B&B Renal: Anatomy & Physiology Flashcards
(85 cards)
1
Q
Germ layer of origin
Kidney Development
A
Mesoderm
2
Q
Pronephros
Kidney Development
A
- 1st embryonic renal structure
- Forms & degenerates by week 4 of gestation
3
Q
Mesonephros
Kidney Development
A
- 2nd embryonic renal strucutre
- Acts as interim kidney during 1st trimester
- Contributes to vas deferens in males
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
5
Q
Kidney Formation
A
2 key structures
1. Ureteric bud
2. Metanephric mesenchyme
6
Q
Ureteric bud
Kidney Formation
A
- Outgrowth of mesonephric (Wolffian) duct
- Forms ureter, renal pelvis & calyces, collecting ducts
7
Q
Metanephric mesenchyme
Kidney formation
A
- Mesoderm tissue around ureteric bud
- Interacts with ureteric bud to form glomerulus through distal tubule of nephron
8
Q
Most common renal malignancy in young children
A
Wilm’s tumor
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
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
11
Q
Renal Agenesis
Pathophysiology
A
- Ureteric bud fails to develop
- Lack of signals to mesenchyme to trigger differentiation
12
Q
Renal dysplasia resulting in replacement of kidney with cysts
* No / little functioning renal tissue
* Usually unilateral
A
Multicystic Dysplastic Kidney
Congenital Anomaly
13
Q
Multicystic Dysplastic Kidney
Pathophysiology
A
Abnormal ureteric bud-mesenchyme interaction
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
15
Q
UPJ obstruction
Complications
A
- Hydronephrosis
- Poor urinary flow –> kidney stones, UTIs
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
17
Q
Duplicated Ureter
Complications
A
- May lead to poor urinary flow; UTIs
- Hydronephrosis
- Associated with vesicoureteral reflux
18
Q
- Backward urine flow from bladder to kidneys
- Leads to recurrent UTIs
A
Vesicoureteral reflux
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
20
Q
Retrograde flow of urine due to high bladder pressure
* Associated with posterior urethral valves
A
Secondary vesicoureteral reflux
21
Q
Retrograde flow of urine due to high bladder pressure
* Associated with posterior urethral valves
A
Secondary vesicoureteral reflux
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
23
Q
Potter’s syndrome
Pathophysiology
A
- Amniotic fluid = fetal urine
- Severe fetal renal malfunction = decreased amniotic fluid
24
Q
- Limb deformities
- Flat face
- Pulmonary hypolasia
- Often fetal death
Signs
A
Potter’s syndrome
25
* Limb deformities
* Flat face
* Pulmonary hypolasia
* Often fetal death
| Signs
Potter's syndrome
26
Low amniotic fluid levels
Oligohydramnios
27
Oligohydramnios
| Etiology
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
28
Potter's syndrome
| Etiology
* 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
29
Fused inferior poles of kidneys
* Kidneys cannot ascend from pelvis to retroperitoneum
* Trapped by inferior mesenteric artery
Horseshoe kidney
30
Horseshoe kidney
| Presentation
* Most pts are asymptomatic
* A/w Turner & Down syndromes
* A/w vesicoureteral reflux
31
* Embryologic structure that connects dome of bladder to umbilicus
* Becomes obliterated at birth & becomes median umbilical ligament
Urachus
32
Urachal remnants
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
33
Urachal remnants
| Complications
Can lead to adenocarcinoma of the bladder
* Key feature: tumor at dome of bladder
* Presentation: adult with painless hematuria
34
Kidney
| Anatomy
3 major regions
1. Cortex: outer region
2. Medulla: middle region
3. Collecting system: inner region
35
Renal cortex
| Anatomy
* Outer region of kidney
* Nephron structures:
* Glomeruli
* Proximal tubules
* Distal tubules
36
Renal medulla
| Anatomy
* Middle region of kidney
* Consists of renal / medullary pyramids
* Nephron structures:
* Loop of Henle
* Collecting ducts
37
Collecting system
| Anatomy
* 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
Renal vasculature
| Anatomy
1. Renal artery
2. Segmental arteries
3. Interlobar arteries
4. Arcuate arteries
5. Interlobular arteries
6. Glomeruli
39
Glomerular blood flow
| Anatomy
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
Afferent & efferent arterioles
| Anatomy
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
Fluid Compartments
| Physiology
* 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
Fluid Compartment Shifts
| Physiology
* Plasma osmolarity = 300 mOsm/kg
* Equilibrium between cells & ECF
* Fluid shifts only occur if there is difference in osmolarity between ICF & ECF
43
Addition / loss of isotonic fluid
| Fluid Compartment Shifts
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
Addition of hypotonic fluid
| Fluid Compartment Shifts
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
Addition of hypertonic fluid
| Fluid Compartment Shifts
Increase in ECF volume; decrease in ICF volume
