Renal - FA Embryo,Anat/Phys p566 -582 Flashcards
(115 cards)
1
Q
pronephros develops in which week?
A
week 4
2
Q
mesonephros contributes to which adult structure?
A
male genital system
3
Q
metanephros appears in which week?
A
week 5
4
Q
uteric bud gives which adult structures?
A
ureter, pelvises, calyces, collecting ducts
5
Q
interaction between uteric bud and metanephric mesenchyme leads to what?
A
differentiation and formation of glomerulus through DCT
6
Q
most common site of obstruction in kidney
A
uteteropelvic junction - bc last to canalize - seen as hydronephrosis
7
Q
A neonate has just been born and looks abnormal at birth. He has low set ears and flattened nose. His GFR is very low. What is the possible Dx, and symptoms associated with it
A
- P ulmonary Hypoplasia (MC cause of death)
- O ligohydramnios
- T wisted face
- T wisted skin
- E xtremity defects
- R enal Failure
8
Q
What causes Potter sequence in utero?
A
Oligohydramnios due to inability of fetus to urinate or because of placental insufficiency
ARPKD
Obstructive uropathy
bilateral renal agenesis
9
Q
A 1 year old boy comes in with severe abdominal pain, and has had a prolonged Hx of malabsorption. The physician diagnoses ischemia of the bowels. He is also irritated that the OB/GYN missed something on the fetal ultrasound. The CT scan shows a drastic abnormality leading to an obstruction in the abdomen. What is the Dx?
A
Horseshoes kidney leading to IMA impingement leading to ischemia of the bowels
10
Q
Horseshoe kidney seen which which genetic issues?
A
turners, trisomies
11
Q
Compare and contrast Multicystic dysplastic kidneys and Duplex collecting System?
A
MCKD and DCS both have abnormal interactions of the ureteric bud leading to congenital rnal pathologies.
MCKD: abnormal intrxn b/w ureteric bud and mesenchyme. Predominantly nonhereditary and usually unilateral; bilateral leads to Potter sequence.
DCS: abnormal movement of ureteric bud to metenephric blastemia creating bifid ureter –> causes increased risk of obstruction and UTIs
12
Q
What leads to unilateral renal agenesis?
A
Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme –> complete absence of kidney and ureter.
13
Q
most common cause of bladder outlet obstruction in male infants? sx?
A
posterior urethral valves; hydronephrosis and dilated/thick walled bladder on US
14
Q
Left renal vein rec which two addtl v?
A
L suprarenal and L gonadal v
15
Q
Which area of kidney is more susceptible to hypoxia, and ischemic damage?
A
renal medulla, it rec much less blood flow.
16
Q
`Which kidney is preferred in living donor transplantation?
A
Left kidney, bc L renal v is longer.
17
Q
A 30 year old labor induced female is going through a C section for her twins. After successfully giving birth, excessive bleeding is observed and the OB/GYN does a hysterectomy. What is a key finding she has to worry about when doing the procedure in order to avoid complications?
A
Water under the bridge - ureters pass under uterine artery/vas deferens. Ligation of the uterine artery (cardinal ligament) and not confuse it with the ureter.
18
Q
What prevents urine reflux?
A
Muscle fibers within the intramural part of the ureter prevent urine reflux.
19
Q
3 common points of ureteral obstruction?
A
ureteropelvic junction, pelvic inlet, ureterovesical junction
20
Q
Blood supply to ureters?
A
Blood supply to ureter:
Proximal—renal arteries
Middle—gonadal artery, aorta, common and internal iliac arteries
Distal—internal iliac and superior vesical arteries
21
Q
Why is albumin not filtered thru BM ?
A
it’s 3.6 nm, so could technically go through but does not bc of (-) ions on endoth/GBM cells
22
Q
Kidney anatomy and pathologies that affect this area
- Small renal a
- Glomeruli
- renal papilla
- calices and ureters
- Bladder
A
- Small renal a - HTN/DB nephropathy
- Glomeruli - acute interstitial nephritis
- Renal papilla - Sickle cell, T2DB, analgesic nephropathy, sever acute pyelonephritis
- Calices ureters - acute renal colic (nephrolithiasis) 5. Bladder - inflammatory process/tumor
23
Q
What % of the body is total body water, ICF, and ECF.
