liquid movement: abnormal lung formation
* Often fatal

A

Potter’s syndrome

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23
Q

Potter’s syndrome

Pathophysiology

A
  • Amniotic fluid = fetal urine
  • Severe fetal renal malfunction = decreased amniotic fluid
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24
Q
  • Limb deformities
  • Flat face
  • Pulmonary hypolasia
  • Often fetal death

Signs

A

Potter’s syndrome

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25
Q
  • Limb deformities
  • Flat face
  • Pulmonary hypolasia
  • Often fetal death

Signs

A

Potter’s syndrome

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26
Q

Low amniotic fluid levels

A

Oligohydramnios

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27
Q

Oligohydramnios

Etiology

A

Causes vary by trimester
* 1st trimester: rare
* 2nd trimester: low fetal urine production
* 3rd trimester: rupture of membranes

1st: 1-12 weeks; 2nd: 13-27 weeks; 3rd: 28 weeks - birth

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28
Q

Potter’s syndrome

Etiology

A
  • Bilateral renal agenesis
    • Often detected in utero
    • U/S: kidneys not seen by 10-12 wks
  • Posterior urethral valve
    • Occurs in males
    • Valve obstructs bladder outflow
    • U/S: dilated bladder, kidneys
    • Both kidneys are affected
  • Autosomal recessive PKD
    • Juvenile cystic kidney disease
    • Cysts form in kidneys & biliary tree
    • Both kidneys are affected
    • Severe: oligohydramnios
    • Less severe: renal failure & HTN in childhood

PKD = polycystic kidney disease

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29
Q

Fused inferior poles of kidneys
* Kidneys cannot ascend from pelvis to retroperitoneum
* Trapped by inferior mesenteric artery

A

Horseshoe kidney

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30
Q

Horseshoe kidney

Presentation

A
  • Most pts are asymptomatic
  • A/w Turner & Down syndromes
  • A/w vesicoureteral reflux
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31
Q
  • Embryologic structure that connects dome of bladder to umbilicus
  • Becomes obliterated at birth & becomes median umbilical ligament
A

Urachus

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32
Q

Urachal remnants

A

Failed / incomplete obliteration of urachus
* Patent urachus: urine can leak from umbilicus
* Failed obliteration of urachus
* Urachal cyst / sinus / diverticulum
* Incomplete obliteration of urachus
* Can lead to infections

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33
Q

Urachal remnants

Complications

A

Can lead to adenocarcinoma of the bladder
* Key feature: tumor at dome of bladder
* Presentation: adult with painless hematuria

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34
Q

Kidney

Anatomy

A

3 major regions
1. Cortex: outer region
2. Medulla: middle region
3. Collecting system: inner region

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35
Q

Renal cortex

Anatomy

A
  • Outer region of kidney
  • Nephron structures:
    • Glomeruli
    • Proximal tubules
    • Distal tubules
36
Q

Renal medulla

Anatomy

A
  • Middle region of kidney
  • Consists of renal / medullary pyramids
  • Nephron structures:
    • Loop of Henle
    • Collecting ducts
37
Q

Collecting system

Anatomy

A
  • Calyx: collects urine draining from medullary pyramid
    * Minor calyx: collects urine from one medullary pyramid
    * Major calyx: collects urine from several minor calyces
  • Papilla: junction between medullary pyramid & calyx
  • Pelvis: collects urine draining from all major calyces
38
Q

Renal vasculature

Anatomy

A
  1. Renal artery
  2. Segmental arteries
  3. Interlobar arteries
  4. Arcuate arteries
  5. Interlobular arteries
  6. Glomeruli
39
Q

Glomerular blood flow

Anatomy

A
  1. Interlobular artery branches into series of afferent arterioles
  2. Each afferent arterioles supplies a glomerular capillary bed
  3. Blood leaves glomerular capillaries via efferent arterioles
  4. Blood from efferent arteriole enters peritublar capillaries
  5. Blood from peritublar capillaries drains into renal vein via series of venules
40
Q

