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CPR > Renal > Flashcards

Renal Flashcards

1
Q

Filtration and ultrafiltrate

A

Filtration by glomerulus forms ultrafiltrate –> same composition of blood except for protein and cells

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2
Q

Sequential renal blood flow

A

Aorta –> Renal artery –> Interlobar arteries –> arcuate artery –> interlobular artery –> afferent arteriole –> glomerular capillaries –> efferent arteriole –> post glomerular capillaries –> venules –> interlobular vein –. Arcuate vein –> interlobar vein –> renal vein

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3
Q

Glomerular and postglomerular capillaries

A

2 capillary beds

Glomerular = filtration

Postglomerular = Absorption

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4
Q

Electrical charge and filtration barriers

A

Negatively charged substances pass less regularly than positve

Electrostatic restriction

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5
Q

More prominent role? Electrostatic restriction or size restriction

A

Electrostatic

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6
Q

Hallmark of gomerular injury and why?

A

Protein in urine

Filtration barrier damaged and more protein being filtered than it can be reabsorbed

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7
Q

Parallel arrangement of filtration barrier capillaries

A

Minimizes hydrostatic pressure drop between entrance and exit

Large surface area for filtration

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8
Q

Filtration forces

A

Glomerular capillary hydrostatic pressure - filtration

Bowmans Space hydrostatic pressure - Absorption

Bowmans space oncotic pressure = 0 - Filtration

Glomerular capillary oncotic pressure - Reabsorption

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9
Q

Difference between capillaries in Renal vs non renal

A

Non renal -

Hydrostatic pressure decreases across length Filtration vs reabsorption changes along length

Filtration = Absorption

Renal - Hydrostatic pressure nearly constant Glomerular oncotic pressure increases along length, never higher than hydrostatic pressure

Bowmans space P is constant and oncotic is 0

NEVER ABSORPTION ALONG GLOMERULAR WALL

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10
Q

Increasing GC plasma flow results in —>

A

More plasma for filtration which slows buildup of proteins in GC –> Lower GC oncotic pressure –> More filtration –> Higher GFR

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11
Q

Forces in peritubular capillaries

A

Capillary hydrostatic pressure (efferent arteriole)

High Plasma oncotic pressure

Oncotic pressure > hydrostatic pressure = NET FILTRATION

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12
Q

Vasoconstriction of afferent arteriole = ?

A

Decreased RBF

Decreased GFR

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13
Q

Increased efferent arteriole resistance = ?

A

Decreases RBF

Increases GFR

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14
Q

Afferent arteriole dilation = ?

A

Increased GFR

Increased RBF

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15
Q

Nitric Oxide effect on A and E arteriole

A

A - Dilate

E - Dilate

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16
Q

Prostaglandin I2 effect on A and E arteriole

A

A - Dilate

E - Dilate

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17
Q

Prostaglandin E2 effect on A and E arteriole

A

A - Dilate

E - No effect

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18
Q

Angiotensin II effect on A and E arteriole

A

A - Constrict

E - Constrict

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19
Q

Vasopressin effect on A and E arteriole

A

A - Constrict

E - Constrict

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20
Q

NE effect on A and E arteriole

A

A - Constrict

E - Constrict

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21
Q

Endothelin effect on A and E arteriole

A

A - Constrict

E - Constrict

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22
Q

Thromboxane effect on A and E arteriole

A

A - Constrict

E - Constrict

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23
Q

ANP effect on A and E arteriole

A

A - Dilate

E - Constrict/no effect

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24
Q

Autoregulation mechanisms of RBF and GFR

A

Myogenic

Tubuloglomerular feedback mechanism

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25
Q

Myogenic

A

Increased constriction if pressure/flow increased

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26
Q

Tubuloglomerular feedback mechanism

A

Increased GFR –> increased flow through tubule and macula dense –> Paracrine signal from MD to afferent arteriole –> Constriction –> Increased resistance –> decreased hydrostatic pressure –> Decreased GFR

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27
Q

How much of filtered Na load is reabsorbed

A

>99%

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28
Q

Proximal tubule Na reabsorption %

A

67%

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29
Q

Loop of Henle Na reabsorption %

A

Intermediate capacity 25%

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30
Q

Dista nephron (DCT and CCT) Na reabsorption %

A

Low capacity ~8%

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31
Q

Proximal tubule Na transporters

A

Na co-transporters

Na/H exchanger

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32
Q

Thick ascending limb Na transporters

A

NKCC

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33
Q

DCT Na transporters

A

Na-Cl co trasporter

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34
Q

Collecting duct Na transporter

A

ENaC

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35
Q

Basolateral membrane Na tranport

A

Na/K ATPase

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36
Q

Glucose handling early proximal tubule

A

Apical SGLT2 - Low affinity, high capacity

Na-glu transport Basolateral - GLUT1

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37
Q

Glucose handling late proximal tubule

A

Apical SGLT1 - High affinity, low capacity 2Na-Glu Basolateral GLUT2

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38
Q

Glucosuria - DM

A

Amount of glucose exceeds threshold and Tm = glucose excreted in urine

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39
Q

Glucosuria - Defects in NaGlu tranporters

A

Familial renal Glucosuria

Glucose-Galactose malabsorption syndrome

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40
Q

Familial renal glucosuria

A

Mutation in SGLT2 decreases transport capacity –> decrease Tm –> glucose excreted

Can result in decreased plasma glucose concentration

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41
Q

Glucose galactose malabsorption syndrome

A

Mutation of SGLT1 – decrease transport capacity –> slight lower Tm –> mild glucosuria

Can effect gut absorption

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42
Q

Urea diffusion

A

Urea remains in renal tubules but concentration increases due to water exit –> travels down concentration gradient to renal venous sytem

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43
Q

PAH and Kidney

A

PAH is filtered and secreted by renal tubules, not reabsorbed

Good measure of Renal plasma flow

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44
Q

[K]ecf

A

Very closely regulated

3.9 < Normal < 4.5

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45
Q

[K]ecf depends on…

A

Total body content of K (input - output)

Distribution between ICF and ECF (Na/K ATPase)

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46
Q

Hormones that cause K uptake into cells

A

Insulin B agonists

Aldosterone

Cause increased activation of Na/K ATPase

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47
Q

pH changes and K

A

Lower pH = Decrease K uptake

Higher pH = Increased K uptake into cels

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48
Q

Glomerular filtration of potassium

A

Freely filtered

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49
Q

Kidney reabsorption of K

A

>90% reabsorbed by proximal tubule and Thick ascending limb

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50
Q

Kidney secretion of K

A

Distal tubule and CCT

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51
Q

Regulation of K excretion

A

Occurs in Distal tubule and CCT

Based on levels of K secretion

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52
Q

Proximal tubule K transport

A

Passive reabsorption H20 reabsorption –> increased K concentration –> K reabsorption down concentration gradient

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53
Q

Loop of Henle K transport

A

Thick ascending limb Apical NKCC

Basolateral K channel

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54
Q

Collecting tubule and collecting duct K transport - a Intercalated cells

A

ICT, CCT, MCD

Apical uptake via H/K ATPase Basolateral K channel

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55
Q

Collecting tubule and collecting duct K transport - principal cells

A

ICT and CCT - active secretion K uptake from peritubular interstitium via basolateral Na/K ATPase

Passive apical K flux

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56
Q

Increased Na/K ATPase activity and K handling

A

Increased intracellular K concentration –> K secretion

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57
Q

Increased tubular flow and K handing

A

Secreted K flushed downstream –> Low K concentration in lumen –> Increase K secretion

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58
Q

Increased negative charge of lumen

A

K secretion due to electrical gradient

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59
Q

K wasting diuretics

A

Agents that block Na reabsorption by proximal tubule of loop of henle Increased tubular flow in distal tubule and collecting duct = K secretion

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60
Q

K sparing diuretics

A

Agents that inhibit Na reabsorption in distal nephron

Tubular flow secretion effect minimized because of tubular electrical status (more positive)

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61
Q

Physiological regulation of K excretion

A

Increased [K] intake –> Increased [K] plasma –> Aldosterone –> Increased distal nephron K secretion –> Increased K excretion Increased [K] intake –> Increased [K] plasma –> Increased distal nephron K secretion –> Increased K excretion

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62
Q

Water handling in proximal tubule

A

AQP1 in apical and basolateral membrane

Promotes water leaving tubules and entering interstitium

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63
Q

Water handling in Loop of Henle

A

Descending limb = water reabsorption

Ascending limb - Water impermeable DCT - Water impermeable

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64
Q

No ADH - collecting duct cells

A

Cells impermeable to water - no basolateral AQP

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65
Q

ADH effect

A

AQP-2 channels inserted onto apical membrane, cells are water permeable

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66
Q

Net effect of kidney response to water intake

A

Formation of dilute urine

Proximal tubule - Isosmotic reabsorption of Na/water

Descending limb - Water reabsorption due to increasing medullary osmolarity (via TAL)

Turn of Loop - Concentrated tubular fluid that is isosmotic to medullary intersititum

Ascending limb - Solute reabsorption and fluid becomes hyposmotic

Slight Na reabsorption in distal nephron

NET EFFECT: Low osmolarity urine excreted

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67
Q

Net effect of kidney to dehydration

A

Requires ADH Formation of dilute urine that reaches distal tubule

CCT - Water permeable tubule comes under effect of intersitial osmolarity –> water reabsorption

Medullary collecting duct - Also water permeable, water reabsorbed

Highly concentrated urine excreted

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68
Q

Synthesis and release of ADH

A

Synthesized in supraoptic and paraventricular neurons of hypothalamus

Stored in nerve endings in posterior pituitary

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69
Q

ADH regulation - osmoreceptors

A

increases in plasma osmolarity = ADH release

Small plasma changes = large ADH release

Most sensitive ADH regulator

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70
Q

ADH regulation - baroreceptors

A

Decrease in blood volume sensed by baroreceptors –> increase ADH release

Need large decrease in blood volume

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71
Q

Other factors that increase ADH secretion

A

Vomiting

Nausea

Morphine

Nicotine

Cyclophosphamide

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72
Q

Factors that decrease ADH secretion

A

Alcohol Clonidine Haloperidol

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73
Q

SIADH

A

Excessive ADH secretion for given plasma osmolarity

Retain water in excess of solute = decreased plasma osmolarity

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74
Q

Diabietes Insipidus

A

Patients produce large volume of dilute urine Increased plasma osmolarity

Neurogenic - Deficient ADH secretion

Nephrogenic - Insensitivity of kidney tubules to ADH

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75
Q

Actions of AngII

A

Retention of Na

Vasoconstriction

Promote acquisition and retention of water

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76
Q

AngII retention of Na

A

Aldosterone activation –> Na reabsorption in collecting duct

Stimulate Na/H exchange –> proximal tubular Na reabsorption

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77
Q

AngII Vasoconstriction

A

Direct effect on vascular smooth muscle

Increase TPR to increase systemic arterial pressure

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78
Q

AngII promote acquisition and retention of water

A

Stimulate thirst –> acquire water

Stimulate ADH release from hypothalamus –> water retention

Decrease medullary blood flow

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79
Q

Aldosterone: Stimuli, action, mechanism

A

Stimuli: Increased AngII, decreased plasma [Na], increased plasma [K]

Action: Increase Na reabsorption by collecting duct

Mechanism: Promote Na entry through apical ENaC and basolateral Na/K ATPase.

