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CVPR > CVPR First Aid: Renal embryology > Flashcards

CVPR First Aid: Renal embryology Flashcards

1
Q

Pronephros

A

Week 4; then degenerates

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2
Q

Mesonephros

A

Functions as interim kidney for 1st trimester, later contributes to male genital system

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3
Q

Metanephros

A

Permanent

First appears in 5th week of gestation

Nephrogenesis continues through weeks 32-36

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4
Q

FIRST AIDKidney embryology diagram

A

562

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5
Q

What is potter sequence syndrome?

A

Oligohydramnios → compression of developing fetus → limb deformities, facial anomalies (eg, low-set ears and retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs → pulmonary hypoplasia (cause of death)

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6
Q

What is the cause of death in Potter Sequence Syndrome

A

lack of amniotic fluid aspiration into fetal lungs → pulmonary hypoplasia (cause of death)

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7
Q

Uteric bud is derived from?

A

Derived from caudal end of mesonephric duct

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8
Q

Uteric bud canalization

A

fully canalized by the 10th week

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9
Q

Ureteric bud gives rise to

A

Gives rise to ureter, pelvises, calyces, collecting ducts

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10
Q

Metanephric mesenchyme and ureteric bud interactions

A

(ie, metanephric blastema)

Uteric bud interacts with this tissue; interaction induces differentiation and formation of glomerulus through to distal convoluted tubule (DCT)

Aberrant interaction between these 2 tissues may result in several congenital malformations of the kidney (eg, renal agenesis, multicystic dysplastic kidney)

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11
Q

Causes of Potter Sequence Syndrome

4 listed

A

ARPKD

Obstructive uropathy (Eg, posterior urethral valves)

Bilateral ren agenesis

Chronic placental insufficiency

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12
Q

What is ARPKD?

A

Autosomal recessive polycystic kidney disease

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13
Q

Ureteropelvic junction

A

Last to canalize → most common site of obstruction (can be detected on prenatal ultrasound as hydronephrosis

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14
Q

Babies who can’t pee in utero develop

A

Potter Sequence Syndrome

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15
Q

POTTER sequence associated with

A

Pulmonary hypoplasia

Oligohydramnios

Twisted face

Twisted skin

Extremity defects

Renal failure (in utero)

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16
Q

What is horseshoe kidney?

A

Inferior poles of both kidneys fuse abnormally

As they descend from pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen

Kidneys function normally

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17
Q

Horseshoe kidney is associated with?

5 listed

A
  • Associated with hydronephrosis (eg, ureteropelvic junction obstruction)
  • renal stones
  • infection
  • chromosomal aneuploidy syndromes (eg, Turner syndrome, Trisomies; 13, 18 and 21)
  • rarely renal cancer
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18
Q

FIRST AID Identify horseshoe kidney

A

563

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19
Q

Trisomies associated with Horseshoe kidney

A

Trisomies; 13, 18 and 21)

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20
Q

Dx of congenital solitary functioning kidney?

A

Prenatally via ultrasound

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21
Q

What is unilateral renal agenesis?

A

Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme → complete absence of kidney and ureter

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22
Q

What is multicystic dysplastic kidney?

A

Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme → complete absence of kidney and ureter

A multicystic dysplastic kidney (MCDK) is the result of abnormal fetal development of the kidney. The kidneyconsists of irregular cysts of varying sizes that resemble a bunch of grapes. A multicystic dysplastic kidney has no function and nothing can be done to save it.

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23
Q

multicystic dysplastic kidney pathophysiology and etiology

A

Ureteric bud fails to induce differentiation of metanephric mesenchyme → nonfunctional kidney consisting of cysts and connective tissue

Predominantly nonhereditary and usually unilateral

Bilateral leads to Potter Sequence

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24
Q

What is duplex collecting system?

A

Bifurcation of ureteric bud before it enters the metanephric blastema creates a Y-shaped bifid ureter

Duplex collecting system can alternatively occur through two ureteric buds reaching and interacting with metanephric blastema

Strongly associated with vesicoureteral reflux and/or ureteral obstruction

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25
Q

What are posterior urethral valves

A

Membrane remnant in the posterior urethra in males

The abnormality occurs when the urethral valves, which are small leaflets of tissue, have a narrow, slit-like opening that partially impedes urine outflow. Reverse flow occurs and can affect all of the urinary tract organs including the urethra, bladder, ureters, and kidneys.

