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Step 1 > Renal > Flashcards

Renal Flashcards

0
Q

Pronephros vs. Mesonephros vs. Metanephros

A

1st: Pronephros = to wk 4, then degenerates
2nd : Mesonephros = 1st trimester. => adult Male genital system
*“ureteric bud” (caudal end) => ureters, pelvises, calices, collecting ducts
3rd: Metanephros = permanent, => adult kidney

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1
Q

Fetus w/ oligohydramnios (can’t pee)

=> consecuences, causes

A

= “Potter Sequence”
Causes: ARPKD, posterior urethral valves, bilat. renal agenesis
Consequences: Limb and facial deformities, pulmonary hypOplasia (= cause of death)

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2
Q

1 site of obstruction of urinary tract in fetus

A

= Ureteropelvic junction,

* Last to canalize => failure -> hydronephrosis

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3
Q

Renin-Ang-Aldosterone signal molecs & actions

A
  1. Renin (from JG cells in kidney) -> Angiotensinogen to Angiotensin I
  2. Ang I –> Ang II via ACE (Angiotensin Converting Enzyme)
  3. Ang II => systemic effects:
    a) vasoconstrict (AT1 Rs), b) constrict eff. arterioles
    c) stimulate aldosterone & ADH, d) increase Na/K exchange in PCT
    e) stimulate thirst @ hypothalamus
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4
Q

signal molecs that respond to low blood volume:

A
  1. Angiotensin II
  2. ADH (=> insert aquaporins in renal collecting duct to retain H2O)
  3. Aldosterone (=> insert more Na+ channels in principle cell to retain Na & H2O, & increase K+ excretion “BK” channels)
    * ANP responds to HIGH volume in heart atria => regulates RAAS*
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5
Q

components of Juxtaglomerular Apparatus

A
  • JG cells: modified sm. muscle on aff. arteriole => secrete renin
    (when low NaCl delivery to DCT, low renal BP, or B1 stim.)
  • Macula Densa: on distal conv. tubule, sense low NaCl
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6
Q

Effect of ANP on kidney

A

(secreted from atria of heart when HIGH pressure/volume)
increase GFR & Na filtration @ distal tubule
=> Na+ & volume loss
(opposes Renin/Ang/Aldosterone)

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7
Q

Effect of PTH on kidney

A

secreted when:
low plasma [Ca2+], high plasma [PO4—], or low 1,25-(OH)2 VitD

=> decrease PO4 resorption (PCT), increase Ca resorption at DCT, and increase 1,25-OH2 vitD activation

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8
Q

Angiotensin II vs. ANP

A

BOTH increase GFR, but
ANP: no compensatory Na resorption => net volume loss
Ang II: w/ compensatory Na resorption => net maintenance of renal BF (& NO volume loss)

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9
Q

Electrolyte changes associated with Aldosterone activity

A

bc aldosterone increases Na resorption at collecting duct,
=> increased K+ and H+ excretion
(may become hypoKalemic or alkalotic)

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10
Q

Causes of K+ shift OUT of CELL

A
  1. Digitalis ==> hypERkalemia
  2. hyperOsmolarity
  3. Insulin deficiency
  4. Lysis of cells
  5. Acidosis
  6. Beta-adrenergic antagonist
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11
Q

Causes of K+ shift INto CELL

A

==> hypOkalemia

  1. hypO-osmolarity
  2. Insulin presence (increases Na/K ATPase)
  3. Alkalosis
  4. Beta-adrenergic AGonist (also increases Na/K ATPase)
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12
Q

Signs/symptoms of Na+ imbalance (High or Low)

A

Both: stupor/coma
High Na+: irritability
Low Na+: nausea, malaise

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13
Q

Signs/Symptoms of K+ imbalance (High or Low)

A

Both: arrhythmias, mm weakness
High K+: Wide QRS complex & peaked T waves
Low K+: U waves on ECG & flattened T waves

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14
Q

Signs/Symptoms of Ca2+ imbalance (High or Low)

A

High Ca2+: “stones, bones (pain), groans (abdom. pain), & psychiatric overtones” (anxiety, altered mental status)