PRINCIPAL CELL OF COLLECTING DUCT

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80
Q

Catecholamine: Stimuli, action, mechanism

A

Stimuli: Activation of SNS

Action: Increase Na reabsorption by proximal tubule

Mechanism: Activate Na/H exchange

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81
Q

Endogenous digitalis like substance: Stimuli, action, mechanism

A

Stimuli: Increased ECF volume

Action: Decrease Na reabsorption by all nephron segments

Mechanism: Direct effect to inhibit basolateral Na/K ATPase

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82
Q

Glomerular-tubular balance

A

Proximal tubule reabsorbs constant fraction, 67%, of filtered Na

Increased GFR –> increased oncotic pressure of peritubular capillaries –> increased reabsorption

Reduces impact of increased filtered load on solute/water delivery to distal nephron

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83
Q

Responses to abrupt increase in Na intake

A

Increased GFR

Decreased Na reabsorption

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84
Q

Factors that increase GFR in response to Na increase

A

Increased Na = Increased ECF = decreased plasma oncotic pressure = Increased GFR via Starling

Increased arterial pressure –> increased capillary hydrostatic pressure –> increased GFR

Decreased AngII –> decreased arteriolar resistance –> increased RBF/GFR

Increased arterial pressure –> decreased SNS –> decreased arterioloar resistance –> Increased RBF/GFR

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85
Q

Factors that decrease tubular Na reabsorption in response to abrupt increase in Na intake

A

Decreased AngII –> decreased proximal tubule Na reabsorption (Na/H)

Decreased aldosterone –> decreased Na reabsorption in collecting duct

Decreased sympathetic tone –> decreased Na reabsorption in proximal tubule

Increased blood volume –> increased ANP –> decreased Na reabsorption in collecting duct

Increased endogenous digitalis like substance –> Decreased Na reabsorption

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86
Q

Pressure Natriuresis

A

Increase in arterial pressure –> Increased Na excretion

Unknown mechanism

IMPAIRED IN HTN

Increased Na intake –> increased ECF volume –> increased arterial pressure –> increased Na excretion –> decreased ECF

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87
Q

Mechanisms of Renin release

A
  1. Low blood volume, JG cells secrete renin into circulation
  2. Decrease in perfusion across macula dense, message sent to JG to secrete renin
  3. Increased sympathetic activity (B1) via baroreceptors in carotid sinus
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88
Q

ANP stimuli, action, mechanism

A

Stimuli: Atrial stretch (High ECF)

Action: Decrease Na reabsorption by collecting duct

Mechanism: ENaC inhibitor

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89
Q

ANP actions

A
  1. Inhibit vasopressin release in hypothalamus
  2. Increase GFR a (vasodilation) and decrease Renin
  3. Inhibit Aldosterone
  4. Decrease BP via medulla oblongata
  5. Decrease Na reabsorption via ENaC inhibition
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90
Q

Aldosterone and Potassium

A

Aldo increases K secretion via compensation for increasing ENaC In collecting duct principal cells

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91
Q

Osmolality definition

A

Total solute concentration but comprised mainly of Sodium salts

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92
Q

Tonicity

A

Effective plasma osmolality

Osmolality of solutes that contribute to water distribution

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93
Q

Requirements to excrete excessive free water

A

Delivery of water/solutes to nephron dilution sites (TAL, DCT)

Proper function of diluting segments (channel function)

No ADH

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94
Q

Requirements for maximal urine concentration (water absorption)

A

Concentrated medullary interstitium (functioning TAL channels)

Presence of ADH

Normal response to ADH

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95
Q

Osmoregulation of ADH

A

Serum osmolality sensed by osmoreceptors in hypothalamus

Increase ADH and thirst Increase urine osmolality, water intake

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96
Q

Volume regulation of ADH

A

Effective tissue perfusion sensed by baroreceptors and macula densa

Activation of RAAS, Aldo, ANP, NE, ADH

Urine sodium and thirst affected

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97
Q

Hypovolemia definition

A

Decreased fluid volume due to decreased total body Na

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98
Q

Hypervolemia definition

A

Increased fluid volume due to increased total body sodium

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99
Q

Determinants of Hyponatremia

A

Plasma tonicity - water distribution

Volume status - Total body Na

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100
Q

Hypertonic hyponatremia osmolar definitions

A

Posm > 290

PNa < normal

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101
Q

Hypertonic hyponatremia definition/cause

A

Increased plasma osmolality with decreased Na concentration

Due to other effective osmole causing fluid movement from ICF –> ECF

Hyperglycemia, glycine, mannitol

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102
Q

Hypertonic hyponatremia treatment

A

Remove underlying cause

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103
Q

Isotonic hyponatremia

A

Lab artifact

Increased protein/lipid concentration that is sensed as decreased Na concentration

Old lab testing

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104
Q

Brain response to hyponatremia

A

Immediate effect - water gain (cerebral edema) and altered mental status (low osmolality)

Rapid adaptation - Loss of sodium/K/Cl to reduce edema (low osmolality)

Slow adaptation - Loss of organic osmolytes (low osmolality)

THERAPEUTIC INTERVENTION:

Slow correction = brain returns to normal osmolality

Rapid correction = Osmotic demyelination - no chill

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105
Q

Hypotonic hyponatremia - Definition and types

A

POsm < 290

PNa < 140

Due to excessive water either because of ADH or impaired water excretion

Hypovolemic Euvolemic Hypervolemic

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106
Q

Hypovolemic hypotonic hyponatremia - Pathogenesis

A

True volume depletion (ECF loss, Na and water)

ADH stimulation –> water retention –> restored ECF volume but NOT Na

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107
Q

Hypovolemic hypotonic hyponatremia - physical exam

A

Signs of volume depletion

Flat neck veins

Tachycardia

Hypotension

Orthostatic hypotension

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108
Q

Hypovolemic hypotonic hyponatremia - Causes

A

Volume losses: GI, blood

Insensible losses - sweating/burns

Renal losses - Loop diuretics, adrenal insufficiency, salt wasting nephropathies

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109
Q

Insensible losses in Hypovolemic hypotonic hyponatremia

A

Burns and sweating

Low Urine [Na] because RAAS active and Na reabsorption is maximal

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110
Q

Renal losses in Hypovolemic hypotonic hyponatremia

A

High urine [Na]

Sodium reabsorption not functioning

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111
Q

Euvolemic hypotonic hyponatremia

A

Euvolemic on exam

SIADH:

High urine Osm

High urine [Na]:

ADH –> water reabsorption –> volume increase –> decrease renin –> decrease RAAS –> decrease Na reabsorption

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112
Q

Primary polydipsia

A

Cause of euvolemic hypotonic hyponatremia

Excessive water intake that overwhelms excretory capacity of kidney

Urine Osm low due to ADH suppression

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113
Q

Hypervolemic hypotonic hyponatremia

A

ECF volume excess with decreased intravascular volume

EDEMATOUS STATES

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114
Q

Hypervolemic hypotonic hyponatremia causes - non renal

A

Heart failure

Liver cirrhosis

Nephrotic syndrome

ADH activated b/c low circulating volume

Urine Osm high b/c ADH

Urine [Na] low b/c RAAS activation

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115
Q

Hypervolemic hypotonic hyponatremia causes - renal

A

Advanced renal failure

Impaired free water excretion

Effective plasma Osm low b/c water retention

Total Plasma Osm may be high b/c excessive urea

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116
Q

Hypovolemic hypotonic hyponatremia treatment

A

Correct intravascular volume w/ isotonic fluid

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117
Q

Euvolemic hypotonic hyponatremia treatment

A

Correct underlying cause

SIADH - Water restrict, increase solute intake, V2 antagonist

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118
Q

Hypervolemic hypotonic hyponatremia treatment

A

Diuretics

Fluid restriction

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119
Q

Hyponatremia management risks

A

DO NOT TREAT QUICKLY

Avoid osmotic demyelination syndrome

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120
Q

Hypernatremia definition and general cause

A

Serum Na >145

Loss of free water

Occurs in patients who cannot express thirst of don’t have access to water

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121
Q

Diabetes insipidus

A

Decreased ADH action - nephrogenic or neurogenic

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122
Q

Central DI

A

Neurogenic

Insufficient release of ADH in response to increased Na osmolality

Lesion in hypothalamic osmoreceptors, supraoptic nuclei, or trauma/surgery

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123
Q

Nephrogenic DI

A

Reduced action of ADH at collecting tubule to due receptor/aquaporin mutation

Lithium

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124
Q

Hypernatremia etiology

A

Hypotonic fluid loss - Na/water loss but solute concentration is hypotonic to plasma osmolality If free water not replaced –> hypernatremia

Hypertonic sodium gain

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125
Q

4 Mechanisms of K balance

A

K intake through diet

GI losses (5-10% absorbed K secreted in GI)

Renal losses (90-95% K regulation)

Transcellular K shift (ECF vs ICF distribution)

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126
Q

Renal handling of K - PCT

A

Freely filtered in glomerulus 65-70% reabsorbed in proximal tubule via passive transport

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127
Q

Renal handling of K - TAL

A

NKCC channel reabsorption of K

K pumped into lumen in TAL to enhance K recycling and NKCC function

Apical K channel inhibited by ATP - More Na enters cell –> transported out by Na/K ATPase –> low ATP –> apical K activation –> NKCC function and more Na absorbed

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128
Q

Renal handling of K - Principal cell

A

K transported into cell by Na/K ATPase

Secreted into tubule via ROMK

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129
Q

Principal cell K transport governing factors

A
  1. Luminal electrical charge
  2. Luminal concentration gradient
  3. K permeability of luminal membrane
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130
Q

4 Main factors that affect K secretion into tubular fluid

A
  1. Aldosterone
  2. Plasma [K]
  3. Distal flow rate
  4. Distal Na delivery
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131
Q

Aldosterone and K secretion

A

Increases # open Na (ENaC) and K (ROMK) channels

Enhances Na/K ATPase activity

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132
Q

Plasma [K] and K secretion

A

Increased plasma K = enhanced Na/K ATPase activity

Increased # open K & Na channels

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133
Q

Distal flow rate and K secretion

A

Increased flow = more K washed away = increased K secretion via favorable gradient

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134
Q

Distal Na delivery and K secretion

A

Na through ENaC = more negative lumen = K secretion More ENaC absorption = more intracellular Na = enhanced Na/K ATPase = more K secreted

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135
Q

a-Intercalated cells and K handling

A

Reabsorption of K via apical H/K ATPase

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136
Q

Main etiologies of hypokalemia

A

Transcellular shift

GI losses

Renal losses

Poor intake

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137
Q

Hypokalemia and transcellular shift etiologies

A

Insulin B2 agonists

Alkalosis

Hypokalemic periodic paralysis

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138
Q

Hypokalemia and insulin

A

Stimulates Na/K ATPase –> more K secretion

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139
Q

Hypokalemia and B2 agonist

A

Increase Na/K ATPase activity –> K secretion

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140
Q

Hypokalemia and alkalosis

A

Alkalosis = high extracellular pH –> H will leave cell –> K enters cell to maintain electroneutrality

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141
Q

Hypokalemic periodic paralysis

A

Acute attacks precipitated by sudden movement of K into cells

Lowers plasma K significantly

Rest after exercise, stress (catecholamines), high carb meal (insulin)

Familial - autosomal dominant mutation Acquired - Thyrotoxicosis

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142
Q

Hypokalemia - GI losses

A

Associated with metabolic alkalosis due to HCL loss –> K entry into cells b/c H exit

Concurrent urinary losses: -

Aldosterone activation

Plasma Bicarb increase = too much Bicarb that can be absorbed –> Na pairs with bicarb –> increased distal delivery of Na –> K secretion

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143
Q

Hypokalemia renal losses categories

A

Metabolic alkalosis

Metabolic Acidosis

Magnesium

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144
Q

Hypokalemia w/ metabolic alkalosis categories

A

Normo-hypotension

Hypertension

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145
Q

Hypokalemia w/ metabolic alkalosis and normo-hypotension

A

Diuretics - Loop/Thiazide

Activation of aldosterone by volume depletion Increased distal delivery of Na (blocked absorption more proximally)

Salt wasting nephropathies

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146
Q

Bartters syndrom

A

THINK LOOP DIURETIC

Defect in solute reabsorption in TAL NKCC2, Luminal K channel, Basolateral Cl channel can be affected

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147
Q

Gitelman’s syndrome

A

THINK THIAZIDE DIURETIC

Defect in thizide sensitive NaCl cotransporter in DCT

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148
Q

Hypokalemia with metbolic alkalosis - Hypertension

A

Mineralocorticoid excess:

Primary hyperaldosteronism (adrenal tumor, BAH)

Glucocorticoid remedial aldosteronism

Renal artery stenosis

11BHSD2 deficiency

CAH

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149
Q

Liddle’s syndrome

A

Gain of function mutation in ENaC

Triad:

Hypertension - Metabolic alkalosis - Hypokalemia

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150
Q

Hypokalemia with metabolic acidosis types

A

Renal tubular acidosis

Nonreabsorbable anion

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151
Q

Hypokalemia with metabolic acidosis - Renal tubular acidosis

A

Hyperchloremic, non anion gap metabolic acidosis

  1. Distal hypokalemic RTA (type I): Impaired distal urine acidification. No protons pumped out = more K secreted
  2. Proximal (type II): Reduction in bicarb reabsorptive capacity –> all bicarb reabsorbed –> metabolic acidosis that inhibits Na reabsorption –> hypokalemia
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152
Q

Hypokalemia with metabolic acidosis - Nonreabsorbable ion

A

Non reabsorbable anion paired with Na –> reduced Na –> Increased distal delivery of Na

Diabetic ketoacidosis - Beta hydroxybuterate pairs with Na

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153
Q

Hypokalemia and Magnesium

A

Hypokalemia occurs in 40-60% of hypoMg diseases

Diseases that waste both K and Mg: Diarrhea, diuretics

Correct Mg to restore K

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154
Q

CV clinical manifestations of Hypokalemia

A

Cardiac arrhythmias:

Sinus bradycardia, AV block, Vtach/Vfib

Decrease amplitude of T wave, increase U wave amplitude

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155
Q

Muscular clinical manifestations of hypokalemia

A

Weakness and muscle cramps

Low K = hyperpolarized skeletal muscle cells = impaired contraction

Reduce blood flow by impairing NO release

Severe K depletion = respiratory weakness –> respiratory failure GI muscle weakness = ileus

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156
Q

Hormonal clinical manifestations of hypokalemia

A

Impaired insulin release and end organ sensitivity to insulin

Worsened glucose control in diabetic patients

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157
Q

Renal clinical manifestations of hypokalemia

A

Tubulointerstitial and cystic changes in parenchyma

Polyuria: Increased thirst and mild nephrogenic DI, concentrating ability impaired

HTN: Increased renal vascular resistance

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158
Q

Hypokalemia diagnosis: Metabolic acidosis + Low urinary K:creatinine

A

Stool losses

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159
Q

Hypokalemia diagnosis: Metabolic acidosis + High urinary K:creatinine

A

RTA

Nonreabsorbable ion

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160
Q

Hypokalemia diagnosis: Metabolic alkalosis + Low urinary K:creatinine

A

Vomiting

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161
Q

Hypokalemia diagnosis: Metabolic alkalosis + High urinary K:creatinine

A

Check BP and volume status

Low-normal BP/volume depleted - diuretics, salt wasting nephropathies

High BP/volume overload - Mineralocorticoid excess, Liddle’s

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162
Q

Main etiologies of hyperkalemia

A

Transcellular shift

Psuedohyperkalemia

Renal - Decreased urinary excretion

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163
Q

Pseudohyperkalemia

A

Elevation in measured serum K due to K movement out of cells during/after blood draw

Hemolysis Thrombocytosis Leukocytosis

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164
Q

Hyperkalemia transcellular shift - etiologies

A

Metabolic acidosis

Hyperglycemia and hyperosmolarity

Nonselective B antagonists

Exercise

Tissue breakdown

Digitalis toxicity

Hyperkalemic familial periodic paralysis

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165
Q

Hyperkalemia - metabolic acidosis

A

H will enter cell in order to buffer extracellular pH –> K will leave and enter ECF/blood vessels

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166
Q

Hyperkalemia - hyperglycemia/hyperosmolarity

A

Elevation in serum osmolality = H20 movement from ICF –> ECF = More K in cell –> K will move out of cell

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167
Q

Hyperkalemia - non selective B antagonists

A

Interfere with K uptake by B receptors

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168
Q

Hyperkalemia - Tissue breakdown

A

Rhabdomyolysis

Lysis of large tumor burden after chemo

Burns

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169
Q

Hyperkalemia and digitalis

A

Block Na/K ATPase

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170
Q

Hyperkalemia - renal etiology categories

A

Renal failure

Volume depletion with decreased distal Na delivery

Functional hypoaldosteronism

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171
Q

Hyperkalemia - renal failure

A

Able to maintain K with distal flow rate and aldosterone secretion is maintained

Hyperkalemia occurs in patients with decreased flow rate + excess K load/Aldo blocker

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172
Q

Hyperkalemia - decreased distal delivery of Na with volume depletion

A

Hypovolemia

Effective arterial volume depletion with ECF excess

Heart failure/liver cirrhosis

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173
Q

Hyperkalemia - functional hyoaldosteronisms

A

Low aldo or resistance to aldo effect

Mineralocorticoid deficiency: primary adrenal insufficiency, hyporeninemic hypoaldosteronism (low renin/aldo)

Tubulointerstitial disease: Sickle cell and urinary tract obstruction -

Distal hyperkalemic RTA - Impaired Na reabsorption reducing K/H secretion

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174
Q

Drug MoA that result in hyperkalemia

A

Block aldo activity - ACE-I, ARB, Aldo antagonists

Decreased renin release - B blocker, NSAIDs

Bind to ENaC - Amiloride, triamterene Calcineurin inhibitors

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175
Q

Clinical manifestations of hyperkalemia

A

Severe muscle weakness/paralysis

Cardiac arrhythmias/ECG abnormalities: BBB, AV block, sinus bradycardia, sinus arrest, Vtach/fib

Early - Tall T waves, short QT

Late - prolonged PR/QRS

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176
Q

Hyperkalemia diagnosis - High renin/low aldo

A

Adrenal insuffieciency

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177
Q

Hyperkalemia diagnosis - Low renin and aldo

A

Type IV RTA

Diabetic nephropathy

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178
Q

Hyperkalemia diagnosis- normal renin/high aldo

A

Aldo resistance

Tubuloinsterstitial disease - sickle cell/urinary obstruction

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179
Q

Treatment methods for hyperkalemia

A

Antagonizing membrane effects of K with Ca

Drive ECF K into cells

Remove excess K from body

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180
Q

Hyperkalemia treatment - Antagonize membrane effects of K with Ca

A

ONLY for patients with ECG changes or acute rise in serum K

CaCl2

Hyperkalemia induces membrane depolarization and inactivation of Na channels –> Ca antagonizes this effect

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181
Q

Hyperkalemia treatment - Drive K into cells

A

Insulin + glucose:

Insulin will activate Na/K ATPase, glucose prevents hypoglycemia

B2 agonist: Stimulate Na/K ATPase

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182
Q

Hyperkalemia treatment - K removal - Diuretics

A

Diuretics: Loop/thizides.

Combine with saline to maintain distal Na delivery and distal flow rate

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183
Q

Hyperkalemia treatment - K removal - Cation exchange resins

A

Uptake of K in exchange for cation

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184
Q

Hyperkalemia treatment - K removal - dialysis

A

Warranted when other measures are ineffective

Use when K rises too rapidly

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185
Q

Acute Kidney injury - definition

A

Abrupt loss of kidney function Retention of urea and other nitrogenous waste products Dysregulation of extracellular volume and electrolytes

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186
Q

AKI general categories

A

Pre renal

Intrinsic renal

Post renal

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187
Q

Pre renal AKI - major causes

A

True volume depletion

Decreased effective arterial blood volume

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188
Q

Pre renal AKI - true volume depletion

A

Loss of Na from ECF

GI losses, hemorrhagic shock, renal losses, cutaneous losses

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189
Q

Pre renal AKI - decreased effective arterial blood volume

A

Increased ECF but decreased blood volume sensed by baroreceptors –> edematous states: HF, cirrhosis, sepsis

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190
Q

Pre renal AKI GFR

A

Renal perfusion decreases –> homeostatic mechanisms activated

Afferent arteriolar vasodilation

Efferent arteriolar vasoconstriction

Increased filtration fraction = increased post glomerular oncotic pressure = increased salt/water

Activation of AngII and ADH = Low urine Na and concentrated urine

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191
Q

Pre renal AKI history/chart review

A

Vomiting Diarrhea GI bleed

HF, liver disease, sepsis

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192
Q

Pre renal AKI physical exam

A

Orthostatic hypotension, skin tenting, dry mucous membranes

Elevated JVP, edema, hypotension

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193
Q

Pre renal AKI lab workup

A

BUN:Creatinine >20:1

Urine osmolality > 500

Urine Na <10 Urine Cl <10

Urinalysis: No protein/blood/WBC, no casts no cells

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194
Q

FENa

A

Measures percent of filtered Na excreted in urine

<1% = patient will be responsive to volume therapy

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195
Q

Intrinsic Renal AKI types

A

Tubulointerstitial Vascular Glomerular

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196
Q

Acute tubular necrosis - Definition, affected area, risk factors

A

Most common cause of acute intrinsic kidney injury

Patch necrosis of proximal tubule and TAL: High metabolic activity so very sensitive to changes in renal perfusion

Risk factors: Volume depletion, CKD, NSAIDs, DM

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197
Q

Pathophysiology of acute tubular necrosis

A

Endothelial/epithelial injury

Intratubular obstruction

Changes in microvascular blood flow

Immunological factors

Tubular cells damaged so cannot absorb salt/water –> increased delivery of salts to macula densa –> afferent vasoconstriction to reduce salt wasting

No TGF = salt wasting and volume depletion = DEATH

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198
Q

Causes of acute tubular necrosis

A

Ischemia - Low BP, volume depletion, sepsis

Toxin - Radiocontrast media (risk with CKD, DM, hypotension)

Toxins

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199
Q

History/chart review for acute tubular necrosis

A

Prolonged hypotension in ICU –> ischemia

Radiocontrast exposure

Sepsis (infections)

Drugs - aminoglycosides, amphotericin B

Crush injuries

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200
Q

Acute tubular necrosis lab evaluations

A

BUN:Creatinine = 10-15:1

Urine Na and Cl >20

FENa >2% (more filtered Na being excreted)

Urine osm <450 May have low grade proteinuria (deficient protein reabsorption in proximal tubule)

Casts and epithelial cells

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201
Q

Acute interstitial nephritis definition and main causes

A

Inflammatory cell infiltration in kidney interstitium caused by immune response -

Medication -

Autoimmune -

Infection

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202
Q

Acute interstitial nephritis drug causes

A

NSAIDs Penicillins Cephalosporins Sulfonamides Rifampin Cipro PPI

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203
Q

Acute interstitial nephritis autoimmune and infection causes

A

Sjogrens Sarcoidosis Legionella, leptospira, CMV

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204
Q

Acute interstitial nephritis clinical presentation

A

Rash, fever, eosinophilia

Full triad only in ~10% patients

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205
Q

Acute interstitial nephritis lab evaluation

A

Acute rise in serum creatinine that temporarily correlates with drug administration

Peripheral eosinophilia

Eosinophiluria

Proteinuria

WBC and WBC casts

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206
Q

Acute tubular obstruction

A

Precipitation of substances in tubules:

Immunoglobulins

Calcium phosphate

Urate

Intratubular crystal precipitations from medications

Volume depletion and acidic urine

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207
Q

Acute tubular obstruction - Cast nephropathy

A

Occurs in multiple myeloma

Overproduction of immunoglobulin light chains that get filtered into urine, can block tubule

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208
Q

Acute tubular obstruction - Tumor lysis syndrome

A

Occurs following chemotherapy

Dead tumor cells release chemicals Intracellular release of uric acid, phosphate, potassium –> all levels high in blood

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209
Q

Acute tubular obstruction - phosphorus containing enemas

A

Bowel preparation for colonoscopy

Acute calcium deposition in tubules with associated interstitial inflammation

Highest risk in patients with underlying CKD

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210
Q

Lab evaluation - tumor lysis syndrome

A

Elevated serum uric acid, potassium, phosphorus

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211
Q

Lab evaluation - phosphate nephropathy

A

High phosphorus

Low calcium

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212
Q

Lab evaluation - Cast nephropathy

A

Elevated free light chains in serum

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213
Q

Vascular intrinsic renal disease causes

A

Renal atheroembolic disease

Vasculitis

Thrombotic microangiopathies

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214
Q

Renal atheroembolic disease

A

Occurs in patients with atherosclerotic disease who undergo aorta/large artery manipulation –> plaque breaks off and can occlude multiple small arteries

Low serum complement, eosinophilia, rash

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215
Q

Intrinsic vascular renal disease - vasculitis

A

Inflammation and necrosis of small arteries

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216
Q

Thrombotic microangiopathies

A

Endothelial injury –> platelet thrombi occluding small vessels –> ischemia Low platelets, hemolytic anemia -

HUS -

Thrombotic thrombocytopenia purpura -

Malignant HTN

Schistocytes (RBC fragments)

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217
Q

Post renal disease - obstructive uropathy

A

Obstruction of the flow of urine anywhere from renal pelvis to urethra

Calculi

Anatomic abnormalities (children)

BPH

Urethral stricture

Malignancy

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218
Q

Proteinuria and hematuria = ?

