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כליה Flashcards

1
Q

Glomerular filtration pressures?

A

Hydrostatic-
afferent arteriole- 55mmHg
fluid pressure created by back propagation of water in capsule of bowmen- (-15)mmHg

[colloid- (-30)mmHg]

net filtration pressure-10mmHg

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2
Q

clearance definition?

A

volume of plasma from which a substance is completely removed per unit time

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3
Q

stages of chronic kidney disease?

A

stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m 2)

stage 2: Mild reduction in GFR 60-89

Stage 3: Moderate reduction in GFR 30-59

stage 4: severe reduction in GFR 15-29

chronic renal failure (end stage) GFR <10-15

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4
Q

GFR measurement?

A

inulin

nuclear medicine lab

BUN-Blood Urea Nitrogen

Creatinine

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5
Q

inulin?

A

100% clearance in urine
no reabsorption
no metabolism

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6
Q

nuclear medicine lab?

A

can differentiate between two kidney

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7
Q

BUN-Blood Urea Nitrogen?

A

urea production rate not constant

proximal massive reabsorption

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8
Q

Creatinine?

A

serum creatinine
men 0.74 to 1.35 mg/dL (65.4 to 119.3mmoles/L)
women 0.59 to 1.04 mg/dL (52.2 to 91.9 mmoles/L)

100% renal clearance- GFR dependent
fast buildup at low kidney function, almost no reduction from basal line at higher kideny function

secreted in proximal tubuli- Cr.clearance> GFR

serum lvl- normal distribute across population
thus steady-state indicator of function,
and is not a sensitive marker of injury

women:
Ccr- 95 ± 20 ml/min

men:
Ccr- 125 ± 25 ml/min

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9
Q

Estimated Cr clearance?

A

Cockcroft-Gault formula?

       (140 - age) x (IBW in kg) Est. CCr = ------------------------------ [x 0.85 women]          
                    72 x Pcr (gr/dl)

IBW = ideal body weight

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10
Q

Tenofovir renal dosing?

A

by Creatinine Clearance

50>
300mg every 24H

30-49>
300mg every 48H

10-29>
300mg every 72-96

less than 10, no hemodialysis- no recommendations

less than 10, with hemodialysis
300mg every 7d or total of 12h dialysis

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11
Q

Gabapentin renal dosing?

A

by Creatinine Clearance

30-59 700mg

30-49> 300mg ever 48H

10-29> 300mg ever 72-96

less than 10, no hemodialysis- no recommendations

less than 10, with hemodialysis> 300mg ever 7d or total of 12h dialysis

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12
Q

Total body water composition and distribution?

A
  1. TBW = 60% ~ 42 Liter

1.1 ICF= 66%
~ 28 Liter

1.2 ECF= 33%
~ 14 Liter

  1. 2.1 ISF = 3/4 ECF
    (10. 5 L)
  2. 2.1 IVF = 1/4 ECF
    (3. 5 L)
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13
Q

Posm – Plasma Osmolarity calculation?

A

Posm = 2(Na) + Glucose/18 + BUN/2.8
(in mg/dl)
שאר עולם

Posm = 2(Na) + Glucose + BUN
(in milimol/liter)
הדסה

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14
Q

effective blood volume definition?

A

blood volume on the arterial side of the circulation

part of IVF

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15
Q

Volume Regulation physiology?

A

Renal sodium handling
Na excretion stand in direct proportion to EBV (GFR)

Sympathetic tone (reveres proportion to EBV, carotic bodeis)
RAAS (reveres proportion to EBV, Afferent arteriole)
ANP (direct proportion to EBV)

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16
Q

Osmoregulation physiology?

A

Normal plasma osmolality = 275 to 290mosmol/kg.

osmolarity sensors in anterior hypothalamus:
ADH > thirst sensitivity

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17
Q

Volume/Osmoregulation in CHF?

A

blood concentrated in veins 🡪 EBV down
🡪 kidney + carotid bodies sensing 🡪 RAAS < ADH secretion 🡪 Posm down but EBV still down 🡪 ADH secretion (although low osmolarity)
EBV signal overcomes the Osmolarity signal
PNa is low but the Total Body Na is high = Edema

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18
Q

Hyponatremia definition?

A

Plasma Na+ concentration < 135 meq/L

usually reflects impaired renal Water excretion

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19
Q

situations of Hyponatremia with normal H2O excretion?