Afferent & efferent arterioles

Anatomy

A

Afferent & efferent arterioles allow body to control blood flow into and out of glomerular capillaries via 2 mechanisms:
* Vasoconstriction of afferent arteriole (AA)
* Reduces blood flow into glomerulus
* Decreases GFR
* Vasoconstriction of efferent arteriole (EA)
* Reduces blood flow out of glomerulus
* Blood spends more time in glomerular capillaries
* Increases GFR

41
Q

Fluid Compartments

Physiology

A
  • Extracellular (ECF): 1/3 of TBW
    • Plasma: 1/4 of ECF
    • Interstitial fluid: 3/4 of ECF
  • Intracellular (ICF): 2/3 of TBW

Body composition: total body water (TBW) = 60%; Non-water: 40%

42
Q

Fluid Compartment Shifts

Physiology

A
  • Plasma osmolarity = 300 mOsm/kg
    • Equilibrium between cells & ECF
  • Fluid shifts only occur if there is difference in osmolarity between ICF & ECF
43
Q

Addition / loss of isotonic fluid

Fluid Compartment Shifts

A

Change in ECF volume; no change in ICF volume
* Example: hemorrhage
* Loss of ECF volume
* No change in ICF volume
* Example: infusion of normal saline
* Increase in ECF volume
* No change in ICF volume

Isotonic = same osmolarity as plasma

44
Q

Addition of hypotonic fluid

Fluid Compartment Shifts

A

Increase in ECF volume & ICF volume
* Decreases plasma osmolarity
* Osmotic gradient drives ECF into cells
* Example: infusion of 5% dextrose

Hypotonic = lower osmolarity than plasma

45
Q

Addition of hypertonic fluid

Fluid Compartment Shifts

A

Increase in ECF volume; decrease in ICF volume
* Raises plasma osmolarity
* Osmotic gradient pulls fluid out of cells into ECF
* Example: mannitol infusion

46
Q

Effective Circulating Volume (ECV)

Physiology

A

Volume of ECF contained in arterial system
* Maintains tissue perfusion
* Modified by: volume, CO, SVR

47
Q

Low ECV

Physiology

A

Low ECV leads to low BP
* Low ECV activates: SNS, RAAS
* Conditions with low ECV:
* Volume depletion: low ECV & TBW
* Heart failure: low ECV, high TBW
* Cirrhosis: low ECV, high TBW

HF = low CO; cirrhosis = low SVR

48
Q

Evaluating renal function

Physiology

A
  1. Glomerular filtration rate (GFR)
  2. Renal blood / plasma flow (RBF/RPF)
  3. Filtration fraction (FF): GFR / RBF
49
Q

Capillary fluid exchange

Physiology

A
  • Hydrostatic pressure: fluid pushing against walls of vessels
    • High pressure drives fluid toward low pressure
  • Oncotic pressure: solutes (albumin) pulling fluid into vessels
    • High pressure draws fluid away from low pressure (osmotic graident)
50
Q

Determinants of GFR

Physiology

A
  • Hydrostatic pressure (P): P-GC vs. P-BC
  • Oncotic pressure (π): π-GC vs. π-BC

GC = glomerular capillary; BC = Bowman’s capsule

51
Q

Dilate afferent arteriole

Changes in GFR

A

More blood flow into glomerular capillary
* RPF: increases
* P-GC: increases
* GFR: increases
* FF: no change

52
Q

Constrict efferent arteriole

Changes in GFR

A

Less blood flow out of glomerular capillary; blood pools behind constricted EA
* RPF: decreases
* P-GC: increases
* GFR: increases
* FF: increases

53
Q

Increase plasma proteins

Changes in GFR

A

Less blood drawn out of glomerular capillary into proximal tubule
* RPF: no change
* GFR: decreases
* FF: decreases

54
Q

Ureteral obstruction

Changes in GFR

A

Urine backs up behind obstruction & hydrostatic pressure in Bowman’s capsule increases; less blood flow from capillary into Bowman’s capsule
* RPF: no change
* P-BC: increases
* GFR: decreases
* FF: decreases

55
Q

Constrict afferent arteriole

Changes in GFR

A

Less blood flow into glomerular capillary
* RPF: decreases
* P-GC: decreases
* GFR: decreases
* FF: no chanfe

56
Q

Renal autoregulation

Physiology

A

Maintains constant GFR / RBF (FF) over range of blood pressures
1. Myogenic mechanism
2. Tubuloglomerular feedback