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26
Q

Complications of Posterior urethral valves

A

Its persistence can lead to a urethral obstruction

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27
Q

Dx of posterior urethral valves

A

Can be diagnosed prenatally by hydronephrosis and dilated or thick walled bladder on ultrasound

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28
Q

What Most common cause of bladder outlet destruction

in male infants

A

posterior urethral valves

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29
Q

What kidney is taken from the donor for transplant

A

Left kidney is taken during donor transplant because it has a longer renal vein

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30
Q

Describe renal blood flow

A

Renal artery → segmental artery → arcuate artery → interlobular artery → afferent arteriole → vasa recta/peritubular capillaries → venous outflow

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31
Q

Diagrams pg

A

564

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32
Q

Describe the course of ureters

A

Pg 564

Arises from renal pelvis and travels under gonadal arteries → over common iliac artery → under uterine artery/vas deferens (retroperitoneal)

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33
Q

Describe the danger to the ureter from gynecologic procedures

A

(eg, ligation of uterine or ovarian vessels)

may damage ureter → ureteral obstruction or leak

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34
Q

What prevents urine reflux?

A

Muscle fibers within the intramural part of the ureter prevent urine reflux

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35
Q

What prevents urine reflux?

A

Muscle fibers within the intramural part of the ureter prevent urine reflux

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36
Q

VUR AKA

A

Vesicoureteral reflux (VUR)

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37
Q

Describe the points of constriction of the ureter

3 Listed

A

Ureteropelvic junction

Pelvic inlet

Ureterovesicle junction

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38
Q

Water (ureters) flows over the iliacs and under the bridge (uterine artery or vas deferens)

A

Diagram pg 564

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39
Q

What is Vesicoureteral reflux?

A

is a condition in which urine flows backward from the bladder to one or both ureters and sometimes to the kidneys. … Normally, urine flows down the urinary tract, from the kidneys, through the ureters, to the bladder

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40
Q

Where is [K+] highest?

A

HIKIN

High K Intracellularly

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41
Q

What is the body water distribution

A

60-40-20 rule

60% total body water

40% ICF

20% ECF

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42
Q

Describe ICF ion concentrations

A

K

Mg

Organic phosphates (eg, ATP)

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43
Q

Describe ECF ion concentrations

4 listed

A

Na+

Cl-

HCO3-

Albumin

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44
Q

Describe ICF ion concentrations

A

K

Mg

Organic phosphates (eg, ATP)

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45
Q

How can plasma volume be measured?

A

Radiolabled albumin

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46
Q

How can extracellular volume be measured

A

Inulin or mannitol

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47
Q

Normal Osmolality of ECF

A

285-295 mOsm/kg H2O

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48
Q

What is the function of the glomerular filtration barrier

A

Responsible for filtration of plasma according to size and charge selectivity

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49
Q

The glomerular filtration barrier is composed of

3 listed

A

Fenestrated capillary endothelium

Basement membrane with type IV collagen chains and heparan sulfate (which is negatively charged)

Epithelial layer consisting of podocyte foot processes

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50
Q

Describe the charge barrier of the glomerular filtration barrier

A

All 3 layers contain (-) charged glycoproteins that prevent entry of (-) charged molecules (eg, albumin)

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51
Q

Describe the size barrier of the glomerular filtration barrier

A

Fenestrated capillary endothelium (prevent entry of > 100 nm molecules/blood cells

Podocyte foot processes interpose with basement membrane

Slit diaphragm (prevent entry of molecules > 50-60 nm

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52
Q

Describe renal clearance

A

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)

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53
Q

Interpretation of renal clearance

A

If Cx < GFR net tubular reabsorption of X

If Cx > GFR net tubular secretion of X

If Cx = GFR no net secretion or absorption

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54
Q

Describe glomerular filtration rate

A

Inulin clearance can be used to calculate GFR because it is freely filtered and is neither reabsorbed nor secreted

GFR = Uinulin x V/Pinulin = Cinulin

= Kf{[PGC-PBS) - (πGC - πBS)]

GC = glomerular capillary

BS = Bowmans space

πBS usually = 0

Kf= filtration coefficient

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55
Q

What is a normal GFR?

A

100 mL/min

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56
Q

What is an appropriate measure of GFR

A

Creatinine clearance is an appropriate measure of GFR but

Slightly overestimates GFR because it is moderately secreted by renal tubules

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57
Q

What do reductions in GFR mean

A

Incremental reductions in GFR define the stages of chronic kidney disease

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58
Q

What is RPF?

A

Renal plasma flow

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59
Q

What is eRPF?

A

effective renal plasma flow

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60
Q

Renal blood flow equation

A

(RBF) = RPF/(1-Hct)

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61
Q

What is filtration fraction?

A

FF= GFR/RPF

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62
Q

Normal FF =

A

20%

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63
Q

Filtered load (mg/min) equation

A

FL = GFR (mL/min) x plasma concentration (mg/mL)

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64
Q

GFR can be estimated with?