A
60% total body water
40% ICF, mainly composed of K+, Mg2+, organic phosphates (eg, ATP)
20% ECF, mainly composed of Na+, Cl–, HCO3–, albumin
24
Q
How do we measure plasma volume level? ECF?
A
radiolabeling albumin for plasma, ECF by inulin or mannitol
25
Serum Osmo level?
Serum osmolality = 285–295 mOsm/kg H2O
26
Components of Glomerular filtration barrier?
Fenestrated capillary endothelium
Basement membrane with type IV collagen chains and heparan sulfate
Visceral epithelial layer consisting of podocyte foot processes
27
if podocytes lack nephrin protein - leads to what Dx?
Congenital nephrotic syndrome
28
Best way to estimate GFR?
Creatinine clearance
29
Renal Clearence
Cx = (UxV)/Px = volume of plasma from which the substance is completely cleared per unit time
```
Cx = clearance of X (mL/min).
Ux = urine concentration of X (eg, mg/mL).
Px = plasma concentration of X (eg, mg/mL).
V = urine flow rate (mL/min).
```
30
Fx for GFR? Normal GFR = ?
GFR = Uinulin × V/Pinulin = Cinulin
GFR = Kf [(PGC – PBS) – (πGC – πBS)]
GC = glomerular capillary; BS = Bowman space; πBS normally equals zero; Kf = filtration coefficient
Normal GFR = 100mL/min
31
Best way to estimated RPF?
PAH clearence
32
Fx for Renal blood flow - what % of CO?
Renal Blood flow = PRF / (1 - Hct)
20-25% of CO
33
Normal FF?
20%
34
How do PGs change GFR, RPF, and FF? What drug would inhibit it?
Prostaglandins preferentially dilate aff arteriole - Inc RPF, Inf GFR, so no change FF. This is inhibited by NSAIDS.
35
What preferentially constricts efferent arteriole? How does that change GFR, RPF, FF? What drug blocks it?
Angiotensin II,
* dec RBF
* inc GFR
* Inc FF.
(-) by ACEI
36
Fill in the chart
37
How much of something (X) was filtered? (Give Fx for filtration rate)
GFR (Creatinine clearence) x Plasma conc of (X)
38
How much of (X) excreted?
Excretion rate = Vol x Urine conc of (X)
39
Reabsorption?
Filtered - excreted
40
Secretion?
Excreted - filtered
41
Normal plasma level of glucose, where and how much reabsorbed?
Glucose at a normal plasma level (range 60–120 mg/dL) is completely reabsorbed in proximal convoluted tubule (PCT) by Na+/glucose cotransport.
42
At what glucose level will glucose begin to appear in urine?
In adults, at plasma glucose of ∼ 200 mg/dL, glucosuria begins (threshold). At rate of ∼ 375 mg/min, all transporters are fully saturated (Tm).
43
How does pregnancy affect GFR and glucose resorption in the kidney?
Normal pregnancy is associated with INC GFR. With INC filtration of all substances, including glucose, the glucose threshold occurs at lower plasma glucose concentrations --\> glucosuria at normal plasma glucose levels.
44
What drugs can lead to glucosuria at plasma concentrations \< 200 mg/dL
Sodium-glucose cotransporter 2 (SGLT2) inhibitors (eg, -flozin drugs) result in glucosuria at plasma concentrations \< 200 mg/dL.
45
What is splay?
Splay is the region of substance clearance between threshold and Tm; due to the heterogeneity of nephrons.
46
Reabsorbs all glucose and amino acids and most HCO3–, Na+, Cl–, PO43–, K+, H2O, and uric acid.
early PCT
47
Generates and secretes NH3, which acts as a buffer for secreted H+.
early PCT
48
Where does PTH work on the nephron? 2 locations, what does it do at each segment?
Early PCT : PTH — inhibits Na+/PO4 cotransport --\> PO4 excretion.
Early DCT - PTH — Inc Ca2+/Na+ exchange --\> Ca2+ reabsorption.
49
What does AT II do in PCT?
AT II — stimulates Na+/H+ exchange --\> inc Na+, H2O, and HCO3 reabsorption (permitting contraction alkalosis).
50
Major function of thin desc loop of Henle? What is it impermeable to?
Thin descending loop of Henle—passively reabsorbs H2O via medullary hypertonicity Impermeable to Na+.