57
Q

Myogenic mechanism

Autoregulation

A
  • Afferent arteriole constricts w/ high BP
    • Responds to changes in stretch
    • High blood pressure causes stretching of arterioles
  • Result: maintenance of normal GFR/RPF
    • Vasoconstriction decreases RPF
58
Q

Tubuloglomerular feedback

Autoregulation

A
  • Increased GFR:
    • Increased flow into proximal tubule
    • Increased NaCl in distal tubule
  • NaCl is detected by macula densa
    • Macula densa stimulates vasoconstriction of AA

Macula densa = part of juxtaglomerular (JG) apparatus

59
Q

Renal clearance

Renal Function

A

C = (U x V) / P
* Clearance (C): volume of blood cleared of substance; excreted volume of blood containing substance
* Urine concentration of substance (U)
* Plasma concentration of substance (P)
* Volume flow of urine (V)

60
Q

Creatinine

Renal Function

A

Creatine clearance is used to estimate GFR
* Product of muscle metabolism
* Closest naturally occurring substance to inulin
* Inulin: all filtered goes out; no secretion / resorption
* Creatinine: all filtered goes out; small amount secreted
* Using Cr to estimate GFR
* Secreted Cr is counted as filtered
* Slightly overestimates GFR

61
Q

Estimating GFR

Renal Function

A

Cockcroft-Gault formula
GFR = [(140-age) x weight (kg)] / (P-Cr x 70 kg)
* If female, multiply estimated GFR by 0.85

62
Q

Serum creatinine (P-Cr) & GFR

Renal Function

A

C-Cr = (V-Cr x U-Cr) / P-Cr = GFR
* Body produces and excretes the same amount of creatinine everyday
* V-Cr x U-Cr = constant
* P-Cr & GFR are inversely proportional
* Increase in GFR = decrease in P-Cr
* Decrease in GFR = increase in P-Cr

63
Q

High serum creatinine

Renal Function

A

Impaired renal function
* Decreased GFR

64
Q

Prostaglandins (PGs) & NSAIDs

Renal Function

A
  • PGs dilate afferent arterioles: increase RPF
  • NSAIDs block production of PGs
    • Vasoconstriction of afferent arterioles
    • Decrease RPF
    • Decrease GFR
  • Clinical effects of NSAIDs:
    • Acute renal failure
    • Acute heart failure
65
Q

ACE inhibitors

Renal Function

A
  • Ang II promotes vasoconstriction of efferent arterioles
  • ACEi block production of Ang II
    • Vasodilation of efferent arterioles
    • Decrease GFR
    • Increase RPF
    • Decrease FF
66
Q

Secretion & Absorption

Renal Function

A

E = F - R + S
* Amount filtered (F) = GFR x P
* Amount excreted (E) = V x U
* Amount resorbed (R) = F - E
* If F > E
* Amount secreted (S) = E - F
* If F < E

67
Q

Regulated solutes: Na+, K+

Solutes in Renal Failure

A
  • Renal failure: decreased GFR
  • Plasma concentration (P-Na, P-K): no change
  • Filterered load (GFR x P): decreases
  • Excretion: no change
  • Fractional excretion: increases

Can adjust K+, Na+ secretion / resorption; filtered load can fall

68
Q

Unregulated solutes: Cr, Urea

Solutes in Renal Failure

A
  • Renal failure: decreased GFR
  • Plasma concentration (P-Cr, P-Urea): increases
  • Filtered load (GFR x P): no change
  • Excretion: no change
  • Fractional excretion: no change

Can only eliminate Cr, Ur via filtration; must maintain filtered load

69
Q

Renal Hormones

Renal Endocrine Function

A
  • Released by kidney:
    • Erythropoietin
    • Renin (enzyme)
    • 1,25-Vit D
  • Act on kidney:
    • Angiotensin II (Ang II)
    • Atrial natriuretic peptide (ANP)
    • Antidiuretic hormone (ADH)
    • Aldosterone
    • Parathyroid hormone (PTH)
70
Q

JG apparatus

Renin

A
  • JG cells: modified smooth muscle of afferent arteriole; secrete renin
  • Macula densa: part of distal tubule
71
Q