A

Glomerular disease

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219
Q

Muddy brown casts in sediment review

A

Acute tubular necrosis

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220
Q

White Blood cell casts in sediment review

A

Acute interstitial nephritis

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221
Q

Dysmorphic RBC, RBC casts, WBC casts in sediment review

A

RPGN

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222
Q

AKI complications - uremia

A

Nausea

Vomiting

Anorexia

Dysguesia

Altered cognition

Pericarditis

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223
Q

AKI electrolyte abnormalities

A

Hyperkalemia (aminoglycosides and cisplatin = hypokalemia via increased flow)

Metabolic acidosis

ECF volume excess

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224
Q

Renal causes of Secondary HTN

A

Renovascular HTN

Renal parenchymal HTN

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225
Q

Renovascular HTN

A

HTN caused by renal artery stenosis

Atherosclerosis (75-90%)

Fibromuscular dysplasia (10-25%)

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226
Q

Renovascular HTN pathophysiology

A

Reduced renal perfusion –> RAAS activation –> AngII mediated vasoconstriction, ADH, Aldo

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227
Q

Renovascular HTN patient history/physical exam

A

Onset in 3-5th decade = FMD

>55yo = Atherosclerotic disease

Sudden onset of uncontrolled HTN

Malignant HTN

Physical: Epigastric bruit

Acute unexplained rise in serum creatinine induced

Asymmetric renal size

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228
Q

Renovascular HTN lab evaluation and imaging

A

Elevated renin and Aldosterone

MRA to asses vessels, contraindicated in high stage CKD

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229
Q

Renovascular HTN treatment - FMD

A

BP meds Lipid lowering meds

FMD - ACE-I or ARB –> percutaneous transluminal angioplasty if ineffective

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230
Q

Renovascular HTN treatment - atherosclerotic disease

A

ACE-I or ARB Lipid lowering meds

Anti platelet therapy

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231
Q

Renal Parenchymal HTN

A

Common feature in acute and CKD

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232
Q

Renal parenchymal HTN - Acute glomerular disease

A

Volume overload and suppression of RAAS

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233
Q

Renal parenchymal HTN - acute vascular disease

A

Ischemic activation of RAAS

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234
Q

Renal parenchymal HTN - CKD

A

Multifactorial pathogenisis

Volume expansion via Na/water retention SNS activation RAAS activation

Secondary hyperPTH Endothelial cell dysfunction

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235
Q

Renal parenchymal HTN - CKD treatment

A

ACE-I/ARB slow GFR decline

Diuretic for volume removal

CCB if neeed

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236
Q

Primary hyperaldosteronism

A

Autonomous production of aldosterone

Adrenal adenoma

Bilateral adrenal hyperplasia

Adrenal carcinoma

Triad: HTN, unexplained hypokalemia, metabolic alkalosis

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237
Q

Primary hyperaldosteronism diagnosis

A

[Plasma aldosterone] : Plasma renin activity Ratio >35-50 and PAC >15 = primary hyperaldosteronism

Discontinue aldo antagonists for accurate results

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238
Q

Primary hyperaldosteronism confirmatory testing

A

Na loading test: If Aldo still high then primary hyperaldosteronism

Isotonic saline administration: Aldo should fall <5

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239
Q

Primary hyperaldosteronism treatment - unilateral adenoma, BAH

A

Unilateral adenoma - Laparoscopic surgical removal

BAH - Spironolactone/other aldo antagonists

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240
Q

Cushings syndrome

A

Excess exogenous or endogenous glucocorticoids

Exogenous administration

Endogenous: Pituitary adenoma, ectopic ACTH production, adrenal adenoma

241
Q

Cushings syndrome clinical features

A

Centripetal obesity

Moon facies

Skin atrophy/abdominal striae

Acne and hirsutism

Proximal muscle weakness

HTN

Glucose intolerance

242
Q

Cushings syndrome diagnosis

A

24hr urinary cortisol excretion

Late evening salivary cortisol

Low dose dexamethasone suppression test

243
Q

Cushings syndrome treatment

A

Cushings disease/pituitary adenoma - Irradiation or resection

Adrenal tumor/ectopic ACTH - Removal

244
Q

Pheochromocytoma

A

Catecholamine secreting tumor

Headache, sweating, palpitations

Diagnosis: - Urinary catecholamines - Fractioned plasma metanephrines

245
Q

Pheochromocytoma treatment

A

Surgical removal of tumor BP control before surgery -

Phenoxybenzamine/Phenotlamine -

Beta blockers after adequate alpha blockade

246
Q

Obstructive sleep apnea

A

Obesity, obstructive sleep apnea and HTN association

SNS abnormalities

Treatment: Weight loss

CPAP

Uvulopalatopharyngoplasty

247
Q

CKD definition

A

Presence of EITHER: Kidney damage

Decreased kidney function for > 3 months with decreased GFR

248
Q

Clinical markers of kidney damage in CKD

A

Proteinuria - >150mg protein, >30mg albumin

Glomerular hematuria

Imaging - polycystic kidney disease, hydronephrosis, small kidney w/thinned cortices

249
Q

Creatinine: Definition, use, limitations

A

Metabolism of creatine in skeletal muscle and dietary meat

Freely filtered, not absorbed

Limitations: Little muscle mass, Secretion by organic pathway in PCT, Does not detect early GFR changes

250
Q

CKD stages

A

Stage I: Kidney damage w/normal GFR

Stage II: Kidney damage w/ mild decreased GFR

Stage III: Moderate GFR decrease (30-59)

Stage IV: Severe GFR decrease (15-29)

Stage V: Kidney failure. <15

251
Q

CKD causes - tubulointerstitial diseases

A

PKD

Autoimmune: Sjogrens, Sarcoidosis

Reflux Nephropathy

252
Q

CKD - PKD

A

Autosomal dominant polycystic kidney disease

Will progress to kidney failure

253
Q

CKD autoimmune disease

A

Sjogrens Sarcoidosis: Inflammatory infiltrates in tubulointerstitium

254
Q

CKD reflux nephropathy

A

Vesicouteral reflux

Passage of urine from bladder to upper urinary tract

Inadequate closure of ureterovesical junction

255
Q

CKD vascular causes

A

Hypertensive vasculopathy - chronic HTN –> thickening and narrowing of large arteries and glomerular arterioles

Renovascular disease - Renal artery stenosis

Renal atheroembolic disease - Emboli caused by large artery manipulation

256
Q

CKD glomerular disease

A

Diabetic nephropathy

Nephritic/nephrotic

257
Q

CKD post renal causes

A

Obstructive uropathy

Prolonged obstruction –> parenchymal loss

Loss of nephron mass due to compression from reflux of urine

258
Q

Pathophysiology of CKD

A

Initial damage to kidney (tubulointerstitial, vascular, glomerular, obstructive) –> renal function maintained by hyperfiltration –> ongoing hyperfiltration –> glomerular capillary HTN –> cytokine activation and podocyte dysfunction –> proteinuria/glomerular sclerosis/tubulointerstitial fibrosis –> renal scarring

259
Q

CKD and diabetes mellitus clinical characteristics

A

Glomerulopathy: mesangial expansion, BM thickening, glomerulosclerosis

Hyperfiltration and golmerular capillary HTN

Microalbuminuria

Overt proteinuria

260
Q

Pathogenesis of diabetic nephropathy

A

Glomerular hyperfiltration

Hyperglycemia and AGE’s

Elevated prorenin

Impaired podocyte-specific insulin signaling

261
Q

CKD consequences - Hypertension

A

Present in 80-85% CKD

Na retention

SNS activation

RAAS activation

Secondary hyperPTH –> increased Ca –> vasoconstriction Impaired NO synthesis so reduced vasodilation

262
Q

CKD consequences - mineral bone disorder

A

Decreased GFR = decreased phosphorus excretion Increased phosphorus = FGF23 increase (to excrete phosphorus) –> FGF23 inhibits 1a-hydroxylase –> decreased calcitrol

Decreased calcitrol –> decreased intestinal Ca absorption –> PTH increase

Vascular calcification

Renal osteodystrophy

263
Q

Consequences of CKD - anemia

A

Kidney damage = decreased erythropoetin

264
Q

Risk factors for CKD –> ESRD

A

Proteinuria HTN

Underlying disease

AA

Male

Obesity (increased glomerular capillary pressure)

Dyslipidemia

SMoking

Hyperphosphatemia

Metabolic acidosis: Bicarb supplementation = good

High protein diet (increased capillary pressure)

Hyperuricemia

265
Q

Interventions that slow CKD progression

A

BP control

Renin-angiotensin-aldosterone antagonism -

Reduce BP - Decrease glomerular capillary pressure

Phosphorus control

Treat metabolic acidosis

Correct anemia

Smoking cessation

Statins

Low protein diet

Treat underlying disease

266
Q

Arteriovenous fistula

A

Connection between artery and vein to arterialize vein and increase blood flow for dialysis needle access

Longest lifespan

Low infection rate

Preferred access

267
Q

Arteriovenous graft

A

Performed when vasculature not able to permit AVF creation

Higher rate of thrombosis and infection

268
Q

Tunneled vascular catheter

A

Least desirable

Highest infection rate

Increased risk of great vessel stenosis

269
Q

Epithelial cells in glomerulus - Podocytes

A

Lines outer aspects of capillary loops

Maintains loop shape

Provides size and charge barrier to filtrate

Maintains GBM

270
Q

Nephrotic syndrome: Definition and components

A

Clinical condition due to DYSFUNCTION OF PODOCYTE

  1. Proteinuria >3.5gm/24hr
  2. Hypoalbuminemia
  3. Hyperlipidemia with lipiduria
  4. Generalized edema
271
Q

H&E stain use

A

General stain

Good for inflammatory cells

272
Q

PAS stain use

A

Mesangium

BM

273
Q

Silver stain use

A

BM

274
Q

Trichrome stain use

A

Fibrosis, necrosis

275
Q

Pathogenesis of immune complex mediated renal diseases - proposed mechanisms

A

Ag/Ab complexes form in blood and deposit in renal tissue

Circulating Ag deposited in kidney, Ab binds Protein intrinsic to kidney acts as auto antigen, Ab recognizes and binds

276
Q

Pathogenesis of immune complex mediated GN

A

Activation of complement –> cytokines/chemokines, recruitment of inflammatory cells –> damage to renal tissue

277
Q

Nephrotic syndrome - glomerular proteinuria

A

Increased filtration of macromolecules across glomerular capillaries

Podocyte abnormality

278
Q

Nephrotic syndrome - hypoalbuminemia

A

Urinary albumin loss = decreased blood albumin

279
Q

Nephrotic syndrome - edema

A

Low blood protein = fluid flow to ecf = edema RAAS activation = Na retention, sympathetic stimulation