Low Ca2+: tetany, seizures

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15
Q

Signs/Symptoms of Mg2+ imbalance (High or Low)

A

High Mg2+: decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa2+

Low: tetany, arrhythmias

16
Q

Signs/Symptoms of PO4(3-) imbalance (High or Low)

A

High: kidney stones, metastatic calcifications, hypoCa2+

Low: bone loss, osteomalacia

17
Q

Calculation for Anion Gap

A

Anion gap = Na+ - (Cl- + HCO3-)

  • normal = 8-12
18
Q

Calculation for respiratory compensation in metabolic acidosis

A

PaCO2 = 1.5([HCO3-]) + 8 +/-2

  • if PCO2 is:
    a) MORE than predicted, = COMBINED met. acidosis & resp. acidosis
    b) LESS than predicted, = MIXED met. acidosis & resp. ALKalosis
19
Q

3 types of RTA (Renal Tubular Acidosis 1, 2, & 4)

A

(normal anion gap metabolic acidosis)
Type 1: “distal” = can’t excrete H+ => urine pH >5.5, hypoK+
Type 2: “proximal” = can’t reabsorb HCO3- => urine pH poor NH3 synth => poor buffer ability, very acidic urine.

20
Q

Type 1 RTA

A

“Distal” = can’t excrete H+
=> urine pH >5.5, hypoK+
*Assoc. w/ Sjogrens & Amphotericin B

21
Q

Type 2 RTA

A

“Proximal” = can’t reabsorb HCO3-

=> urine pH s anemia, mult. myeloma, carb.anhydrase Is

22
Q

Type 4 RTA

A

“HyperK+” = hypoAldo or no response to aldosterone
=> poor NH3 synth. = poor buffer ability, very acidic urine.
*assoc. w/ Diabetes, adrenal insuff., ACE Is

23
Q

Kidney stones that occur in ACIDIC environment:

vs. alkaline

A 
LOW pH (acidic) 
#1: Calcium oxalate, 2. uric acid, 3. cysteine (hexagonal)

Basic (high pH):
Ca-phosphate, Struvite (NH3-Mg-PO4, *from urease+ bacteria)

24
Q

RadioLUCENT kidney stones

A

= Uric acid stones => need CT or ultrasound to visualize (NOT xray)
in acidic environment w/ hyperuricemia

25
Q

Acute vs. Chronic Pyelonephritis

A

Acute: WBC casts in urine, neutrophilic infiltration into renal cortex

Chronic: from recurrent acute episodes, => eosinophilic casts, corticomedullary scarring/fibrosis & blunted calyces.

26
Q

Drugs that can induce interstitial nephritis (5 total)

A

(drugs act as haptens, induce hypersensitivity)
1-2 weeks after taking: diuretics, penicillins, sulfonamides, or rifampin
OR
1 mo. after taking NSAIDs

27
Q

Common nephrotoxins (known to induce Acute Tubular Necrosis)

A
  1. Antibiotics (Aminoglycosides & amphotericin B)
  2. radiocontrast (*decrease risk if taken w/ prednisone)
  3. acetaminophen overdose
  4. cisplatin
  5. heme (ie: myoglobin, hemoglobin)
28
Q

Stages of Acute Tubular Necrosis (“ATN”)

A
  • # 1 cause of INtrinsic renal failure!
    1. inciting event (renal ischemia)
    2. maintenance phase: oliguria, 1-3 wks. *risk hyperK
    3. recovery phase: polyuria => decrease creatinine & BUN, risk hypOK!
29
Q

Pathogenesis of oliguria in Acute Tubular Necrosis

A

ATN = necrosis/apoptosis AND sublethal injury to TUBULAR epithelial cells.
because of damage, low Na+ delivery to macula densa
=> retain Na & H2O ==> low urine output (despite normotension)

30
Q

Sign of acute renal failure & 3 types of causes

A

increasing Creatinine AND BUN (also often oliguria, 20!

  • intrinsic renal failure (ATN, AIN, or RPGN) *BUN/Creatinine ratio <15
  • post-renal (outflow obstruction) *exclude w/ ultrasound

Step 1 (15 decks)

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