A 
Primary polydipsia
Reset Osmostat (pregnancy)
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20
Q

Isotonic (280-290) Hyponatremia mechanism?

A

HyperProteinemia, Hyperlipidemia 🡪 H2O fraction of TBW lowers + hyponatremia 🡪 [Na] is kept normal.

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21
Q

Hypertonic (<295) Hyponatremia mechanism?

A
  1. Posm = 2(Na) + Glucose/18 + BUN/2.8 (in mg/dl)
    NA has the major influence but not a single player.

diabetes 🡪 Posm of blood is up (Hypertonic) 🡪 water moves form ISF TO ECF 🡪 [Na] goes down 🡪 “pseudohyponatremia” / dilutional hyponatremia

A 2.4-meq/L reduction in the plasma sodium concentration for every 100-mg/dL elevation in the plasma glucose

  1. mannitol
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22
Q

hypotonic hyponatremia (remember it represents concentration and not total mg) mechanism and Treatment?

A

hypovolemia-
TBW↓ Total Na ↓↓
U[na]> 20- renal losses, diuretic excess
U[na]< 10- extra renal losses, diarrhea/ vomiting
Give Salt & water == 0.9% saline

euvolemia-
TBW↑ Total Na –
U[na]> 20- SIADH
Vasopressin receptor antagonists

hypervolemia-
TBW↑↑ Total Na↑
U[na]> 20- Renal failure (acute/ chronic)
U[na]< 10- cardiac failure (keep secrete ADH)
Diuretics, Low salt diet

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23
Q

SIADH - Criteria?

A

Hyponatremia & Hypoosmolarity
Uosm inappropriatly high>100 mosmol/kg
Una >40 mosmol/kg*
Normovolemia

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24
Q

SIADH - ETIOLOGY?

A

Increased production-

Neuropsychiatric disorders 
Drugs- thiazides 
Pulmonary Disease
Post operative
Severe nausea

Ectopic production (Carcinoma)

Exogenous administration (Oxytocin; Vasopressin)

etc…

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25
Q

Symptoms of Hyponatremia?

A

intracellular volume varies inversely with the P(Na)

Brain Edema:
Nausea Malaise Headache
Lethargy 🡪 Seizures 🡪 Coma

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26
Q

Treatment of Hyponatremia – symptomatic patient?

A

Calculate Sodium deficit

Do not attempt to raise PNa to normal

Do not attempt to raise PNa quickly

Hourly evaluate clinical & biochemical status

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27
Q

Calculation of sodium deficit?

A

Na+ deficit = TBW x (Na target-plasma Na+)
TBW- men 0.6/ female 0.5
NA target: 125

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28
Q

hyponatremia rate of correction?

A

asymptomatic-
less than 8 on the first day (24 hours)
Less than 18 meq/L over the first 2 days
0.5meq/L/h

symptomatic-
1.5 to 2 meq/L/h for 3 to 4 h or until the severe neurological symptoms have abated
additional rescue (till 8meq/L) in remaining time (<24h)

take fucking re-measurments every 1-2h to ensure right correction

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29
Q

osmotic demyelination pathophysiology?

A

hyponatremia 🡪 low osmolarity 🡪 brain edema 🡪 rapid adaptation of brain, loss of Na, K, Cl 🡪 slow adaptation, loss of organic osmolytes 🡪 ICF reduction 🡪 rapid external correction (therapy) 🡪 osmotic shrinkage of axons

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30
Q

osmotic demyelination symptoms?

A

paraparesis or quadriparesis, dysarthria, dysphagia, and coma; seizures also may occur but are less common.

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31
Q

hypernatremia (remember it represents concentration and not total mg) mechanism and Treatment?

A 
hypovolemia- 
TBW↓↓ Total Na ↓
U[na]> 20- renal losses: loop diuretic  
U[na]< 20- extra renal losses: diarrhea, fistula. sweating, burns
correct of water deficit (5% dextrose)
euvolemia- 
TBW↓ Total Na -- 
U[na] variable
renal losses: diabetes, hypodipsia
extrarenal losses: respiratory, dermal 
correct of water deficit

hypervolemia-
TBW↑ Total Na↑↑
U[na]> 20- sodium gain: primary, hyperaldo, cushing’s,
removal of NA: furosemide

Hypernatremia usually dose not develop unless there is limited access to H2O

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32
Q

Diabetes Insipidus physiology?