280
Q

Nephrotic syndrome - hyperlipidemia/lipiduria

A

Decreased oncotic pressure stimulates hepatic lipoprotein synthesis –> hypercholestrolemia, hypertrigliceridemia

Lipid in urine trapped in protein material in renal tubules: Maltese crosses under polarized light

281
Q

Nephrotic syndrome complications - altered coagulation/thromboembolism

A

Loss of anticoagulation factors through GC

Volume depletion from diuretics –> decreased oncotic pressure –> hemoconcentration and increased platelet aggregation

Thrombus formation - hemoconcentration in post glomerular circulation

282
Q

Nephrotic syndrome complications - infection

A

Ig loss in urine

283
Q

Generalized treatment of Nephrotic syndrome

A

ACE-I or ARB: Reduce intraglomerular pressure, reduce proteinuria

Loop diuretics, low Na diet

BP control <130/80

Statin for hyperlipidemia

284
Q

Minimal change disease epidemiology and etiology

A

Most common cause of nephrotic syndrome in children Etiology: Idiopathic, Drugs (NSAIDs), Neoplasm

285
Q

Minimal change disease pathogenesis

A

Exact cause unknown

Key feature: Podocyte injury -

Systemic T cell dysfunction -

Production of glomerular permeability factor –> podocyte injury –> effacement of foot processes = proteinuria

286
Q

Minimal change disease Biopsy finding: Light microscopy, immunofluorescence, EM

A

Light microscopy: Normal

Immunofluorescence: Negative

EM: Diffuse effacement of podocyte foot processes

287
Q

Clinical course of Minimal change disease

A

Nephrotic syndrome

Untreated MCD associated with mortality due to infection or thromboembolism

Good prognosis, no progression

288
Q

Minimal change disease treatment

A

All receive nonspecific Rx: Diuretics, low Na, BP control

High dose steroids (prednisone)

Cyclophosphamide - steroid dependent patients

Cyclosporine - Steroid resistant

289
Q

FSGS

A

Focal segmental glomerulosclerosis

Most common cause of nephrotic syndrome in adults

Increased incidence in AA and males

290
Q

FSGS etiology - primary

A

Idiopathic

Genetic/Familial: Genetic defect in genes that code slit diaphragm proteins in foot processes of podocytes

291
Q

FSGS etiology - secondary

A

Heterogenous - Occurs in many forms of renal injury and systemic disease

Loss of renal mass, obesity, HIV, sickle cell, drugs

Often presents with nephrotic range proteinuria but not full syndrome

292
Q

Primary FSGS pathogenesis

A

Immune dysregulation/T cell function

Circulating toxin

293
Q

Secondary FSGS pathogenesis

A

Hyperfiltration+increased glomerular capillary pressure: reduced renal mass, obesity, sickle cell

Direct podocyte injury from virus/drugs: HIV, pamidronate/heroin

294
Q

FSGS biopsy results

A

Light microscopy: Focal glomeruli with scarring/sclerosis of glomerular capillary tuft

IF: Trapping of C3/IgM in areas of sclerosis

EM: Accumulation of matrix material, cells, plasma protein in sclerotic area

No immune deposits

Primary = diffuse effacement of podocyte foot processes

Secondary = patchy effacement of foot processes

295
Q

Clinical course primary FSGS

A

Mat present with acute or insidious onset

Hematuria in 30% patients, HTN, variable degrees of reduced function

No complement abnormalities

296
Q

Secondary FSGS clinical course

A

Always presents with insidious onset

Full nephrotic syndrome NOT always present

297
Q

Untreated primary FSGS and clinical course

A

Follows progressive course to ESRD

298
Q

Risk factors for primary FSGS progression

A

High level proteinuria

Reduced renal function

Presence of tubulointerstitial fibrosis

299
Q

Primary FSGS treatment

A

ACE-I, ARB, loop, low Na, BP control, statin

High dose steroids

Cyclophoshamide/cyclosporine

No response to therapies = slit diaphragm mutations

300
Q

Secondary FSGS treatment

A

ACE-I, ARB, loop, BP control, low Na, statin

Treat underlying disease - Weight loss - Anti viral -

Discontinue bad drugs

301
Q

Membranous nephropathy etiology

A

Primary/idiopathic (70%)

Secondary (30%) - Drugs/Malignancy/SLE/Infections

302
Q

Membranous nephropathy pathogenesis

A

Primary - Autoimmune - Circulating IgG antibodies directed against renal tissue (Type M phospholipase A2 receptor on podocyte foot processes)

Secondary - Circulating IgG Ab directed against extrinsic antigens (viral proteins, tumor proteins, drug)

303
Q

Membranous nephropathy specific pathogenesis

A

Immune complex formation activates complement cascade

MAC inserts into podocyte membrance

Podocyte foot process effacement

Podocyte death and necrosis

304
Q

Membranous nephropathy biopsy

A

Light microscopy: Thick GBM with spikes

IF: Diffuse fine granular deposits on capillary walls, IgG/C3

EM: Subepithelial immune deposits, spikes of GBM, effacement of podocyte foot processes

305
Q

Membranous nephropathy clinical course and risk for pregression

A

Nephrotic syndrome 40% progress to ESRD if untreated

Progression risk factors:

  • Older age of onset
  • Male
  • Increased creatinine
  • >8gm proteinuria
  • Tubulointerstitial fibrosis
306
Q

Membranous nephropathy treatment

A

ACE-I, ARB, Na low, B control, statin

Immune targeted therapy

  • Cyclophosphamide
  • Cyclosporine
  • Rituximab
307
Q

Diabetic Nephropathy

A

Most common systemic illness to cause nephrotic syndrome

308
Q

Diabetic nephropathy pathophysiology

A

Metabolic: - Hyperglycemia + pro inflamm molecules –> biochemical change in glomeruli –> profibrotic growth factors and increased synthesis of collagen/matrix - Non enzymatic glycosylation of proteins

Hemodynamic - Hyperfiltration –> increased glomerular capillary pressure and hypertrophy –> injury

309
Q

Diabetic nephropathy biopsy findings

A

LM: Glomerular nodules of matrix material. Thick GBM, thick tubular BM, interstitial fibrosis, vascular sclerosis

IF: No immune deposits. Pseudolinear staining of glomerular/tubular BM with IgG and albumin due to sticky BM

EM: Diffuse thickening of GBM

  • Mesangium expansion with increased matrix
  • No immune deposits
  • Variable foot process effacement
310
Q

Diabetic nephropathy clinical course

A

Proteinuria:

Early - microalbuminuria

Late - Overt proteinuria and neprotic syndrome

Progression: Depends on BP and glycemic control

311
Q

Diabetic nephropathy treatment

A

ACE-I/ARB (important to reduce capillary pressure),

Low Na, BP control

Strict blood sugar control

Kidney pancreas transplant

312
Q

Amyloidosis

A

Cause of proteinuria/nephrotic syndrome in adults

Extracellular deposition of abnormally folded proteins

Poor prognosis

313
Q

AL type amyloidosis

A

Multiple myeloma - neoplasm of plasma cells

Amyloid made of monoclonal Ig light chains

314
Q

AA tyep amyloidosis

A

Chronic inflammatory disease

Amyloid made of serum amyloid A protein

315
Q

Amnyloidosis biopsy findings

A

LM: Congo red stain positive

IF: Variable

EM: Haphazardly arranged fibrils

316
Q

Amyloidosis clinical course and treatment

A

Poor prognosis, ESRD common

Treatment: ACE-i, ARB, Low Na, Lop, BP control, statin

Primary - chemo, stem cell transplant

Secondary - Treat underlying disease

317
Q

Cystitis definition

A

Inflammation of urinary bladder, usually due to infection

318
Q

Cystitis triad of symptoms

A
  1. Frequency of urination
  2. Lower abdominal pain
  3. Dysuria
319
Q

Most common cystitis organism

A

E. Coli >> Proteus, Klebsiella, Enterobacter

320
Q

Predisposing factors for cystitis

A

Bladder calculi

Urinary obstruction

DM

Instrumentation

Immune deficiency

Cytotoxic drugs

Radiation

321
Q

Cytotixic drug cystitis risk

A

Cyclophosphamide

Hemorrhagic cystitis

322
Q

Gross pathalogical findings of acute cystitis

A

Hyperemia (redding) of mucosa

Exudate

Large amounts of hemorrhage = hemorrhagic cystitis

323
Q

Microscopic pathological findings of acute cystitis

A

Neutrophilic infiltrate

Hemorrhage

Ulceration of mucosa

Large areas of ulceration = ulcerative cystitis

324
Q
A

Acute cystitis

325
Q
A

Hemorrhagic cystitis

326
Q
A

Acute cystitis

327
Q
A

Acute cystitis

328
Q

Chronic cystitis pathological findings

A

Longer duration of infection

Chronic infiltrate - lymphocytes/plasma cells

Heaped up and reactive urothelium

Fibrous thickening of muscularis propria

329
Q
A

Chronic cystitis

330
Q

Special histological forms of chronic cystitis

A

Follicular

Eosinophilic

Interstitial

Malacoplakia

Polypoid

Emphysematous

Cystitis cystica

331
Q
A

Chronic follicular cystitis

Germinal center

332
Q
A

Eosinophilic cystitis

333
Q

Interstitial cystitis

A

Most frequent in women

Inflammation and fibrosis in all layers of bladder wall, often with ulceration

Highliy incapacitating and difficult to treat

334
Q

Symptoms of interstitial cystitis

A

Intermittent and severe suprapubic pain

Frequency

Urgency

Hematuria

Dysuria

335
Q

Malacoplakia

A

Unique form of chronic cystitis, chronic E coli infection

Immunosuppressed patients

336
Q

Gross pathology of malacoplakia

A

Multiple yellowish plaques in mucosa and submucosa

337
Q
A

Malacoplakia

338
Q

Microscopic pathological features of malacoplakia

A

Large foamy macrophages, multinucleate giant cells, lymphocytes

Michaelis Gutmann bodies: Round intracytoplasmic concretions within macrophages and between cells

339
Q
A

Michaelis Gutmann bodies

340
Q

Polypoid cystits cause and mucosal appearance

A

Results from mucosal irritation - bladder catheter

Broad polypoid projections due to submucosal edema

341
Q
A

Polypoid cystitis

342
Q
A

Polypoid cystitis

343
Q
A

Emphysematous cystitis

344
Q
A

Cystitis cystica

345
Q

Pyelonephritis major causes

A

Majority (>95%) are ascending bladder infections

Most are bacterial infections: 85% gram(-) rods from intestinal tract

E. COLI

346
Q

Pyelonephritis nosocomial infections

A

Hospital acquired

Due to indwelling bladder catheters, patients on antibiotics

Most are due to E coli

347
Q

Pyelonephritis hematogenous spread

A

Associated with virulent organisms

Staph aureus, salmonella

348
Q

Pyelonephritis predisposing factors to infection

A

Urinary tract obstruction

Catheters

Vesicouteral reflux

Pregnancy

Pre existing renal disease

DM

Immunosuppression

349
Q

Pathophysiology of pyelonephritis

A

Colonization of urethra then bladder

  • Usually by intestinal flora
  • Bacterial adhesion molecules interact with urothelium receptors –> promote migration to kidney and persistent infection

Multiplication of organisms in bladder: Outflow obstruction/bladder dysfunction –> STASIS –> bacterial growth

Bacteria gain access to upper tract: Catheter. Vesicoureteral reflux (back flow)

Intrarenal reflux

350
Q

Factors preventing pyelonephritis infection

A

Active peristalsis of ureters

Ureterovesical valves

Complete voiding of bladder

Turbulent flow of urine exiting urethra

351
Q

Clinical presentation of acute pyelonephritis

A

Fever, chills

Flank pain, CVA tenderness

Constitutional symptoms: malaise, anorexia, vomiting, diarrhea, headache

Cystitis symptomsL Urgency, frequency, dysuria

352
Q

Acute pyelonephritis lab findings

A

Leukocytosis - Left shift increase WBC

Urinalysis - Pyuria (>5WBC/HPF), WBC casts

Urine culture - colony formation

Positive blood culture - 15-30% cases

353
Q

Acute pyelonephritis Gross path findings

A

Focal abscesses, wedge shaped areas of suppuration, hemmorhage

354
Q

Acute pyelonephritis microscopic path findings

A

Early: PMN infiltrate in interstitium and within tubule, abscess, tubule destruction