A

creatinine clearance

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65
Q

RPF is best estimated with?

A

PAH clearance

Prostaglandins Dilate Afferent arteriole (PDA)

Angiotensin II Constricts Efferent arteriole (ACE)

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66
Q

Bowman’s capsule

A

Pg 567

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67
Q

Afferent arteriole constriction effect on GFR

A

↓

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68
Q

Efferent arteriole constriction effect on GFR

A

↑

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69
Q

↑ plasma protein concentration effect on GFR

A

↓

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70
Q

↓ plasma protein concentration effect on GFR

A

↑

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71
Q

Constriction of ureter effect on GFR

A

↓

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72
Q

Dehydration effect on GFR

A

↓

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73
Q

Afferent arteriole constriction effect on RPF

A

↓

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74
Q

Efferent arteriole constriction effect on RPF

A

↓

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75
Q

↑ plasma protein concentration effect on RPF

A

-

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76
Q

↓ plasma protein concentration effect on RPF

A

-

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77
Q

Constriction of ureter effect on RPF

A

-

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78
Q

Dehydration effect on RPF

A

↓↓

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79
Q

Afferent arteriole constriction effect on FF

A

-

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80
Q

Efferent arteriole constriction effect on FF

A

↑

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81
Q

↑ plasma protein concentration effect on FF

A

↓

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82
Q

↓ plasma protein concentration effect on FF

A

↑

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83
Q

Constriction of ureter effect on FF

A

↓

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84
Q

Dehydration effect on FF

A

↑

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85
Q

What is FF?

A

GFR/RPF

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86
Q

Calculation of reabsorption and secretion rate

A

Filtered load = GFR x Px

Excretion rate = V x Ux

Reabsorption rate = filtered - excreted

Secretion rate = excreted - filtered

FeNa = fractional excretion of sodium

FeNa = Na excreted / Na filtered = (V x Una) / (GFR x Pna)

Where GFR = (Ucr x V/ (PCr) = (PCr x Una) /(Ucr x Pna)

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87
Q

Describe glucose clearance

A

Glucose at a normal plasma level (range 60-120 mg/dL) is completely reabsorbed in proximal convoluted tubule (PCT) by Na/glucose cotransport

Glucose at a normal plasma level (range 60-120 mg/dL) is completely reabsorbed in proximal convoluted tubule (PCT) by Na/glucose cotransport

In adults at plasma glucose of 200 mg/dL glucosuria begins begins (threshold)

At a rate of 375 mg/min, all transporters are fully saturated (T(m))

Normal pregnancy is associated with ↑GFR

with ↑ filtration of all substances including glucose, the glucose threshold occurs at lower plasma glucose concentrations → glucosuria at plasma concentrations < 200 mg/dL

Glucosuria is an important clinical clue to diabetes mellitus

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88
Q

Splay phenomenon -

A

Tm for glucose is reached gradually rather than sharply due to the heterogeneity of nephrons (ie, different Tm points); represented by the portion of the titration curve between threshold and Tm

ALL THIS PG 568

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89
Q

Nephron physiology early PCT

A

Early PCT - contains brush border. Reabsorbs all glucose and amino acids and most HCO3-, Na, Cl, PO4, K, H2O and uric acid

Isotonic absorption

Generates and secretes NH3 which enables the kidney to secrete more H+

PTH inhibits Na/PO4 cotransport → PO4 excretion

ATII - stimulates Na/H exchange → ↑Na, H2O, and HCO3 reabsorption (permitting contraction alkalosis)

65-80% Na reabsorbed

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90
Q

Thin descending loop of Henle

A

Passively reabsorbs H2O via medullary hypertonicity (impermeable to Na)

Concentrating segment

makes urine hypertonic

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91
Q

Thick ascending loop of Henle

A

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

10-20% Na reabsorbed

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92
Q

Early DCT

A

Reabsorbs Na, Cl

Impermeable to H2O

Makes urine fully dilute (hypotonic)

PTH - ↑ Ca/Na exchange → Ca reabsorption

5-10% Na reabsorbed

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93
Q

Collecting tubule

A

Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone)

Aldosterone - acts on mineralocorticoid receptor → mRNA → protein synthesis

In principal cells ↑ apical K conductance, ↑ Na/K pump, ↑ epithelial Na channel (ENaC activity) → lumen negativity → K secretion

In α-intercalated cells: lumen negativity → ↑H+ ATPase activity → ↑H+ secretion → ↑ HCO3/Cl exchanger activity

ADH - acts at V2 receptor → insertion of aquaporin H2O channels on apical side

3-5% Na reabsorbed

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94
Q

What is SAME?