A

Central: complete or partial failure of ADH secretion

Nephrogenic: renal response to ADH is diminished or absent

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33
Q

Central Diabetes Insipidus etiology?

A

Idiopathic – familial (30%)

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34
Q

Nephrogenic Diabetes Insipidus Etiology?

A
  1. Decreased water permeability of the collecting tubule
    a. Congenital
    b. Hypercalcemia
    c. Hypokalemia
    d. Drugs (lithium)
    e. Sjogren’s syndrom
    f. Amyloidosis
  2. Interference with countercurrent mechanism
    a. Osmotic diuresis
    b. Loop diuretics
    c. Renal failure
    d. Hypercalcemia
    e. Hypokalemia
    f. Sickle cell anemia
  3. Increased peripheral degradation of ADH (pregnancy)
  4. Unknown mechanism
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35
Q

CDI vs NDI?

A

Uosm should be ~800-1400 mosmol/kg

If PNa>150 meq/L but Uosm<800 mosmol/kg=
There is at least a partial defect in ADH

ADH will increase the Uosm only in CDI

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36
Q

Symptoms of Hypernatremia?

A

intracellular volume varies inversely with the P(Na)

Brain dihydration:
Nausea Malaise Headache
Lethargy 🡪 Seizures 🡪 Coma

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37
Q

Treatment of Hypernatremia

A
  1. Calculate Water deficit
  2. Rate of correction 0.5 meq/L/h (12meq/L/24h)
  3. Hourly evaluate clinical & biochemical status

H2O deficit = TBW x ((Plasma Na-Target Na)/ Target Na)
NA target is 140
TBW= Weight x 0.5 male
Weight x 0.4 female

shock correction first to be corrected== Isotonic saline should be used if the patient is hypotensive

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38
Q

polyuria definition?

A

Urine volume > 3 liters per day

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39
Q

polyuria etiology?

A

water diuresis =Uosm< 250:
primary- intravenous infusion of dilute solution
CDI

solute diuresis= Uosm> 300:
saline loading 
post obstructive (BPH)
hyperglycemia 
high protein tube feeding
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40
Q

polyuria diagnosis?

A
  1. Patient history
  2. Estimate volume status
  3. Measure Glucose level in plasma (for DI)
  4. Plasma osmolarity
  5. Urine osmolarity
  6. If DI is suspected but no hyperosmolarity is present, perform water restriction test:

a. induce hyperosmolarity to stimulate maximal ADH secretion at 295osm (withhold water)
b. give exogenous ADH
c.
urine osmolarity goes all the way up (1000+) + no exo.ADH response = normal

urine osmolarity goes half the way up (600+)
-+ exo.ADH response= partial N/CDI

urine osmolarity does not go way up (0)
-+ exo.ADH response= complete N/CDI

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41
Q

Na+-K+-ATPase Pump regulation?

A

K+ balance
Insulin- upregulate ,naturally coupled with dietary K+ load.
Catecholamines- b2 activate, a-receptors inhibit
availability of ATP.

chronic diseases the pump activity is down regulated = hyperkalemia if renal failure diminishes K+ excretion

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42
Q

exercise influence on Distribution of K+?

A

muscle work 🡪 depolarization 🡪 k move to ECF

muscle work 🡪 ATP depletion 🡪 k move to ECF

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43
Q

Extracellular pH influence on Distribution of K+?

A

entrance of H+ to cells and exit of K+ and Na+

EXEPT:
K+ losses accompany the acidosis: RTA or diarrhea
organic acids production: lactate, ketoacids

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44
Q

Hyperosmolarity influence on Distribution of K+?

A

passive K+ movement out by channels (osmotic gradient)

Solvent Drag: Water drag K+

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45
Q

Rapid increase in cell production influence on Distribution of K+?

A

shift of K+ into the new cells:
severe megaloblastic anemia
G-CSF (neutropenia)
Refeeding Syndrome

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46
Q

Tubular Handling of K+?

A

filtered in the glomerulus, Most reabsorbed in the proximal tubule and loop of Henle.

secretion- distal tubule (principal cells, ROMK) and connecting segment and outer medullary collecting tubule

reabsorption- distal tubule segments (intercalated cells, H/K antiporter)

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47
Q

Regulation of K+ Secretion?