Concentrating segment. Makes urine hypertonic.
51
Major function of thick asc loop of Henle? what is it impermeable to?
Thick ascending loop of Henle—**reabsorbs Na+, K+, and Cl−.**
Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through ⊕ lumen potential generated by K+ backleak.
Impermeable to H2O. Makes urine less concentrated as it ascends.
52
Function of early DCT?
Early DCT—reabsorbs Na+, Cl−. Makes urine fully dilute (hypotonic).
53
Function of collecting tubule? Regulated by what hormone?
Collecting tubule—**reabsorbs Na+** in exchange for **secreting K+ and H+**, Regulated by Aldosterone
54
Aldosterone's effect in principal cells?
In principal cells: Inc apical K+ conductance, Na+/K+ pump, epithelial Na+ channel (ENaC) activity --\> lumen becomes more neg --\> **inc K+ secretion**
55
Which drug works at early PCT - MOA?
Acetazolamide - *inhibits CA*, therefore causing **NaHCO3 to be excreted**, **dec HCO3 in body**
56
Aldosterone effect on intercalated cells?
In α-intercalated cells: lumen negativity --\> inc H+ ATPase activity --\> **inc H+ secretion** --\> inc HCO3 −/Cl− exchanger activity. (HCO3 out, Cl in)
57
ADH works on what receptor at what part of tubule? main effect?
ADH—acts at V2 receptor insertion of aquaporin H2O channels on apical side. V2 is at the 2-bules. (of kidney)
58
What drug works at the thick asc loop? MOA?
Loop diuretics, inhibit N/K/2Cl transporter. This stops that medullary hyperconc, which disallows the concentration of urine.
59
Which drug works at early DCT? MOA?
Thiazides, (-) Na/Cl transporter, makes urine less dilute (bc w/o the Na, Cl absorption, H2O won't follow in)
60
Which drugs work at collecting tubule? MOA?
K sparing diuretics
**Spironolactone and eplerenone** are competitive aldosterone receptor antagonists in cortical collecting tubule.
**Triamterene and amiloride** act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
61
Bonus Q - How do loops affect the vascular tone in the kidney? What drug prevents this effect?
Loops stimulate PGE release --\> VD effect on aff art. Effect (-) by NSAIDS
62
Thiazide effect on Ca?
Dec Ca excretion (notice - OPP of loops) - used in osteoporosis, therefore
63
In Fanconi syndrome - where along the tubule is defect? end result?
Generalized reabsorptive defect in PCT. Associated with excretion of nearly all amino acids, glucose, HCO3 and PO4.
64
Bartter - where along the tubule is defect? end result? What drug is that similar to?
Reabsorptive defect in thick ascending loop of Henle. Autosomal recessive. Affects Na+/K+/2Cl– cotransporter. Presents similarly to chronic loop diuretic use. Results in hypokalemia and hypercalciuria
65
Gitelman - where along the tubule is defect? end result? What drug is that similar to?
Reabsorptive defect of NaCl in DCT. Similar to using lifelong thiazide diuretics. Result - hypoKalemia, hypoMg, hypoCa-uria, and Metabolic alkalosis
66
Looks like Hyperalosteronism, but with nearly undetectable aldosterone
Liddle syndrome
67
Liddle - where along the tubule is defect? end result?
Gain of function mutation - Inc Na+ reabsorption in collecting tubules ( inc activity of epithelial Na+ channel)
68
glycyrrhetinic acid (present in licorice) block what enzyme?
blocks activity of 11β-hydroxysteroid dehydrogenase.
69
SAME - def of what enzyme? what metabolic issues?
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase, which normally converts cortisol (can activate mineralocorticoid receptors) to cortisone (inactive on mineralocorticoid receptors)
Excess cortisol in these cells from enzyme deficiency --\> inc mineralocorticoid receptor activity --\> hypertension, hypokalemia, metabolic alkalosis.
70
71
3 stimulations to secrete renin?
* Dec BP (JG cells)
* Dec Na+ delivery (macula densa cells)
* Inc sympathetic tone (B1-receptors)
72
Why do you not get reflex brady with AT II?
Affects baroreceptor function; limits reflex bradycardia, which would normally accompany its pressor effects. Helps maintain blood volume and blood pressure.