A

Syndrome of apparent mineralocorticoid excess

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95
Q

Describe renal defects in Fanconi syndrome

A

Generlized reabsorption defect in PCT → ↑ excretion of amino acids, glucose, HCO3 and PO4 and all substances reabsorbed by the PCT

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96
Q

Describe renal defects in Bartter syndrome

A

Resorptive defect in thick ascending loop of Henle (affects Na/K/2Cl cotransporter)

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97
Q

Presentation of renal defects in Gitelman syndrome

A

Reabsorption defect of NaCl in DCT

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98
Q

Describe renal defects in Liddle syndrome

A

Gain of function mutation → ↑ activity of Na channel → ↑ Na reabsorption in collecting tubules

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99
Q

Describe the renal defects in Syndrome of apparent mineralocorticoid excess

A

In cells containing mineralocorticoid receptors 11β-hydroxysteroid receptors, 11β-hydroxysteroid dehydrogenase converts cortisol (can activate these receptors to cortisone (inactive on these receptors)

Hereditary deficiency of 11β-hydroxysteroid → excess cortisol → ↑ mineralocorticoid activity

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100
Q

Presentation of the effects of the renal defect in Fanconi syndrome

A

May lead to metabolic acidosis (proximal RTA)

hypophosphatemia

osteopenia

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101
Q

Describe the effects of the renal defect in Bartter syndrome

3 listed

A
  • Metabolic alkalosis
  • Hypokalemia
  • hypercalciuria
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102
Q

Describe the effects of the renal defect in Gitelman syndrome

4 listed

A
  • Metabolic alkalosis
  • Hypomagnesemia
  • Hypokalemia
  • Hypocalciuria
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103
Q

Describe the effects of the renal defect in Liddle syndrome

4 listed

A
  • Metabolic alkalosis
  • Hypokalemia
  • Hypertension
  • ↓ aldosterone
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104
Q

Describe the effects of the renal defect in Syndrome of apparent mineralocorticoid excess

A

Metabolic alkalosis

Hypokalemia

Hypertension

↓ serum aldosterone level

Cortisol tries to be SAME as aldosterone so ↑ cortisol levels

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105
Q

Causes of Fanconi syndrome

A

Hereditary defects

(eg, Wilson disease, tyrosinemia, glycogen storage disease)

Ischemia

Multiple myeloma

Nephrotoxins/drugs (eg, ifosfamide, cisplatin, expired tetracyclines)

Lead poisoning

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106
Q

Causes of Bartter syndrome

A

Autosomal recessive

107
Q

Causes of Gitelman syndrome

A

Autosomal recessive

108
Q

Causes of Liddle syndrome

A

Autosomal dominant

109
Q

Causes of SAME

A

Autosomal recessive

Can acquire disorder from glycyrrhtinic acid (present in licorice) which blocks activity of 11β-hydroxysteroid dehydrogenase

110
Q

Special considerations of Bartter syndrome

A

Presents similarly to chronic loop diuretic use

111
Q

Special considerations of Gitelmen syndrome

A

Presents similarly to lifelong thiazide diuretic use

Less severe than Bartter syndrome

112
Q

Special considerations of Liddle syndrome

A

Presents similarly to hyperaldosteronism but aldosterone is nearly undetectable

113
Q

Treatment of Liddle syndrome

A

Amiloride

114
Q

What is amiloride?

A

The potassium-sparing diuretics are competitive antagonists that either compete with aldosterone for intracellular cytoplasmic receptor sites, or directly block sodium channels (specifically epithelial sodium channels (ENaC) by amiloride).

115
Q

Treatment of SAME

A

Treat with K-sparring diuretics (↓ mineralocorticoid effects)

Or

Corticosteroids (exogenous corticosteroid ↓ endogenous cortisol production →↓ mineralocorticoid receptor activation

116
Q

Renal tubular defect that presents similarly to chronic loop diuretic use

A

Bartter syndrome

117
Q

Renal tubular defect that presents similarly to lifelong thiazide diuretic use

A

Gitelmen syndrome

118
Q

Renal tubular defect that presents similarly to hyperaldosteronism but aldosterone is nearly undetectable

A

Liddle syndrome

119
Q

Describe the relative concentrations along the proximal convoluted tubule

A

571

Tubular inulin ↑ in concentration (but not amount) along the PCT as a result of water reabsorption Cl- reabsorption occurs at a slower rate than Na in early PCT and then matches the rate of Na reabsorption more distally

Thus its relative concentration ↑ before it plateaus

120
Q

Describe the factors that stimulate renin secretion

A

Secreted by juxtaglomerular cells in response to:

↓ renal perfusion pressure (detected by renal baroreceptors in afferent arteriole)

↑ renal sympathetic discharge (β1 effect)