A

ALDOSTERONE
number of open channels of luminal membrane ↑
Na+/K+-ATPase activity ↑

plasma [K] ↑- 
Electrical gradient↑
Na+-K+-ATPase activity↑
aldosterone secretion ↑
H+/K+-ATPase ↓

Distal Sodium Delivery ↑(principal cells, ENAC)
Distal Flow Rate↑ 🡪 keep gradient at high lvl 🡪secretion ↑

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48
Q

Periodic paralysis definition?

A

recurrent episodes of muscle weakness or paralysis
[AD] or aquired
α-subunit of the dihydropyridine-sensitive calcium channel defect 🡪 Increased K+ Entry into Cells

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49
Q

Hypokalemia: Increased Gastrointestinal Losses mechanism?

A

decreased intake or hyperaldosteronism accompany the GI loss and aggravate the hypokalemia

Vomiting\gastric fluids-

-If vomiting is of biliary or pancreatic fluids

-Hypovolemia induced hyperaldostronism
Distal Sodium Delivery:

  • increased HCO3- in urine, delivered to distal tubule with Na+, reabsorption of Na and secretion of K
  • contributes to hypokalemia through K+ movement into cells
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50
Q

Bartter’s syndrome in hypokalemia?

A

Na+-K+-2Cl- cotransporter mutation

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51
Q

Gitelman’s syndrome in hypokalemia?

A

thiazide sensitive Na+-Cl- cotransporter mutation 🡪 less activation 🡪 less Na+ secretion in distal tubule 🡪 less K excretion
hypermagnesuria
hypocalciuria.

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52
Q

inhibition of 11β-hydroxysteroid dehydrogenase mechanism of hypokalemia? (licorice ingestion)

A

11β-hydroxysteroid converts cortisol to cortisone.
inhibition.
cortisol ↑ (cortisol have same affinity of aldosterone to mineralo-corticoid receptor in principal cells) 🡪
ENAC↑ Na+/K+-ATPase ↑

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53
Q

Glucocorticoid Remediable Hyperaldosteronism (GRA)

mechanism of hypokalemia?

A

translocation 🡪 chimeric gene 🡪 ACTH (cortisol regulator regularly) regulation of secretion of Aldosterone

treatment: give glucosteroids to inhibit ACTH secretion

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54
Q

Liddle’s syndrome definition?

A

[AD] activating mutation of ENaC 🡪 Na+ reabsorption ↑ 🡪 gradient ↑ 🡪 hypokalemia

mimics primary hyperaldo – hypertension, hypokalemia and alkalosis.
but: aldosteron↓ renin↓

treatment:
1. amiloride- Blocks ENAC
2. not spironolactone (ARBs/ACEs)!!! Liddle’s syndrome is not mediated by aldosterone.

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55
Q

Amphotericin B hypokalemia mechanism?

A

tubuli injury 🡪 cell membrane destroyed 🡪 solvents go to waste
renal failure

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56
Q

Hypomagnesemia induced hypokalemia mechanism?

A

ROMK naturally inhibited by Mg+2🡪 less Mg+2🡪 less inhibition 🡪 K enters cells

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57
Q

RTA induced hypokalemia mechanism?

A

type 1 (distal)- impaired hydrogen ion secretion in the distal nephron (thus K+ wasting, H+/K+atpase)

  • Decreased net activity of the proton pump
  • Increased hydrogen ion permeability of the luminal membrane

Proximal (type 2) RTA is characterized by a decrease in proximal bicarbonate (HCO3 ion) absorptive capacity

🡪 metabolic acidosis diminish proximal sodium reabsorption 🡪 may be sufficient to cause some hypovolemia and secondary hyperaldosteronism 🡪 sodium reabsorption and potassium secretion in the cortical collecting tubule

🡪alkali is administered 🡪 Increased distal tubule delivery of sodium, bicarbonate, and water 🡪 modest hypovolemia 🡪 hyperaldosteronism 🡪 potassium secretion in the cortical collecting tubule

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58
Q

Hypokalemia: Symptoms?

A 
Muscle weakness or paralysis.
Cardiac arrhythmias.
Rhabdomyolysis.
Renal dysfunction:
-Impaired concentrating ability.
-Increased ammonia production.
-Impaired urinary acidification.
-Increased bicarbonate reabsorption.
-Renal insufficiency
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59
Q

Hypokalemia: ECG?

A 
ST depression.
Decreased amplitude of T wave.
Increased amplitude of U wave.
Prolonged PR interval.
Widened QRS complex.

Polymorphic VT – torsade de pointes.