* Raises plasma osmolarity
* Osmotic gradient pulls fluid out of cells into ECF
* Example: mannitol infusion
46
Effective Circulating Volume (ECV)
| Physiology
Volume of ECF contained in arterial system
* Maintains tissue perfusion
* Modified by: volume, CO, SVR
47
Low ECV
| Physiology
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
Evaluating renal function
| Physiology
1. Glomerular filtration rate (GFR)
2. Renal blood / plasma flow (RBF/RPF)
3. Filtration fraction (FF): GFR / RBF
49
Capillary fluid exchange
| Physiology
* 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
Determinants of GFR
| Physiology
* Hydrostatic pressure (P): P-GC vs. P-BC
* Oncotic pressure (π): π-GC vs. π-BC
| GC = glomerular capillary; BC = Bowman's capsule
51
Dilate afferent arteriole
| Changes in GFR
More blood flow into glomerular capillary
* RPF: increases
* P-GC: increases
* GFR: increases
* FF: no change
52
Constrict efferent arteriole
| Changes in GFR
Less blood flow out of glomerular capillary; blood pools behind constricted EA
* RPF: decreases
* P-GC: increases
* GFR: increases
* FF: increases
53
Increase plasma proteins
| Changes in GFR
Less blood drawn out of glomerular capillary into proximal tubule
* RPF: no change
* GFR: decreases
* FF: decreases
54
Ureteral obstruction
| Changes in GFR
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
Constrict afferent arteriole
| Changes in GFR
Less blood flow into glomerular capillary
* RPF: decreases
* P-GC: decreases
* GFR: decreases
* FF: no chanfe
56
Renal autoregulation
| Physiology
Maintains constant GFR / RBF (FF) over range of blood pressures
1. Myogenic mechanism
2. Tubuloglomerular feedback
57
Myogenic mechanism
| Autoregulation
* 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
Tubuloglomerular feedback
| Autoregulation
* 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
Renal clearance
| Renal Function
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
Creatinine
| Renal Function
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
Estimating GFR
| Renal Function
Cockcroft-Gault formula
GFR = [(140-age) x weight (kg)] / (P-Cr x 70 kg)
* If female, multiply estimated GFR by 0.85
62
Serum creatinine (P-Cr) & GFR
| Renal Function
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
High serum creatinine
| Renal Function
Impaired renal function
* Decreased GFR
64
Prostaglandins (PGs) & NSAIDs
| Renal Function
* 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
ACE inhibitors
| Renal Function
* Ang II promotes vasoconstriction of efferent arterioles
* ACEi block production of Ang II
* Vasodilation of efferent arterioles
* Decrease GFR
* Increase RPF
* Decrease FF
66
Secretion & Absorption
| Renal Function
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
Regulated solutes: Na+, K+
| Solutes in Renal Failure
* 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
Unregulated solutes: Cr, Urea
| Solutes in Renal Failure
* 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
Renal Hormones
| Renal Endocrine Function
* 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
JG apparatus
| Renin
* JG cells: modified smooth muscle of afferent arteriole; secrete renin
* Macula densa: part of distal tubule
71
RAAS
| Renal Endocrine Function
1. Angiotensinogen (plasma protein; from liver)
Renin (from JG cells in kidneys)
2. Ang I
ACE (in lungs)
3. Ang II
72
Stimuli for renin release
| RAAS
* 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
Activates RAAS
* Converts angiotensinogen to Ang I
| RAAS
Renin
74
Ang II
| RAAS
* 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
Capillary effect
| Proximal Tubule
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
Collecting duct effects
* Resorption of Na+, H2O
* Excretion of K+, H+
| RAAS
Aldosterone
77
Lower blood pressure
* Block converstion of Ang I to Ang II
| RAAS Drugs
ACE-inhibitors
78
Lower blood pressure
* Block effects of Ang II
| RAAS Drugs
Ang II receptor blockers (ARBs)
79
Beta-Blockers
| RAAS Drugs
Lower blood pressure
* Block sympathetic stimulation of JG apparatus
* Inhibit renin release
80
Lower blood pressure
* Block effects of aldosterone
* Increase serum K+ & H+ (reduce pH)
| RAAS Drugs
Aldosterone antagonists
* Spironolactone
* Eplerenone
81
Lower blood pressure
* Inhibit ENaC
* Inhibit Na+ & H2O resorption
* Inhibit K+ secretion
Potassium-sparing diuretics
* Triamterene
* Amiloride
82
Natriuretic peptides
| Hormones Acting on Kidneys
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
PTH
| Hormones Acting on Kidneys
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
Renal effects of PTH
| Hormones Acting on Kidneys
* 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
Erythropoietin (EPO)
| Renal Hormones
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