↓ NaCl delivery to macula densa cells

121
Q

ATII

A

Helps maintain blood volume and blood pressure

Affects baroreceptor function; limits reflex bradycardia which would normally accompany its pressor effects

122
Q

ANP & BNP

A

Release from atria (ANP) and ventricles (BNP) in response to ↑ volume; may act as a “check” on renin-angiotensin-aldosterone system; relaxes vascular smooth muscle via cGMP → ↑ GFR. ↓renin

Dilates afferent arteriole

Constricts efferent arteriole

Promotes natriuresis

123
Q

ADH

A

Primarily regulates serum osmolality; also responds to low blood volume states

Stimulates reabsorption of water in collecting ducts

Also stimulates reabsorption of urea in collecting ducts to maintain corticopulmonary osmotic gradient

124
Q

Aldosterone

A

Primarily regulates ECF volume and Na content; responds to low blood volume states

Responds to hyperkalemia by ↑ K excretion

125
Q

Diagram 572

A

572

126
Q

Describe the juxtaglomerular apparatus

A

Consists of mesangial cells

JG cells (modified smooth muscle of afferent arteriole)

Macula Densa (NaCl sensor located in at the distal end of loop of Henle

JG cells secrete renin in response to

↓ renal perfusion pressure (detected by renal baroreceptors in afferent arteriole)

↑ renal sympathetic discharge (β1 effect)

↓ NaCl delivery to macula densa cells and cause efferent arteriole vasoconstriction → ↑ GFR

127
Q

JG cells are what kind of cells?

A

(modified smooth muscle of afferent arteriole)

128
Q

What is the macula densa?

A

(NaCl sensor located in at the distal end of loop of Henle)

129
Q

JG cells secrete renin in response to

A

↓ renal perfusion pressure (detected by renal baroreceptors in afferent arteriole)

↑ renal sympathetic discharge (β1 effect)

↓ NaCl delivery to macula densa cells and cause efferent arteriole vasoconstriction → ↑ GFR

130
Q

How is GFR maintained?

A

The JGA maintains GFR via renin-angiotensin-aldosterone system

131
Q

ANP and BNP effect on Renin

A

decrease renin by increasing GFR

my assumption^

132
Q

Β-blockers and RAAS

A

In addition to vasodilatory properties β-blockers can decrease BP by inhibiting β1 receptors of the JGA →↓ renin release

133
Q

What are the kidney endocrine functions?

4 listed

A
  • Erythropoietin
  • Calciferol
  • Prostaglandins
  • Dopamine
134
Q

Describe kidney erythropoietin

A

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

Stimulates RBC proliferation in bone marrow

135
Q

Chronic kidney disease and EPO

A

EPO is often supplemented in CKD

136
Q

Describe kidney calciferol

A

PCT cells convert 25-OH vitamin D3 to 1, 25- (OH) vitamin D3 (calcitriol, active form)

137
Q

PTH and Vitamin D

A

PTH activates 1α-hydroxylase to convert to active form calcitriol

138
Q

Describe kidney prostaglandins

A

Paracrine secretion vasodilates the afferent arterioles to ↑ RBF

NSAIDS block renal-protective prostaglandin synthesis → constriction of afferent arteriole and ↓ GFR; this may result in acute renal failure in low renal blood flow states

139
Q

Describe kidney dopamine effects at low doses

A

At low doses

Promotes natriuresis

Dilates interlobular arteries, afferent arterioles and efferent arterioles →↑ RBF

Little or no change in GFR

140
Q

contraction alkalosis

A

ATII - stimulates Na/H exchange → ↑Na, H2O, and HCO3 reabsorption

in the PCT

141
Q

Describe kidney dopamine effects at high doses

A

At higher doses

acts as a vasoconstrictor

142
Q

Dopamine is secreted by what in the kidney?

A

Secreted by PCT cells

143
Q

Hormones acting on the kidney

A

574

144
Q

Where does Angiotensin II act in the nephron?

A

Proximal convoluted tubule

145
Q

Where does PTH act in the nephron?

A

Proximal convoluted tubule

DCT

146
Q

Where does ANP act in the nephron?

A

Distal convoluted tubule

147
Q

Where does aldosterone work in the nephron?

A

Distal convoluted tubule and collecting ducts

148
Q

Where does Vasopressin work in the nephron?

A

Collecting duct

149
Q

ADH is secreted in response to?

