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Evan's Step 1 Prep Material > Renal Physiology EC > Flashcards

Renal Physiology EC Flashcards

1
Q

Fluid compartments and percent of body weight

A 
60%= Total body water (TBW)
2/3TBW Intracellular
1/3TBW Extracellular (EC)
1/4 EC Plasma
3/4 EC Interstitial
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2
Q

What are the components of the glomerular filtration barrier? Loss of barrier leads to what syndrome?

A

Fenestrated capillary endothelium (size barrier)
Fused basement membrane w/ heparan sulfate (-charge barrier)
Epithelial layer w/ podocyte foot processes

Loss of barrier leads to nephrotic syndrome

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3
Q

What is the equation for renal clearance?

A

Clearance= ([Urine]*Volume) /[Plasma]

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4
Q

How do you calculate GFR? What substance is used? What is a normal value?

A

GFR=Clearance of inulin or creatinine (freely filtered and not absorbed or secreted - creatinine used clinically but overestimates GFR)

Normal GFR=100mL/min

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5
Q

How do you calculate RPF (renal plasma flow)?

A

RPF= Clearance of PAH

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6
Q

How do you calculate RBF (renal blood flow)?

A

RBF= RPF / (1-hematocrit)

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7
Q

How do you calculate FF (filtration fraction)?

A

FF= GFR/RPF

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8
Q

How do you calculate Filtered Load?

A

FL= GFR * [Plasma]

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9
Q

How do NSAIDs affect RPF, GFR, and FF?

A

NSAIDs decrease RPF and GFR by blocking production of prostaglandins that usually dilate afferent arteriole

FF does not change because RPF and GFR both decrease

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10
Q

How do ACE inhibitors affect RPF, GFR, and FF?

A

Constrict efferent arteriole
Decrease RPF
Increase GFR
so Increase FF (GFR/RPF)

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11
Q

Where is glucose reabsorbed? At what plasma level does glucosuria begin? At what plasma level are transporters saturated?

A

Reabsorbed in proximal tubule by Na/glucose cotransport

Glycosuria begins at 160mg/dL
Saturation begins at 250mg/dL

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12
Q

How are amino acids reabsorbed?

A

Reabsorbed via Na-dependent transporters in proximal tubule

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13
Q

Hartnup’s Disease

A

Deficiency in neutral amino acid transporter

Tryptophan deficiency leads to pellagra (diarrhea, dermatitis, dementia)

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14
Q

Early Proximal tubule: What is reabsorbed? What is secreted? What hormones act on?

A

Reabsorbs:
Glucose, AA’s, bicarb, Na, Cl, PO4, H2O via isotonic absorption

Secretes:
H+, Ammonia (acts as buffer for H+)

PTH: Inhibits phosphate reabsorption
AT II: Increases Na, H2O, and Bicarb reabsorption

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15
Q

Thin descending loop of Henle

A

Passively reabsorbs water via medullary hypertonicity

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16
Q

Thick ascending loop of Henle: What is reabsorbed? What is it’s function? What diuretics act here/what affect do they have on body Ca?

A

Reabsorbs:
Na/K/2Cl actively, parallel reabsorption of Mg and Ca (driven by K leak-back into tubule)

Dilutes urine

Loop diuretics act here
LOOPS LOSE CALCIUM (cause hypocalcemia)

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17
Q

Early distal tubule: What is reabsorbed? What is it’s function? What hormones act here? What diuretics act here/what affect do they have on body Ca?

A

Reabsorbed:
Na/Cl actively

Dilutes urine

PTH increases Ca reabsorption

Thiazide diuretics act here (cause hypercalcemia)

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18
Q

Collecting tubules:

A

Reabsorb:
Na

Secrete:
K, H+

Aldosterone - causes Na reabsorption and K/H secretion
ADH- causes water reabsorption (Aq channel insertion)

19
Q

What is the function of the juxtaglomerular apparatus?

A

JG cells = secrete renin in response to decreased BP

Macula densa= NaCl sensor that increases sympathetic tone in response to decrease (Beta-1 receptors)

Beta blockers decrease BP by blocking receptors on JGA

20
Q

Erythropoietin

A

Released by interstitial cells in the peritubular capillary bed in response to hypoxia

21
Q

1,25-(OH)2 vit. D

A

Proximal tubule cells convert to active form via 1-alpha-hydroxylase

22
Q

Renin

A

Secreted by JG cells in response to decreased renal BP and increased renal sympathetic discharge

23
Q

Prostaglandins

A

Paracrine regulation of renal blood flow via dilation of afferent arteriole

(NSAIDs can cause acute renal failure by inhibiting)

24
Q

ANP (atrial natriuretic peptide) action on kidney

A

Secreted in response to INCREASED RA pressure

Causes increased GFR and Na filtration with no compensatory Na reabsorption (Na and volume loss)

25
Q

PTH (parathyroid hormone) action on kidney

A

Secreted in response to decreased plasma Ca, increased PO4, or decreased vit D

Causes Ca reabsorption (DCT), PO4 dumping (PCT), 1-OH-D production

26
Q

Angiotensin II action on kindey

A

efferent arteriole constriction (increase GFR) w/ compensatory Na reabsorption

Preservation of renal function in low volume state w/ Na reabsorption

27
Q

Aldosterone action on kidney

A

Secreted in response to decreased blood volume

Causes increased Na reabsorption, K and H secretion in collecting duct

28
Q

ADH action on kidney

A

Secreted in response to increased plasma osmolarity

Increases number of aquaporin channels (increase water reabsorption)

29
Q

What shifts K out of the cell?