RAAS

Renal Endocrine Function

A
  1. Angiotensinogen (plasma protein; from liver)
    Renin (from JG cells in kidneys)
  2. Ang I
    ACE (in lungs)
  3. Ang II
72
Q

Stimuli for renin release

RAAS

A
  • Low perfusion pressure
    • Low BP or low ECV
    • Sensed by afferent arteriole –> renin release
  • Low NaCl delivery
    • Sensed by macula densa –> renin release
    • Also constricts afferent arteriole: TGF
  • Sympathetic activation
    • Renal B1-receptors –> renin release
    • Renal A1-receptors –> constricts arterioles
    • Decreases GFR to limit Na/H2O excretion

TGF: tubuloglomerular feedback

73
Q

Activates RAAS
* Converts angiotensinogen to Ang I

RAAS

A

Renin

74
Q

Ang II

RAAS

A
  • Efferent arteriole vasoconstriction
    • RPF: decreases; less renal blood flow
    • GFR: increases; more Na/H2O filtration
  • Increased Na/H2O reabsorption
    • Proximal tubule: increases Na+ resorption via capillary effect, Na+/H+ exchange
    • Stimulates aldosterone release
75
Q

Capillary effect

Proximal Tubule

A

Efferent arteriole constriction increases NaCl resorption
* Ang II induces efferent arteriole constriction
* Efferent arteriole constriction decreases blood flow beyond constriction
* Decreased RBF reduces hydrostatic pressure in peritubular capillaries
* Favorable gradient for reabsorption of Na & H2O in proximal tubule: capillary effect
* Efferent arteriole constriction increases GFR
* More fluid is filtered from glomerular capillaries into Bowman’s capsule leaving concentrated plasma proteins
* Increased oncotic pressure favors reabsorption of Na & H2O

76
Q

Collecting duct effects
* Resorption of Na+, H2O
* Excretion of K+, H+

RAAS

A

Aldosterone

77
Q

Lower blood pressure
* Block converstion of Ang I to Ang II

RAAS Drugs

A

ACE-inhibitors

78
Q

Lower blood pressure
* Block effects of Ang II

RAAS Drugs

A

Ang II receptor blockers (ARBs)

79
Q

Beta-Blockers

RAAS Drugs

A

Lower blood pressure
* Block sympathetic stimulation of JG apparatus
* Inhibit renin release

80
Q

Lower blood pressure
* Block effects of aldosterone
* Increase serum K+ & H+ (reduce pH)

RAAS Drugs

A

Aldosterone antagonists
* Spironolactone
* Eplerenone

81
Q

Lower blood pressure
* Inhibit ENaC
* Inhibit Na+ & H2O resorption
* Inhibit K+ secretion

A

Potassium-sparing diuretics
* Triamterene
* Amiloride

82
Q

Natriuretic peptides

Hormones Acting on Kidneys

A

Hormones released by the heart that act on the kidneys
* Response to increased cardiac volume
* Increased volume causes myocyte stretch
* ANP: released by atrial myocytes
* BNP: released by ventricular myocytes
* Opposite effects of RAAS
* Relax VSM via cGMP
* Vasodilation: reduces SVR
* Increased diuresis: decreases ECV

83
Q

PTH

Hormones Acting on Kidneys

A

Maintains Ca2+ levels
* Released by chief cells of parathyroid gland
* Stimulus: low serum [Ca]
* Net effects:
* Increases plasma [Ca]
* Decreases plasma [PO4]
* Increases urine [PO4]

84
Q

Renal effects of PTH

Hormones Acting on Kidneys

A
  • DCT: increased Ca2+ resorption
    • PTH stimulates Na/Ca2+ exchanger
  • PCT: decreased PO4 resorption
    • PTH inhibits Na/phosphate cotransporter
  • PCT: increased production of 1,25-(OH)2-Vit D
    • PTH stimulates 1a-Hydroxylase
85
Q

Erythropoietin (EPO)

Renal Hormones

A

Stimulates RBC in bone marrow
- Produced by interstitial cells of peritubular capillaries
- Released in response to hypoxia
- Decreased production in renal failure
- Results in normocytic anemia

gu / gyn & renal (23 decks)

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