Later: Mixed inflamm infiltrate, PMN/lymphocytes/plasma cells

355
Q
A

Acute pyelonephritis

356
Q
A

Acute pyelonephritis

357
Q
A

Acute pyelonephritis

358
Q
A

Acute pyelonephritis

359
Q

Natural history of acute pyelonephritis

A

Most cases follow benign course - antibiotics and supportive care

Adults with normal urinary tract = no rogressive disease

Bacteruria may persist after therapy

360
Q

Complications of acute pyelonephritis

A

Bacteremia/sepsis - 15-30%

Papillary necrosis - necrosis of distal medullary tips, diabetics

Pyonephrosis - Exudate filling renal pelvis and ureters. Severe obstruction

Perinephric abscess - Extension of inflmmation through renal capsule into perinephric fat

361
Q
A

Severe papillary necrosis

362
Q

Polyoma virus

A

Cause of acute ciral pyelonephritis in renal allografts

Immunosuppression –> latent virus activation –> inflammation of tubules and interstitium

Treatment: Reduce immunosuppression

363
Q
A

Polyoma virus nephropathy

364
Q

Chronic pyelonephritis: Definition, cause, progression

A

Chronic disorder characterized by chronic tubulointerstitial inflammation and progresive scarring

Causes:

  1. Chronic reflux (reflux nephropathy): Usually in childhood
  2. Chronic obstruction: Recurrent infection superimposed on obstruction

Abnormal urinary tract –> repeated infections –> progressive injury

365
Q

Clinical presentation of chronic pyelonephritis

A

Vague/nonspecific symptoms: Flank pain, low grade fever. History of UTI’s. ESRD w/out prior history

Common cause of HTN in children (via CKD)

Nocturia, polyuria - tubular dysfunction and loss of ability to concentrate urine

Secondary FSGS

366
Q
A

Chronic pyelonephritis

367
Q
A

Chronic pyelonephritis

368
Q

Microscopic path findings of chronic pyelonephritis

A

Chronic interstitial inflammation with fibrosis

Tubular atrophy and dilation with hyaline casts

Glomeruli vary from normal to ischemic to obsolescent

369
Q
A

Chronic pyelonephritis

370
Q

Xanthogranulomatous pyelonephritis

A

Special form of chronic pyelonephritis

Proteus infections, obstruction

Mixed inflammation with large amouns of foamy macrophages

371
Q
A

Xanthomatous pyelonephritis

372
Q
A

Xanthogranulomatous pyelonephritis

373
Q

Staghorn calculi

A

Associated with chronic infections due to urea splitting bacteria

Proteus

Klebsiella

Ureaplasma

Struvite crystals –> Stones

Difficult to treat

374
Q
A

Staghorn calculi

375
Q
A

Staghorn calculi

376
Q

Chronic pyelonephritis natural history

A

Caught early: Surgical correction of abnormal urinary tract allows normal function, prevents progressive scarring

End stage: No effective therapy

377
Q

Allergic interstitial nephritis

A

Inflammatory disorder involving interstitium and tubules - non infectious, hypersensitivity reaction

Penicillins, NSAIDs, antibiotics, thiazdes

378
Q

Clinical presentation - allergic interstitial nephritis

A

Fever

Skin rash

Eosinophilia

379
Q

Microscopic path of allergic interstitial nephritis

A

Mixed inflammation within interstitium: Eosinophils, lymphocytes, PMN, plasma

Tubular inflammation, tubular injury

Early - interstitial edema

Late - interstitial fibrosis, tubular atrophy

380
Q
A

Allergic interstitial nephritis

381
Q
A

Allergic interstitial nephritis

382
Q
A

Allergic interstitial nephritis

Chronicity with fibrosis

383
Q

Treatment allergic interstitial nephritis

A

Discontinue offending drug ASAP

Corticosteroids

Supportive care

384
Q
A

Myeloma cast nephropathy

Intratubular cast

385
Q

Components of nephritic syndrome

A

Glomerular hematuria: Dysmorphic RBC’s, RBC casts

Proteinuria: Can be nephrotic range

Azotemia: Elevated BUN

Oliguria

HTN: Volume overload via Na retention - RAAS suppression and icnreased Na/K ATPase

386
Q

Etiology of Membranoproliferative Glomerulonephritis

A

Idiopathic/autoimmune

Infectious:

  • Hep C
  • Chronic bacterial infection

Neoplasia

  • Mulitple myeloma
  • CML
387
Q

Pathogenesis of MPGN

A

Immune complex mediated disease

Idiopathic: Antibody directed at unknown antigen

Secondary: Antibody directed at viral/bacterial

Deposition of Ab/Ag complex in glomerulus OR formation of complex in situ

Immune complex formation –> complement activation –> MAC

388
Q

MPGN blood analysis

A

Low C3, C4, total complement

389
Q
A

MPGN

Global hypercellularity and lobular formation

390
Q
A

MPGN

Silver stain

GBM duplication

391
Q
A

MPGN

IgM deposits

Smooth BM because deposits are subendothelial

392
Q
A

MPGN

Subendothelial deposits

393
Q

MPGN biopsy findings

A

LM: Hypercellular, lobulated glomeruli. Duplication of GBM

IF: IgG, IgM, C3 in mesangium or inner aspect of GBM

EM: Immune deposits in mesangium, subendothelium locations. GBM duplication

394
Q

MPGN clinical course: Idiopathic and secondary

A

Idiopathic/autoimmune: Prolonged course with slow rate of progression

Secondary: Good prognosis if underlying disease treated

395
Q

MPGN treatment

A

Idiopathic/autoimmune: Steroids

Secondary: Treat underlying condition

396
Q

Dense Deposit Disease

A

Rare

Excessive activation of alternatic complement pathway

397
Q

Dense Deposit Disease pathogenesis

A

Circulating autoantibody: C3 Nephritic Factor

Deficient regulatory protein: Factor H/Factor I

Leads to persistent degradation of C3 and constitutive activation of alternative pathway

LOW C3 ONLY

398
Q

DDD diagnosis

A

Low C3, C4, total complement

Assay for C3 nephritic factor, Factor H, Factor I

399
Q

C3

A

DDD

400
Q

DDD biopsy

A

LM: Similar to MPGN

IF: Mesangial and capillary wall C3

EM: Linear deposition of electron dense material along GBM (ribbon like)

401
Q
A

DDD

402
Q

Dense Deposit Disease clinical course

A

Poor prognosis

70% –> ESRD at 9 years

403
Q

DDD treatment

A

Non specific therapy if nephrotic

Plasmapharesis - Patients with C3 nephritic factor

Plasma infusion - Factor H/I deficiency patients

Eculizumab - antibody to C5 protein, prevents MAC formation, expensive

404
Q

IgA Nephropathy Etiology

A

Mucosal infection triggered by environmental antigens –> pathogenic IgA complexes

Antigens: Viral, bacterial, food

Genetic predisposition: Polygenic

405
Q

IgA Nephropathy pathogenesis

A

Increased synthesis of abnormal IgA/IgG

Abnormally glycosylated IgA produced –> immune complexes don’t clear –> IgG antibodies directed against abnormal IgA –> Large fucker of a macromolecule –> Deposition in mesangium and complement activation

406
Q
A

IgA Nephropathy

Increased size of mesangium

407
Q
A

IgA nephropathy

408
Q

IgA Nephropathy biopsy

A

LM: Variable, increased mesangium

IF: Mesangial IgA, C3

EM: Immune deposits in mesangium, increased mesangial matrix and cellularity

409
Q

IgA Nephropathy clinical presentation

A

40% present with gross hematuria following URI (Synpharyngitic hematuria)

30% present with microscopic hematuria and mild proteinuria

5-10% with acute nephritic syndrome

Associated abnormalities:

  • Skin lesions
  • GI (celiac, cirrhosis)
  • IgA vasculitis
410
Q

IgA nephropathy treatment

A

No treatment if normal renal function and low proteinuria

ACE-I/ARB if >1gm proteinuria

Fish oil

Prednisone - Patients with proteinuria even with ACE-I/ARB, progressive disease

411
Q

Post infectious Glomerulonephritis

A

Most common cause of acute nephritic syndrome

Children 5-12 and adults >60

412
Q

Post infectious glomerulonephritis etiology

A

Develops in response to infection

Acute nephritis 1-6 weeks following infectious illness

Strep pharyngitis/impetigo

413
Q

Post infectious glomerulonephritis Pathogenesis

A

Immune complex disease caused by specific nephritogenic strains of bacteria

  • Group A beta hemolytic Strep
  • Elevated strep titers

Hypotheses:

  1. Circulating immune complexes comprised of Strep antigen and antibody deposit within glomeruli and activate complement
  2. Infection causes alterations of intrinsic GBM proteins, Ab bind and activate complement
414
Q

Post infectious glomerulonephritis clinical presentation

A

Variable

Range from asymptomatic with microscopic hematuria to full blown nephritic syndrome

415
Q

Post infectious glomerulonephritis Diagnosis

A

Active urine sediment: Dysmorphic RBC, RBC casts, WBC, WBC casts

Low C3, CH50, normal C4

Elevated Strep antibody titers - Streptozyme test

416
Q
A

PIGN

Hypercellular with numerous PMN

417
Q
A

PIGN

418
Q

Post infectious glomerulonephritis Biopsy

A

LM: Hypercellular glomerulus with abundant PMN

IF: Large granular deposits of IgG, C3

EM: Large, hump like subepithelial deposits

419
Q

Post infectious glomerulonephritis Prognosis/Treatment

A

Good prognosis - most recover

Children - 95% recover without complications

Adults - More insidious, slow progression to chronic GN

Treatment - Supportive Care

  • Treat underlying infection
  • Manage HTN, edema, proteinuria
420
Q

Pools of serum calcium in body

A

50% ionized

10% complexed to phosphate, citrate, carbonate, other ions

40% bound to protein

421
Q

Sites of Ca reabsorption

A

PCT - 65%. Mostly passive via gradients

TAL - 20%. Mainly passive, driven by lumen charge

DCT - 10%. Transcellular transport, active

422
Q

PTH and calcium

A

Increases serum calcium

  1. Ca release from bone
  2. Ca reabsorption from kidney
  3. Conversion of vit D to calcitrol by stimulating 1-a-hydroxylase –> increase Gi absorption
423
Q

Calcitrol and Ca

A

Increase intestinal Ca absorption

424
Q

Factors that affect renal calcium excretion

A
  1. Sodium - saline infusion increases Ca excretion
  2. Ca - Dietary Ca increases excretion
  3. Phosphate - Dietary of IV phosphate increases excretion
  4. Proton - acidosis increases excretion
  5. PTH and Calcitrol
425
Q

Renal handling of phosphate

A

12% filtered phosphate is excreted, remainder reabsorbed

PCT:

Enter apical membrane via Na dependent transporter (type II, I) –> cross basolateral membrane via Na dependent transport (type III)

426
Q

PTH and Phosphate

A

Principal regulator of phosphate reabsorption

Inhibits Type II Na dependent phosphate transporter –> reduces reabsorption

Increases phosphate release from bone

427
Q

Calcitrol and phosphate

A

Principal phosphate regulator in GI

Increases intestinal reabsorption

Increases renal reabsorption

428
Q

Phosphatonin and phosphate

A

FGF 23

Inhibits calcitrol synthesis and NaPi2a synthesis

Calcitrol and high phosphate increase FGF23 –> reduce calcitrol and phosphate

429
Q

Factors affecting renal phosphate excretion

A

Sodium - saline infusion = excretion

Calcium - Hypercalcemia = excretion

Proton - Acidosis = excretion

PTH/calcitrol/phosphatonin - major regulators

Decreased GFR = hyperphosphatemia

430
Q

Secondary hyperPTH and CKD

A

Decreased kidney f(x) = decreased Vit D = phosphate retention/Ca decline

Decreased Ca = PTH activation

431
Q

Vascular calcification and CKD

A

CKD CV risk factors can accelerate vascular calcification - PTH, calcitrol, advanced AGE’s, lipoproteins