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60
Q

Hypokalemia - Diagnosis?

A

history

Physical examination: estimate blood pressure.

Acid base status.

Urinary K+ excretion:

  • 24 hour urine Collection: >25 mEq/day suggest at least contribution of a renal source.
  • Urinary [K+]/[Cr]: <13 mEq/g suggest extra-renal cause.
  • TTKG: ratio of luminal K+ concentration at the end of the CCD to plasma K+ would help in assessing whether K+ secretion\retention is adequate.
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61
Q

Hypokalemia: Treatment?

A

food

KCl:

I.V- very slowly up to 20 mEq/h, and at low concentration up to 60 mEq/l (if not high extracellular K will cause arrhythmias)

orally- can cause pill esophagitis and gastric ulcers.
preferred unless severe hypokalemia or CI.

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62
Q

Hyperkalemia: Etiology?

A

Increased intake.

shift of K+ from ICF to ECF.

  • Pseudohyperkalemia (lab).
  • Metabolic acidosis.
  • Insulin deficiency (DKA).
  • Hyperosmolarity (DKA).
  • Tissue catabolism.
  • β-adrenergic blockade.
  • Severe exercise
  • Digitalis Overdose.
  • Periodic Paralysis.
  • Post Cardiac Surgery.
  • Succinylcholine – induces cell membrane depolarization.

Decreased urinary excretion.

  • Renal failure.
  • EBV depletion.
  • Low aldosterone or disturbances in RAAS.
  • Type 4 renal tubular acidosis.
  • Selective potassium secretory defect.
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63
Q

Pseudohypoaldosteronism (Type 1) induced hyperkalemia?

A

Resistance to aldosterone

Acquired –
mostly in tubulointerstitial diseases of the kidney
Type 4 RTA.

Congenital – rare!

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64
Q

Pseudohypoaldosteronism (Type 2) induced hyperkalemia?

A

(Gordon Syndrome) the opposite to gitelman’s syndrome

Mutation regulatory proteins (WNK1 or WNK4) 🡪 Increased activation of the NCC in the distal convoluted tubule 🡪 Na+↓ in distal tubule 🡪 excretion of K+ ↓

Thiazides effective

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65
Q

disturbance in RAAS axis?

A 
impaired renin release- 
NSAIDS
beta blocker 
cyclosporine 
diabetes 
elders

renin inhibitors

ACE inhibitors

ARBs

impaired aldosterone metabolism- Heparin

aldosteron receptor blockers-
spironolactone
eplerenone

sodium channel blocker-
amiloride
triamterene
trimethoprim

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66
Q

Hyperkalemia: ECG?

A

progression by order:

  1. Peaked, narrowed T waves.
  2. Short QT interval & prolongation of PR interval.
  3. Loss of P wave.
  4. Widening of QRS complex.
  5. Sine-wave pattern (QRS complex merges with the T wave).
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67
Q

Hyperkalemia treatment?

A
  1. Antagonism of membrane instability: (and thus prevent arrhythmias):
    I.V calcium gluconate
  2. increase K+ entry into cells:
    Glucose and insulin IV.
    β2 adrenergic agonists (Ventolin)
    NaHCO3.
3. Remove excess K+ 
Diet.
Cation exchange resin: sodium polystyrene sulfate (kayexalate), Patiromer, Zirconium cyclosilicate.
Diuretics.
Dialysis.

Be ready with external pacemaker\defibrillator.

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68
Q

pH calculation?

A

-log[H+]
For 0.1 increase in pH (>7.45)– multiply 40nM by 0.8
For 0.1 decrease in pH (<7.35)- multiply 40nM by 1.2

[H+]=24*Pco2/ [HCO3-]

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69
Q

Chemical Buffering?

A

Extracellular
HCO3- + H+ 🡪 H2CO3
HPO4-2 + H+ 🡪 H2PO4-1
Protein- + H+ 🡪 ProteinH (Albumin)

Intracellular
Protein- + H+ 🡪 ProteinH (Hemoglobin)
organic and inorganic phosphates

Bone
NaHCO3- + H+ 🡪 H2CO3 + Na +
KHCO3- + H+ 🡪 H2CO3 +  K +
CaCO3- + 2H+ 🡪 H2CO3 + Ca +2
CaHPO4- + H+ 🡪 H2PO4- + -Ca +2

~ 40% of acute acid load is buffered by the Bone. More in chronic acidosis

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70
Q

H excretion (general)?