73
ANP, BNP - what second mediator? effects on arterioles?
cGMP, VD aff art, VC eff art -\> inc GFR, dec renin
74
Aldosterone is released in response to what change in blood? (Don't say AGII)
dec blood volume and Inc plasma K+
75
3 cells of JGA? Which of these cells actually secrete renin?
Consists of mesangial cells, JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of DCT). JG cells secrete renin.
76
enhances K+ and H+ excretion by way of principal cells, K+ channels and intercalated cell H+ ATPases
Aldosterone
77
aquaporin insertion in principal cells? end result?
ADH - leads to inc H20 absorption
78
3 effects of AG II (other than hormones)
VC, (via ATII1-R) of vasc smooth musc VC of eff art --\> preserve FF
inc PCT Na+/H+ activity --\> Na, HCO3, H20 reabsorption
(+) HT --\> thirst
79
Released by interstitial cells in peritubular capillary bed in response to hypoxia.
EPO
80
Paracrine secretion vasodilates the afferent arterioles to inc RBF.
PGs
81
Secreted by PCT cells, promotes natriuresis. Difference between low and high dose?
Dopamine At low doses, dilates interlobular arteries, afferent arterioles, efferent arterioles --\> Inc RBF, little or no change in GFR. At higher doses, acts as vasoconstrictor.
82
62 yr old man comes to primary physician with complaints of urination at night, lethargy, and general malaise. BUN = 4.0, Creatine 3.5, ttl Ca = 7.4 mg/dL, se PO4 = 5.5 mg/dL. Has normochromic, normocytic anemia. Started on Ca supplements, and PO4 restricted diet. Primary Tx for pt's anemia?
EPO - EPO is likely low in this pt with chronic renal failure, bc it's made with peritubular capillaries lining the renal cortex.
83
A young man brings in his 3yr old daughter to ER, She began vomiting 2 hrs ago. As he looked thru the medicine cabinet for something to give her, he noticed a few bottles were missing. The daugher admitted to taking them, and eating "candy" from one of them 2 days ago. The bottle turns out to be expired tetracyclin. . Lab show se PO4 of 1.8, and urine shows high amts of glucose. 24 hr urine show hyperphosphaturia. What is this pt at risk of developing?
1. AML
2. Acute tubular necrosis
3. Diarrhea and dermatitis
4. kidney stones
5. systemic acidosis
Choice E is correct. Glucosuria + HyperPO4 = Fanconi syndrome
Can be caused by inherited disorders like Wilson's or acquired (like the expired tetracycline)
Pt will have dysfunctional proximal renal tubules and do not reabsorb glucose, phosphorous, amino acids, or bicarbonate.
It is one cause of **renal tubular acidosis** --\> pts develop **systemic acidosis with normal anion gap**.
Another possible complication of Fanconi syndrome = hyperphosphatemic rickets Fanconi syndrome due to tetracycline degradation will resolve in few months.
AML = Fanconi anemia
ATN = death of tubular cells (not just temporary dysfunction) - muddy brown casts in urine, due to nephrotoxic Rx and pre-renal azotemia
Diarrhea+dermatitis - Hartnup disease, pellagra like sx, dec Trp absorption in renal tubules
Kidney stones - AR cysteinuria, cant absorb cysteine in renal tubules --\> cysteine stones
84
Two drugs that target ENac?
Triamterene, Amiloride
85
Spironolactone used in what non renal disease?
PCOS (due to anti androgen effect)
86
BB effect on JG apparatus?
BB dec BP by (-) B1-R on JGA, causing dec renin
87
Which shift K+ out of the cell? (causing Hyperkalemia)
* **D**igitalis
* Hyper**O**smolarity
* **L**ysis of cells
* **A**cidosis
* **B**B
* High blood **S**ugar - Insulin def
* **S**uccinylcholine
Hyperkalemia? DO LABS
88
What shifts K+ into cells? (causing hypokalemia)
Hypo-osmolarity Insulin (inc N/K ATPase) Alkalosis Beta (+)'r - inc Na/K ATPase
89
Na - normal value? low conc effects? high conc effects?
135-145 mmol/L Low - nausea, malaise, stupor, coma, seizures High - irritability, stupor coma
90
K+ - normal value? low conc effects? high conc effects?
3.5-5.5
low - U waves on ECG, flattened T waves, arrythmias, muscle weakness, cramps
high - Wide QRS, peaked T waves, muscle weakness
91
Ca2+ - normal value? low conc effects? high conc effects?