Relationship between CKD and abnormal phosphate/Ca, PTH levels, and vascular calcification

432
Q

Clinical consequences of vascular calcification

A

Severe organ dysfunction

Heart valve dysfunction

Calciphylaxis - necrotizing skin caused by calcific uremic arteriolopathy

Large vessel stiffening

433
Q

Renal Osteodystrophy classifications

A

High turnover bone disease

Osteomalacia

Mixed uremic bone disease

Adynamic bone disease

434
Q

High turnover bone disease

A

High PTH

Increased osteoclasts and osteoblasts

Bone structure disruption

435
Q

Adynamic bone disease

A

Low PTH

Low turnover

Decrease osteoblasts/clasts

No mineralization defect

Low rate of bone formation

436
Q

Osteomalacia

A

Adynamic bone disease with mineralization defect

437
Q

Mixed uremic bone disease

A

Histologic features of ostetitis fibrosa and osteomalacia

438
Q

Clinical manifestations of renal osteodystrophy

A

Bone pain

Muscle weakness

Skeletal deformities

Growth retardation in children

439
Q

Management of CKD-MBD

A

Early prevention

Control hyperphosphatemia: Diet, phosphate binders, dialysis

Control Ca: Supplements for Low Ca, Low Ca dialysate for high Ca

Vit D analogs: Inhibit PTH synthesis and secretion

Calcimimetic agent: Blocks PTH secretion

440
Q

Phosphate level goals in CKD Stage III, IV, V

A

Stage III: <70

Stage IV: <110

Stage V: 150-300

441
Q

4 Disease categories of hematuria

A

Infection

Kidney stones

Cancer

Glomerular disease

442
Q

Types of kidney stones

A

Calcium oxalate stones - increased Ca

Sturvite stones - Urea splitting organisms. High NH4 and high uring pH

Uric acid stones - Low urine pH

Cystine stones - Defect is cystine transporter

443
Q

Glomerular diseases that can cause isolated hematuria

A

IgA nephropathy

Familial hematuria/Thin BM disease - GBM collagen defect

Alports syndrome - Hereditary nephritis, collagen defect. Basket weave GBM

444
Q
A

Uric acid crystals

445
Q
A

Calcium oxalate crystals

446
Q
A

Cystine crystals

447
Q
A

Cholesterol crystals

448
Q
A

RBC cast

449
Q
A

RBC cast

450
Q
A

ATN

451
Q
A

Waxy cast - chronic disease

452
Q

Lupus Nephritis epidemiology and etiology

A

Occurs in 50% SLE patients

Genetic

Environmental - Lower SES, viral antigens

Genetic - Loss of tolerance

453
Q

Lupus Nephritis pathogenesis

A

Immune complex mediated disease

Antibody target - nucleosome

Cells undergoing apoptosis/necrosis fail to exit circulation –> intracellular contents exposed to immune system

454
Q

Lupus nephritis: Mechanisms of immune complex formation

A

Circulating nucleosome Ag/Ab complex deposits in kidney

Anti nucleosome Ab cross reacts with intrinsic renal antigen

Nucleosome antigen deposits first –> Ab binds antigen

455
Q

Lupus Nephritis Diagnosis: Non biopsy

A

Serology: Anti ds DNA, ANA

Low complement: C3, C4, total

Active urine sediment

456
Q

Classification of Lupus Nephritis

A

Class I: Minimal LN

Class II: Mesangial Prolferative LN

Class III: Focal LN

Class IV: Diffuse LN

Class V: Membranous LN

Class VI: Advanced sclerosing LN

457
Q

Class IV LN biopsy findings

A

LM: Hypercellularity involving capillary loops

Necrosis, crescent formation

Immune complexes visible, wire loop capillaries (thickened)

458
Q
A

Lupus Nephritis:

Wire loops

Intra capillary immune deposits

Hypercellular areas with capillary loop destruction

459
Q
A

Full house IF

Lupus Nephritis

460
Q
A

Lupus Nephritis

Global immune deposits

Subepithelial, subendothelial, mesangial

461
Q

Lupus Nephritis EM findings

A

Immune complexes in all compartments: Subendothelial, subepithelial, mesangial

462
Q

Lupus nephritis clinical presentation

A

Variable, depends on pattern of injury

Relapsing and remitting disease symptoms

463
Q

Lupus Nephritis treatment

A

Depends on clinical presentation and biopsy results

Class III-V treated aggressively

Active lesions - Cyclophosphamide, steroids –> induce remission

Maintenence therapy - Cellcept, azathioprine, steroids

Alternative agents: Rituximab

464
Q

RPGN definition

A

Rapidly progressive glomerulonephritis

Sever acute nephritic syndrome, progressive loss of renal function over days-weeks –> ESRD if untreated

465
Q

Categories of RPGN

A

Type I: Anti GBM

Type II: Immune complex mediated

Type III: Pauci immune

466
Q

Type I RPGN

A

Anti GBM - Goodpastures

Formation of autoantibodies against Type IV collagen

Immune deposits in GBM and pulmonary BM

467
Q

Type II RPGN

A

Immune complex mediated

IgA nephropathy

PIGN

Lupus Nephritis

468
Q

Type III RPGN

A

Pauci Immune type

ANCA

C-ANCA: Proteinase3 target antigen. Renal limited or associated with granulomatosis with polyangitis

P-ANCA: MPO target antigen. Renal limited or associated with microscopic polyangitis

469
Q

RPGN diagnosis, non biopsy

A

Serologic tests:

Anti GBM

P/C-ANCA

470
Q

RPGN biopsy

A

LM: Necrosis of glomerular capillaries. Crescent formation, proliferation of cells in urinary space

Anti GBM/Pauci: Non involved glomeruli look normal

IF:

Type I - Linear IgG along capillary walls

Type II - Positive, depends on cause

Type III - NEgative

EM: Immune deposits only in Type II

471
Q

RPGN treatment

A

High dose steroids

Cyclophosphamide

Rituximab

Azathioprine

Plasmapharesis - Anti GBM

472
Q
A

RPGN

Note crescent

473
Q
A

RPGN

Note crescent

474
Q

Fibrinogen stain

A

RPGN

Fibrinogen crescent

475
Q

IgG

A

Type I RPGN

Linear IgG deposits

476
Q

Chronic Glomerulonephritis Definition and Clinical presentation

A

End result of many forms of GN

Clinical presentation:

Renal failure with elevated creatinine

Uremia

Proteinuria and/or hematuria

477
Q

Chronic GN biopsy

A

LM: Globally sclerosed glomeruli, interstitial fibrosis, arteriolosclerosis, arteriolar hyalinosis

IF: Variable
EM: Variable

478
Q

Renal Papillary adenoma

Behavior, path features

A

Common neoplasm

Benign

Papillary/tubular architecture

Bland nuclei, no atypia

No fibrous capsule or desmoplastic response

479
Q
A

Renal papillary adenoma

480
Q

Angiomyolipoma

Behavior, association, path features

A

Benign, rare

Association with tuberous sclerosis

Microscopic path: Blood vessels, smooth muscle, adipose tissue

481
Q
A

Angiomyolipoma - adipose tissue

482
Q
A

Angiomyolipoma

Smooth muscle

483
Q
A

Angiomyolipoma

Blood vessels

484
Q
A

Angiomyolipoma

485
Q

Oncocytoma

Behavior and path features

A

Benign neoplasm

Nest arrangement of cells

Eosinophilic granular cytoplasm

Bland, round central nuclei

486
Q
A

Oncocytoma

487
Q
A

Oncocytoma

488
Q

Renal cell carcinoma

Behavior

A

85% of all primary renal malignancies

Behavior related to:

Size

Stage: Involvement of surrounding fat, vascular invasion, lymph node mets

Grade

489
Q

Renal cell carcinoma clinical features

A

Adults, male > female

Triad of symptoms:

Costovertebral angle pain

Palpable mass

Hematuria

Polycythemia: Paraneoplastic syndrome, erythropoietin secretion

490
Q

Renal cell Carcinoma treatment

A

Partial nephrectomy

Radical nephrectomy: Whole kidney

Adjunct chemotherapy

491
Q

Renal Cell carcinoma classifications

A

Clear Cell

Papillary

Chromophobe

492
Q

Renal cell carcinoma: Clear cell

Chromosomal abnormalities

A

Deletion of chromosome 3p

Loss of VHL

Promote tumor angiogenesis through VEGF

493
Q

Renal cell carcinoma: Papillary

Chromosomal abnormalities

A

Trisomy 7

MET mutation (proto-oncogene)

494
Q
A

Renal Cell Carcinoma

495
Q
A

Renal Cell carcinoma

496
Q
A

Renal Cell carcinoma

497
Q

Clear Cell Renal cell carcinoma

Path features

A

Cells arranged in nests/sheets

Delicate fibrovascular network

CLEAR CYTOPLASM

498
Q
A

Clear Cell RCC

499
Q
A

Clear Cell RCC

500
Q

Papillary RCC path features

A

Cuboidal/low columnar epithelial tumor cells

Papillary formation of cells with fibrovascular core

Papillae may contain prominent macrophages

501
Q
A

Papillary RCC

502
Q
A

Papillary RCC

503
Q

Chromophobe RCC path features

A

Eosinophilic cytoplasm with plant like cell borders

Greater nuclear atypia

504
Q
A

Chromophobe RCC

505
Q

RCC pattern of spread

A

Invasion through renal capsule into perinephric fat

Invasion into renal vein, proximal spread along IVC

Lymph nodes - Renal hilum/para-aortic

Distant mets - Adrenal, liver, brain, lungs, bone

506
Q

Wilms Tumor

Definition, genetic abnormality, associations

A

Malignant renal tumor of chilfren

Mutation of WT-1 gene on chromosome 11

WAGR syndroms: Wilms, Aniridia, Genital anomalies, retardation

Denys-Drash syndrome: Wilms, gonadal dysgenesis, early onset nephropathy w/ renal failure

507
Q

Wilms tumor clinical features

A

Abdominal mass

Ab pain, hematuria, intestinal obstruciton, HTN

508
Q
A

Wilms Tumor

509
Q

Wilms tumor path features

A

Triphasic Pattern

  1. Primitive blastema
  2. Epithelial component - abortive tubules/glomeruli
  3. Stroma - Fibrous or myxoid patters
510
Q
A

Wilms Tumor

511
Q
A

Wilms tumor

Epithelial elements

512
Q

Consequence of Wilms tumor

A

Anaplasia of tumor cells

Correlates with more aggressive behavior

513
Q
A

Wilms tumor - Anaplasia

514
Q

Wilms tumor treatment

A

Combined therapy

Surgical nephrectomy, radiation, chemo

515
Q

Urothelial carcinoma: Origin, clinical features

A

Origin in urothelium lining the renal pelvis

Clinical features:

Associated with urothelial carcinoma elswhere in urinary tract

Hematuria, urinary obstruction, hydronephrosis, flank pain

516
Q
A

Urothelial cell carcinoma

517
Q
A

Urothelial cell carcinoma

518
Q

Urothelial cell path features

A

Papillary: Papillae with vascular cores, lined by malignant urothelial cells

Flat: no papillary growth, disordered polarity/maturity of cells

519
Q
A

Normal Urothelium

520
Q
A

Papillary urothelial cell carcinoma

521
Q
A

Low grade papillary urothelial cell carcinoma

522
Q
A

High grade urothelial cell carcinoma - papillary

523
Q
A

Flat urothelial cell carcinoma

524
Q

Behavior and prognosis of urothelial cell carcinoma

A

Presence/absence of invasion

High grade = invasion

Tumor infiltrates adjacent tissue into renal parenchyma

525
Q
A

Invasive urothelial cell carcinoma

526
Q
A

High grade invasive urothelial cell carcinoma

527
Q

Bladder neoplasm: Pathogenesis

A

Cigarette smoking - most important

Chemical carcinogens

Infectious agent - Schistosoma haematobium (Bladder SCC)