A

Secreted in response to ↑ plasma osmolarity and ↓ blood volume

150
Q

Describe the effects of ADH in the nephron

A

Binds to receptors on principal cells causing ↑ number of aquaporins and ↑H2O reabsorption in the collecting duct

151
Q

Stimuli for aldosterone secretion

2 listed

A

Secreted in response to ↓ blood volume (via AT II) and ↑ plasma [K+]

152
Q

Effects of aldosterone

A

causes ↑Na reabsorption, ↑K secretion, ↑H+ secretion in the DCT and collecting ducts

153
Q

Describe the effects of ANP in the nephron

A

Secreted in response to ↑ atrial pressure

Causes ↑ GFR and ↑ Na filtration with no compensatory Na reabsorption in the distal nephron

Net effect Na loss and volume loss

154
Q

Describe the effects of AT II in the nephron

A

Synthesized in response to ↓ BP

Causes efferent arteriole constriction → ↑GFR and ↑ FF but with compensatory Na reabsorption in proximal and distal nephron

Net effect: preservation of renal function (↑FF) in low-volume state with simultaneous Na reabsorption (both proximal and distal) to maintain circulating volume

155
Q

Describe the effects of PTH

A

Secreted in response to ↓ plasma [Ca], ↑ plasma [PO4] or ↓ plasma 1, 25-(OH)2 D3

Causes ↑Ca reabsorption in the DCT and ↓ PO4 reabsorption in the PCT and ↑1, 25(OH)2 D3 production leading to ↑Ca and PO4 absorption from the gut via vitamin D

156
Q

Describe the effects of aldosterone in the nephron

A

Secreted in response to ↓blood volume (via ATII) and ↑plasma [K+]

Causes ↑Na reabsorption ↑K+ secretion ↑H+ secretion

157
Q

Digitalis potassium shift

A

Digitalis (blocks Na/K+ATPase) causing shift of K+ out of cell causing hyperkalemia

158
Q

Hyperosmolality effect on potassium

A

Shifts K+ out of cells causing hyperkalemia

159
Q

Cell lysis effect on potassium

A

Shifts K+ out of cells causing hyperkalemia

160
Q

Examples of processes that can cause cell lysis

A

crush injury

Rhabdomyolysis

Tumor lysis syndrome

161
Q

Alkalosis effect on potassium

A

Shifts K+ into cells causing hypokalemia

162
Q

Acidosis effect on potassium

A

Shifts K+ out of cells causing hyperkalemia

163
Q

β-adrenergic agonist effect on potassium

A

↑Na/K ATPase causing shift of K into cells causing hypokalemia

164
Q

β-blocker effect on potassium

A

↓ Na/K ATPase activity

Shifts K+ out of cells causing hyperkalemia

165
Q

Insulin effect on potassium

A

↑ Na/K ATPase causing K+ shift into cells causing hypokalemia

166
Q

High blood sugar effect on potassium

A

Insulin deficiency causes ↓ Na/K ATPase leading to K+ shift out of cells causing hyperkalemia

167
Q

Insulin potassium mnemonic

A

Insulin shift K into cells

168
Q

Succinylcholine effect on potassium

A

↑ risk of burns/muscle trauma causing shift of K+ out of cells causing hyperkalemia

169
Q

Hyperkalemia Mnemonic

A

Hyperkalemia? DO LAβSS

Digitalis

HyperOsmolality

Lysis

Acidosis

β-Blocker

High blood Sugar

Succinylcholine

170
Q

Conn Syndrome AKA

A

Primary hyperaldosteronism

171
Q

Symptoms of low serum [Na+]

4 listed

A

Nausea and malaise

Stupor

Coma

Seizures

172
Q

Symptoms of high serum [Na+]

3 listed

A

Irritability

Stupor

coma

173
Q

Symptoms of low serum [K+]

5 listed

A

U waves and flattened T waves on ECG

Arrhythmias

Muscle cramps

Spasm

Weakness

174
Q

Symptoms of high serum [K+]

3 listed

A

Wide QRS and peaked T waves on ECG

Arrhythmias

Muscle weakness

175
Q

Symptoms of low serum [Ca2+]

5 listed

A

Tetany

Seizures

QT prolongation

Twitching (Chvostek sign)

Spasm (Trousseau sign)

176
Q

Symptoms of high serum [Ca2+]

5 listed

A

Stones (renal)

Bones (pain)

Groans (abdominal pain)

Thrones (↑ urinary frequency)

Psychiatric overtones (anxiety, altered mental status)

177
Q

Symptoms of low serum [Mg2+]

4 listed

A

Tetany

Torsades de pointes

Hypokalemia

Hypocalcemia (when [Mg2+] < 1.2 mg/dL)

178
Q

Symptoms of high serum [Mg2+]

6 listed

A

↓DTRs

Lethargy

Bradycardia

Hypotension

Cardiac arrest

Hypocalcemia

179
Q

Symptoms of low serum [PO43-]

A

Bone loss

Osteomalacia (adults)

Rickets (children)

180
Q

Symptoms of high serum [PO43-]