8.4- 10.2 low - tetany, seizures, QT prolongation, Chvotek sx Trousseau sx high - renal stones, bone pain, abdom pain, psych issues (anxiety, etc)
92
Mg2+ - normal value? low conc effects? high conc effects?
1.5-2.0
low - tetany, torsades de pointes, hypokalemia, hypocalcemia (when [Mg2+] \< 1.0 mEq/L)
high - Dec DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
93
PO4 3- - normal value? low conc effects? high conc effects?
3.0-4.5 low - bone loss, rickets, osteomalacia high - renal stones, metastatic calcification, hypocalcemia
94
Which renal disorder causes an inc in urine Ca?
Bartter syndrome
95
Which renal disorder causes an dec in serum Mg and urine Ca?
Gitelman syndrome
96
Both Liddle and Conn sydrome causes an inc in BP and dec renin - diff b/w them?
Conn has high aldos, where as Liddle has low aldos
97
Normal levels of pH, PCO2, and HCO3?
pH - 7.35-7.45
PCO2 - 33-45
HCO3 - 22-28
98
pH, pCO2, HCO3 and compensation for - metabolic acidosis?
pH - dec pCO2 - dec HCO3
dec Compensation - immediate hyperventilation
99
pH, pCO2, HCO3 and compensation for - metabolic alkalosis?
inc pH inc pCO2 inc HCO3 Compensation - immediate hypoventilation
100
pH, pCO2, HCO3 and compensation for - respiratory acidosis?
dec pH INC pCO2 INC HCO3 Compensation - inc renal HCO3 resorption - delayed
101
pH, pCO2, HCO3 and compensation for - respiratory alkalosis?
inc pH DEC pCO2 DEC HCO3 Compensation - dec renal HCO3 reabsorption - delayed
102
what Causes efferent arteriole constriction
AG II
103
causes of Resp Acidosis
Hypoventilation –Airway obstruction –Acute lung disease –Chronic lung disease –Opioids, sedative weakness of resp muscles
104
what is the formula of anion gap
Na - (Cl + HCO3)
105
Inc Anion Gap
MUDPILES:
* Methanol (formic acid)
* Uremia
* Diabetic ketoacidosis
* Propylene glycol
* Iron tablets or Isoniazid
* Lactic acidosis
* Ethylene glycol (oxalic acid)
* Salicylates (late)
106
normal anion gap btw 8-12 meq/l
HARD-ASS:
* Hyperchloremia / Hyperalimentation
* Addison disease
* Renal tubular acidosis
* Diarrhea
* Acetazolamide
* Spironolactone
* Saline infusion
107
causes of respiratory alkalosis
* Anxiety/panic attack
* Hypoxemia (eg, high altitude)
* Salicylates (early)
* Tumor
* Pulmonary embolism
108
causes of metabolic alkalosis
H+loss / HCO3 excess
-Loop/thiazide diuretics
–Vomiting
–Antacid use
–Hyperaldosteronism
109
what is type 1 (distal) renal tubular acidosis
Defect in ability of α intercalated cells to secrete H+, hypokalemia and urine pH \>5.5.
110
Causes of distal renal tubular acidosis
Causes: amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases
111
Pathology assoc w/ RTA type 1
Inc risk for calcium phosphate stones, bc of inc urine pH and bone turnover
Type One = StONEs
112
what is type 2 (proximal) renal tubular acidosis
Defect in PCT HCO3− reabsorption--\> Inc excretion of HCO3− in urine --\> metabolic acidosis.
113
Causes of type 2 renal tubular acidosis? Inc risk of what patho?
Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
W/ Fanconi syndrome - inc risk for hypophosphatemic rickets
114
what is hyperkalemic renal tubular acidosis (type 4)
Hypoaldosteronism or aldosterone resistance --\> hyperkalemia --\> dec NH3 synthesis in PCT --\> dec NH4+ excretion.
115
Cause of type 4 RTA
Dec aldosterone production
* diabetic hyporeninism,
* ACE inhibitors, ARBs,
* NSAIDs,
* heparin,
* cyclosporine,
* adrenal insufficiency
aldosterone resistance
* K+-sparing diuretics,
* nephropathy due to obstruction,
* TMP-SMX