Radiation, cyclophosphamide

528
Q

Clinical features of bladder neoplasms

A

Hematuria

Dysuria

529
Q

Diagnosis of bladder neoplasms

A

Urine Cytology - Less invasive, detect high grade. Less specific for low grade

Cytoscopy with biopsy

530
Q

Benign bladder neoplasms

A

Leiomyoma

Urothelial papilloma

531
Q

Common malignant bladder neoplasms

A

Urothelial cell carcinoma

SCC

532
Q
A

Papillary urothelial cell carcinoma

533
Q
A

Invasive urothelial cell carcinoma - bladder

534
Q

Squamous cell carcinoma - bladder

Background, association, appearance, treatment

A

Background: Often due to chronic irritation/inflammation

Association with schistosomiasis

Appearance: Intercellular bridges, keratinazation of single cells, keratin pearls

Radical cystectomy

535
Q
A

Squamous cell carcinoma

536
Q

Rare bladder cancer - adenocarcinoma

A

Gland forming tumor, mucin production

May arise from urachal remnant

Treat: Radical cystectomy +/- radiation

537
Q

Rare bladder carcinoma - Small cell carcinoma

A

Poorly differentiated appearance

Treatment: Chemo+cystectomy+radiation if localized

Chemo if systemic

538
Q

Bladder carcinoma T1/2/3

A

T1 - invasion into lamina proprial

T2 - Invasion into muscularis

T3 - Invasion into soft tissue outside bladder

539
Q

Bladder urothelial cell carcinoma: Clinical course and prognosis

A

Clinical course: 60% tumors single, 70% confined to bladder

New tumors after excision ==> higher grade

Prognosis: Depends on grade and stage

540
Q

Bladder urothelial cell carcinoma trreatment

A

Transuretheral resection - Low grade, non invasive papillary lesions

Bacillus Calmette Guerin - Attenuated TB. USed for high grade non invasive lesions. Incites granulomatous response against tumor

Radical cystectomy - T2 or higher tumors

Chemotherapy - Advanced disease

541
Q

Causes of elevated anion gap metabolic acidosis

A

Diabetic ketoacidosis

Lactic acidosis

Renal failure

Toxins (Aspirin)

542
Q

Causes of non elevated anion gap metabolic acidosis

A

Diarrhea

RTA

Carbonic anhydrase inhibitors

543
Q

Proximal tubule drug: MoA, usage, benefits to treat HTN?

A

Acetazolamide

Carbonic Anhydrase inhibitor

Not good for HTN because solutes delivered to TAL and can be reabsorbed

Used for epilepsy, glaucoma, altitude sickness

544
Q

TAL drug: Name, usage, benefit to HTN, consequences

A

Loop diuretics, Furosemide

NKCC2 inhibitor

Not the best for HTN

Increased excretion of Ca, Mg, K, H

Use for hypervolemic states: HF, cirrhosis

545
Q

DCT drug: MoA, usage, benefits, consequences

A

Thiazide drugs (HCTZ, chlorthalidone)

Na/Cl symporter blocker

FIrst line HTN

Not as good as loop for edematous states

546
Q

Collecting duct/Late DCT drugs: MoA, uses, benefits, consequences

A

Amilorde/Triamterene

ENaC blockers

Prevents K and H secretion

Use adjunct with Loop/thiazide to prevent hypokalemia

Can cause hyperkalemia

Not great diuretics

547
Q

Hydrochlorothiazide

A

DCT Na/Cl symporter blocker

First line HTN drug

Can increase K and H secretion via collecting tubule mechanisms

548
Q

Chlorthalidone

A

Na/Cl symporter blocker

First line HTN drug

549
Q

Furosemide

A

Loop Diuretic

NKCC2 blocker

Use for treating hypervolemic states (HF, cirrhosis)

Increase excretion of Ca, Mg via electrostatic mechanisms

Not best diuretic for HTN treatment

550
Q

Mannitol

A

Osmotic laxative

Helps treat cerebral edema

551
Q

Spironolactone

A

Mineralocorticoid receptor blocker

Prevent Aldosterone action - No ENaC uptake

Potassium sparing diuretic b/c no K secretion - Even with increased Na, charge restriction prevents K secretion

552
Q

Acetazolamide

A

Carbonic Anhydrase inhibitor

Acts in PCT

Affects acid/base status without disrupting ion balance

553
Q

Amiloride/Triamterene

A

ENaC inhibitors

Can result in hyperkalemia (no K secretion)

Use adjunct with thiazides/Loop to prevent hypokalemia

554
Q

NSAIDs

A

The devil incarnate for kidneys

Causes arteriolar vasoconstriction and decreased GFR

555
Q

Cyclophosphamide

A

Immunosuppressant

Can be used in inflammatory nephrotic syndromes

MCD, FSGS, Membranous nephropathy

556
Q

Cyclosporine

A

Immunosupressant

Can be used to treat inflammatory nephrotic syndromes: MCD, MN

557
Q

Phenoxybenzamine

A

Non selective irreversible alpha blocker

Use for Pheochromocytoma

558
Q

Penicillin

A

Antibiotic

Can cause AIN

559
Q

Lithium

A

Bipolar medication

Can cause DI

560
Q

Calcium Chloride

A

Use in hyperkalemia ONLY if ECG changes

Short term drug

561
Q

Kayexalate

A

Cation exchange resin

Hyperkalemia

562
Q

Pronephros

A

Non functional in humans

563
Q

Mesonephros

A

Most degenerates, small structure remains

Becomes ducts of reproductive system: Wolffian, mesonephric

564
Q

Metanephros

A

Final and definitive kidney and ureter

565
Q

Urogenital ridge: Origin, development

A

Derived from intermediate mesoderm

Lateral folding results in dorsolateral ridges that run along length of embryo (urogenital ridge)

566
Q

Pronephros development

A

Begins to form and regresses at week 4

567
Q

Mesenephros development

A

4th week - mesonephric tubules form in IM, cranial –> caudal

Mesonephric duct forms (solid rod of cells) and fuses with cloaca

Mesonephric tubules fuse with duct, create passage from mesonepchric excretory unit to cloaca

568
Q

Metanephric kidney: Origin

A

Arises from ureteric bud and metanephric blastema

569
Q

Ureteric bud origin and induction

A

Buds off mesonephric duct

Induces IM to form metanephric blastema

570
Q

Ureteric bud develops into…

A

Urine collecting elements

Collecting tubules, major/minor calyces, ureters

Undergoes repeated branching

571
Q

Metanephric blastema gives rise to…

A

Portion of kidney between glomerular capillaries and collecting duct

Bowmans capsule, PCT, Loop of Henle, DCT

572
Q

Regulation of kidney development overall

A

Reciprocal induction of ureteric bud and metanephric blastema are required for normalbranching and tubulation

Mutations anywhere in pathway cause problems

573
Q

Ascent of kidney

A

Metanephric kidney originates deep in pelvic region

Shift towards abdominal region (week 6-8)

90 degree medial rotation, face inward

574
Q

Urinary bladder formation

A

Base of allantois and attachment to urogenital sinus expands and forms urinary bladder

Urachus closes and becomes median umbilical ligament

575
Q

Bladder formation and mesonephric duct/ureteric bud

A

Growth of bladder incorporates mesonephric duct and ureteric bud into bladder wall

Remaining ureteric bud = ureters

Trigone (smooth part of bladder) formed from entry of mesonephric duct and ureters

576
Q

Horseshoe kidney

A

Forms when bilateral metanephric blastema fuse

Get suck under IMA during ascention

577
Q

Unilateral multicystic dysplasia

A

Kidney epithelia overexressing PAX2 –> atretic ureter

578
Q

Bilateral polycystic/multi cystic kidneys

A

Renal dysplasia characterized by multiple cysts and dysplastic kidney tissue

POTTER

Pulmonary hypoplasia

Oligohydraminos

Twisted face

Twisted skin

Extremity defects

Renal failure in utero

579
Q

Primary zone of incontinence

A

External urethral spincter (Rhabdosphincter)

580
Q

Male urethra and site of incontinence

A

Bladder neck/prostate –> membranous urethra –> bulbar urethra –> Pendulous urethra

Membranous urethra is site of incontinence

581
Q

Female urethra and incontinence

A

Shorter than males, fused to anterior vaginal wall

Incontinence can be caused by:

  1. Childbirth that damages pudendal nerve –> external sphincter
  2. Childbirth –> anterior vaginal wall damage
  3. Menopause –> low estrogen –> atrophy or urethra
582
Q

Detrusor autonomics

A

Rich in M3 receptors

M3 activation –> detrusor contraction –> relaxed bladder outlet –> void urine

583
Q

Bladder body autonomics

A

Beta adrenergic receptors (B3)

NE release –> detrusor relaxation –> urine storage

584
Q

Bladder base and proximal urethra autonomics

A

Alpha receptors

NE –> constriction –. Storage

585
Q

Pelvic parasympathetics and bladder control

A

S2-S4

Detrusor contraction, urethral relaxation

Detrusor contracts via Ach relsease

Urethra probably through NO

586
Q

Lumbar sympathetics and bladder control

A

NE release

B3 receptors on bladder –> relaxation via cAMP

Constrict urethra (alpha receptors)

587
Q

Pudendal nerve and bladder control

A

Somatic cholinergic

Ach release on nicotinic receptors on rhabdosphincter –> contraction –> stop void

588
Q

Urinary afferent pathways

A

A delta fibers in detrusor - Sense wall stretch/tension

C fibers in bladder mucosa - Stretch and nociception

589
Q

Bladder irritation and afferent fibers

A

Irritation = afferent fibers firing with decreased filling –> frequency/urgency

590
Q

Guarding Reflex

A

Storage reflex - based on spinal pathways

Filling –> afferents fire –> reflex firing from hypogastric nerve –> NE release =

Inhibit detrusor contraction

Contract bladder neck/proximal urethra

Block PS transmission

Pudendal nerve also fires = contracted rhabdosphincter

591
Q

Spino-bulbo-spinal reflex

A

Filling sends signal to PMC –> PMC only fires when threshold is reached

If threshold reached and PMC disinhibited –>

Stimulate PS transmission - detrusor contraction/urethral relaxation

Inhibit Pudendal nerve mediated rhabdosphincter contraction

Inhibit Guarding reflex via hypogastric nerve - No NE release

592
Q

Secondary bladder reflex

A

Urine flow through urethra –> facilitates bladder contraction and more voiding

593
Q

Detrusor Overactivity: Etiology, presentation

A

Excessive bladder contraction –> involuntary urine losses

Urge incontinence - Immediate need to urinate that cannot be suppressed

Urgency and frequency

594
Q

Urethral incompetence

A

Loss of normal function of bladder outlet

Stress incontinence - Laugh/cough etc

Can result after surgery –> damage to nerves

595
Q

Overflow incontinence

A

Primary problem is failure to empty bladder fully

Results in buildup of urine –> overflow trickles out into urethra

Etiology:

Unable to contract bladder

Retention due to blockage (enlarged prostate)

596
Q

Lesions above brainstem and bladder abnormalities

A

Detrusor overactivity –> overactive bladder

Impaired PMC inhibition

597
Q

Spinal cord injury above S2 and bladder abnormalities

A

Detrusor Sphincter Dyssynergia

No connection with PMC so no relaxed sphincter

598
Q

Spinal cord injury below S2 and bladder abnormality

A

Detrusor areflexia, fixed external sphincter

No bladder contraction

Sphincter retains residual tone

Urinary retention and overflow incontinence

599
Q
A

CPR (3 decks)

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