A

Renal stones

Metastatic calcifications

Hypocalcemia

181
Q

BP in Bartter syndrome

A

Normal

182
Q

BP in Gitelman syndrome

A

normal

183
Q

BP in Liddle syndrome

A

↑

184
Q

BP in SAME

A

↑

185
Q

BP in SIADH

A

Normal/↑

186
Q

BP in Primary hyperaldosteronism

A

↑

187
Q

BP in Renin-secreting tumor

A

↑

188
Q

Plasma renin in Bartter syndrome

A

↑

189
Q

Plasma renin in Gitelman syndrome

A

↑

190
Q

Plasma renin in Liddle syndrome

A

↓

191
Q

Plasma renin in SAME

A

↓

192
Q

Plasma renin in SIADH

A

↓

193
Q

Plasma renin in Primary hyperaldosteronism

A

↓

194
Q

Plasma renin in Renin-secreting tumor

A

↑(important differentiating feature)

195
Q

Aldosterone in Bartter syndrome

A

↑

196
Q

Aldosterone in Gitelman syndrome

A

↑

197
Q

Aldosterone in Liddle syndrome

A

↓(important differentiating feature)

198
Q

Aldosterone in SAME

A

↓(important differentiating feature)

199
Q

Aldosterone in SIADH

A

↓

200
Q

Aldosterone in primary hyperaldosteronism

A

↑(important differentiating feature)

201
Q

Aldosterone in Renin-secreting tumor

A

↑

202
Q

Serum Mg2+ in Gitelman syndrome

A

↓

203
Q

Urine Ca2+ in Bartter syndrome

A

↑ (important differentiating feature)

204
Q

Urine Ca2+ in Gitelman syndrome

A

↓(important differentiating feature)

205
Q

pH in metabolic acidosis

A

↓

206
Q

pH in metabolic alkalosis

A

↑

207
Q

pH in respiratory acidosis

A

↓

208
Q

pH in respiratory alkalosis

A

↑

209
Q

PCO2 in metabolic acidosis

A

↓

210
Q

PCO2 in metabolic alkalosis

A

↑

211
Q

PCO2 in Respiratory acidosis

A

↑(1° disturbance)

212
Q

PCO2 in Respiratory alkalosis

A

↓(1° disturbance)

213
Q

[HCO3-] in metabolic acidosis

A

↓ (1° disturbance)

214
Q

[HCO3-] in metabolic alkalosis

A

↑ (1° disturbance)

215
Q

[HCO3-] in respiratory acidosis

A

↑

216
Q

[HCO3-] in respiratory alkalosis

A

↓

217
Q

Compensatory response to metabolic acidosis

A

Hyperventilation (immediate)

218
Q

Compensatory response to metabolic alkalosis

A

Hypoventilation (immediate)

219
Q

Compensatory response to respiratory acidosis

A

↑ renal [HCO3-] absorption (delayed)

220
Q

Compensatory response to respiratory alkalosis

A

↓ renal [HCO3-] absorption (delayed)

221
Q

Henderson-Hasselbach equation

A

pH=6.1 + log ([HCO3-]/0.03PCO2)

222
Q

How to predict the respiratory compensation for a simple metabolic acidosis

A

Can be calculated using the Winter’s Formula

If measured PCO2 > predicted CO2 → concomitant respiratory acidosis

If measured PCO2 < predicted CO2 → concomitant respiratory alkalosis

PCO2 = 1.5[HCO3-] + 8 +/- 2

223
Q

Acidosis and alkalosis flow chart

A

576

224
Q

Common causes of respiratory acidosis

A

Airway obstruction

Acute lung disease

Chronic lung disease

Opioids

Sedatives

Weakening of respiratory muscles

225
Q

Common causes of ↑ anion gap metabolic acidosis

A

MUDPILES

Methanol (formic acid)

Uremia

Diabetic ketoacidosis

Propylene glycol

Iron tablets or INH

Lactic acidosis

Ethylene glycol

Salicylates (late)

226
Q

Common causes of normal anion gap metabolic acidosis

A

HARDASS

Hyperalimentation

Addison disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion

227
Q

Common causes of respiratory alkalosis

A

Hyperventilation

Anxiety/panic attack

Hypoxemia (eg, high altitude)

Salicylates (early)

Tumor

Pulmonary embolism

228
Q

Common causes of metabolic alkalosis

A

H+ loss/HCO3- excess

Loop diuretics

Vomiting

Antacid use

Hyperaldosteronism

229
Q

Anion gap equation

A

Na - (Cl+HCO3) = AG

230
Q

What is renal tubular acidosis

A

Disorder of renal tubules that causes normal anion gap (hyperchloremic) metabolic acidosis

231
Q

Types of renal tubular acidosis

A

Distal renal tubular acidosis (type 1)

Proximal renal tubular acidosis (type 2)

Hyperkalemic tubular acidosis (type 4)

232
Q

What is Type 1 renal acidosis

A

Distal renal tubular acidosis

233
Q

What is type 2 renal acidosis?