A

“pt’s w/ hyperkalemia? DO INSULIN LAB”

Digitalis
hyperOsmolarity 
INSULIN deficiency
Lysis of cells
Acidosis
Beta-antagonist
30
Q

Na effects of low and high serum concentration

A

Low Na:
Nausea, malaise, stupor, coma

High Na:
Irritability, stupor, coma

31
Q

K effects of low and high serum concentration

A

Low K:
U waves, flattened T waves on ECG, muscle weakness

High K:
Wide QRS, peaked T waves on ECG, muscle weakness

32
Q

Ca effects of low and high serum concentration

A

Low Ca:
Tetany (ie Chovek’s sign), Seizures

High Ca:
“Stones (renal), Bones (pain), Groans (abdominal pain), Psychiatric overtones”

33
Q

Mg effects of low and high serum concentration

A

Low Mg:
Tetany, arrhythmias

High Mg:
Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

34
Q

PO4 effects of low and high serum concentration

A

Low PO4:
Bone loss

High PO4:
Renal stones, metastatic calcifications/hypocalcemia (drives Ca into cells)

35
Q

pH < 7.4 with a PCO2 of 50 (what is this and what are the causes)

A

Respiratory acidosis (no compensation)

Caused by hypoventilation

36
Q

pH of 7.38 w/ a PCO2 of 35 (what is this and what are the causes)

A

Metabolic acidosis with respiratory compensation

Check ion gap for causes (see other card)

37
Q

Causes of metabolic acidosis with an increased ion gap (>12)

A

“MUDPILES”

Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or Isoniazid 
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates
38
Q

Causes of metabolic acidosis with normal ion gap (8-12)

A

“HARD-ASS”

Hyperalimentation
Addison's
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
39
Q

Renal tubular acidosis type 1

A

Defect in collecting tubules ability to excrete H+

Present w/ low plasma pH, hypokalemia, and calcium phosphate stones

40
Q

Renal tubular acidosis type 2

A

Defect in proximal tubule bicarb reabsorption (may be seen with Fanconi syndrome)

Presents with low plasma pH, hypokalemia, and hypophosphatemic rickets

41
Q

Renal tubular acidosis type 3

A

Hypoaldosteronism (or lack of response to aldosterone)

Hyperkalemia impairs ammoniagenesis in proximal tubule leading to decreased buffering capacity and decreased urine pH

42
Q

Case study: A woman has a history of weakness, weight loss, orthostatic hypotension, increased pulse rate, and increased skin pigmentation. She has decreased serum [Na], decreased serum osmolarity, increase serum [K], and arterial blood gases consistent with metabolic acidosis.

A

Hypoaldosteronism

Lack of aldosterone (Na dumping, K saving, H+ saving) resulting in ECF VOLUME CONTRACTION, HYPERKALEMIA, and METABOLIC ACIDOSIS

ECF contraction leads to ADH which leads to fluid retention which worsens hyponatremia

43
Q

Case study: A man is admitted to the hospital for evaluation of severe epigastric pain. He has had persistent nausea and vomiting for 4 days. Upper GI endoscopy shows pyloric ulcer with partial gastric outlet obstruction. He has orthostatic hypotension, decreased serum [K] and [Cl] with blood gases consistent with metabolic alkalosis and decreased ventilation rate.

A

Vomiting response

Loss of H+ and Cl causes metabolic alkalosis and ECF contraction
Decreased ventilation as respiratory compensation
ECF contraction leads to decreased RBF and aldosterone causes increase bicarb reabsorption WORSENING METABOLIC ALKALOSIS (aka contraction alkalosis)
Also causes K secretion

44
Q

Case study: A man returns from a trip abroad with “traveler’s diarrhea.” He has weakness, weight loss, orthostatic hypotension, increased pulse rate, increased breathing rate, pale skin, and serum [Na] of 132, [Cl] of 111 and [K] of 2.3. His arterial blood gases are pH=7.25, PCO2=24, HCO3=10.2

A

Diarrhea

Losing HCO3 from GI tract leads to metabolic acidosis
HCO3 replaced by Cl to maintain normal anion gap
Hyperventilation for compensation
ECF volume contraction activates baroreceptor reflex, resulting in sympathetic outflow
ECF volume contraction also activates Renin-Ang system leading to Hypokalemia

Evan's Step 1 Prep Material (72 decks)

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