A

Proximal renal tubular acidosis

234
Q

What is type 3 renal acidosis?

A

IDK?

235
Q

What is type 4 renal acidosis?

A

Hyperkalemic tubular acidosis

236
Q

Describe the defect in Distal renal tubular acidosis

A

Inability of α-intercalated cells to secrete H+ → no new HCO3- is generated → metabolic acidosis

237
Q

Describe the defect in proximal renal tubular acidosis

A

Defect in PCT HCO3- reabsorption → ↑ excretion of HCO3- in urine → metabolic acidosis

Urine can be acidified by α-intercalated cells in the collecting duct, but not enough to overcome the increased excretion of HCO3- → metabolic acidosis

238
Q

Describe the defect in Hyperkalemic tubular acidosis

A

Hypoaldosteronism or aldosterone resistance;

Hyperkalemia → ↓ NH3 synthesis in PCT →↓ NH4+ excretion

239
Q

Describe urine pH in distal renal tubular acidosis

A

> 5.5

240
Q

Describe urine pH in Proximal renal tubular acidosis

A

<5.5

241
Q

Describe urine pH in Hyperkalemic tubular acidosis (type 4)

A

< 5.5 (or variable)

242
Q

Serum K in distal renal tubular acidosis

A

↓

243
Q

Serum K in proximal renal tubular acidosis

A

↓

244
Q

Serum K in hyperkalemic tubular acidosis

A

↑

245
Q

Causes of distal renal tubular acidosis

4 listed

A

Amphotericin B toxicity

Analgesic nephropathy

Congenital anomalies (obstruction) of urinary tract

Autoimmune diseases (eg, SLE)

246
Q

Causes of proximal renal tubular acidosis

A

Fanconi syndrome

Multiple myeloma

Carbonic anhydrase inhibitors

247
Q

Causes of hyperkalemic tubular acidosis

A

↓ aldosterone producton (eg, diabetic hypereninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency)

Or aldosterone resistance (eg, K+ sparring diuretics, neprhopathy dut to obstruction, TMP-SMX)

248
Q

Distal renal tubular acidosis associations

A

↑ risk for calcium phosphate kidney stones (due to ↑ urine pH and ↑ bone turnover)

249
Q

Proximal renal tubular acidosis associations

A

↑ risk for hypophosphatemic rickets (in Fanconi syndrome)

250
Q

What are casts in urine?

A

Presence of casts indicates that hematuria/pyuria is glomerular or renal tubular origin

251
Q

Are there urine casts in bladder cancer or kidney stones?

A

No

252
Q

ATN AKA

A

Acute tubular necrosis

253
Q

What is reabsorbed in the PCT?

9 listed

A

Reabsorbs all glucose and amino acids and most HCO3-, Na, Cl, PO4, K, H2O and uric acid

254
Q

PTH and phosphate

A

PTH inhibits Na/PO4 cotransport → PO4 excretion

PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means morephosphate is excreted through the urine. However,PTH enhances the uptake of phosphate from the intestine and bones into the blood. … The absorption of phosphate is not as dependent on vitamin D as is that of calcium.

255
Q

ATII and contraction alkalosis

A

ATII - stimulates Na/H exchange → ↑Na, H2O, and HCO3 reabsorption (permitting contraction alkalosis)

256
Q

Thick ascending loop of Henle resorbs?

A

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

257
Q

Thick ascending loop of Henle % Na resorbed

A

10-20%

258
Q

Na reabsorption in early PCT

A

65-80% Na reabsorbed

259
Q

Thick ascending loop of Henle Reabsorbs?

A

Reabsorbs Na, K and Cl

Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through (+) lumen potential generated by K backleak

260
Q

Aldosterone acts on what in the where?

A

Aldosterone - acts on mineralocorticoid receptor → mRNA → protein synthesis

in the collecting duct

261
Q

Principal cells of the CD

A

In principal cells ↑ apical K conductance, ↑ Na/K pump, ↑ epithelial Na channel (ENaC activity) → lumen negativity → K secretion

262
Q

Describe α-intercalated cells in the CD

A

lumen negativity → ↑H+ ATPase activity → ↑H+ secretion → ↑ HCO3/Cl exchanger activity

263
Q

ADH actions in the CD

A

ADH - acts at V2 receptor → insertion of aquaporin H2O channels on apical side

CVPR (93 decks)

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