A

Tmax for HCO3- reabsorption is 26 meq/L

proximal tubule-
3500-4400mmon/day of bicarbonate reabsorption
CA2 🡪 bicarbonate move to interstitium by natrium bicarbonate cotransporter- 1 on basolateral 🡪 H move to lumen by NHExchanger-1 🡪 CA4 on brush border produce Carbonic acid 🡪 co2 + h20 🡪 co2 moves back to tubuli cells through membrane

cortical collecting tubule- 50-150 mmon/day Of H+ excretion (from non-volitile acids)
intercalated alfa cell CA2 🡪 bicarbonate move to interstitium by natrium AnionExchanger1 🡪 H move to lumen by Hatpase + H/K antiporter 🡪 H buffered with NH3 or HPO4

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71
Q

respiratory acidosis buffering?

A

intracellular RBC buffering 🡪 CO2 enters RBC 🡪 CA2 produce carbonic acid 🡪 H connects with negative Hb 🡪 HCO3 moves to blood or stays inside RBC

Acute-
For every 10mmHg increase in PCO2 there is an increase of 1-1.5 meq/L of HCO3-

chronic (3-5d, synthesis of proteins)-
For each 10 mmHg increase in PCO2, an increase of 3.5 meq/L of HCO3- is expected

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72
Q

Respiratory Alkalosis buffering?

A

release of H+ from intracellular proteins (hemoglobin mainly)

Acute- mainly from intracellular buffers. For every 10mmHg decrease in PCO2, a decrease of 2 meq/L in HCO3- is expected.

Chronic- For every 10 mmHg decrease in PCO2, a decrease of 4-5 meq/L in HCO3- is expected .

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73
Q

Respiratory Alkalosis Symptoms?

A

Headaches, Light-headedness, altered consciousness

albumin releases H+ 🡪 connects with Ca+2 🡪 hypocalcemia 🡪 Paresthesia, cramps and carpopedal spasm

more common in acute respiratory alkalosis than in chronic

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74
Q

Metabolic Acidosis Compensation?

A

For every decrease of 1 meq/L of HCO3-, a decrease of 1.1-1.3 mmHg in PCO2 is expected.

proximal tubule production of NH3 ↑
distal tubule secretion of H+ titrated by NH3 ↑

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75
Q

Metabolic Alkalosis Compensation?

A

For every increase of 1 meq/L of HCO3-, an increase of 0.7-0.8 mmHg in PCO2 is expected

proximal tubule re-absorption of HCO3- ↓
distal tubule H+ secretion ↓

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76
Q

Metabolic Acidosis Etiology?

A

Normal Anion Gap:

  1. Diminished H+ excretion
Type 1 (distal) Tubular Acidosis (RTA)
Hypoaldostronism (type 4 RTA)
Renal failure
  1. Increased HCO3- loss
Gastrointestinal
Diarrhea
Pancreatic, Biliary
Ureterosigmoidostomy
Cholestiramine

Renal
Type 2 (proximal) RTA
Carbonic Anhydrase Inhibitors

Increased Anion Gap:

1.Increased H+ load

Lactic acidosis
Ketoacidosis
Ingestions:
ASA, methanol, metformin

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77
Q

blood Anion Gap?

A

Anion Gap = [Na+ + K+] – [Cl- + HCO3-] =
Un-Measured Anion - Un-Measured Cations

Normal Values 15-17 meq/L if calculating K+
Normal Values 10-12 ,eq/L if not adding K+

In metabolic acidosis: if HCO3- ↓ and AG is normal than Cl had to ↑

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78
Q

RTA?

A

Type 1 – Distal RTA

Type 2 – Proximal RTA

Type 3 – Type 1 +Type 2 RTA

Type 4 – Hypoaldostronemia RTA

All are Hyperchloremic- Normal Anion Gap

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79
Q

Type 2 – Proximal RTA?

A

Can be Isolated or as part of combined proximal tubule reabsorption defect, i.e. Fancony Syndrome

Rickets in Children
Osteomalacia in adults

Urine pH – low due to Normal Distal H+ excretion

treatment-
citrate or bicarbonate salts, mainly as K+ salts, 10-15 meq/Kg/d (due to hypokalemia)

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80
Q

Type 1- Distal RTA?

A 
Can be complete, no urine acidification (infantile)
or incomplete (adult)

Nephrocalcinosis secondary to bone release of Calcium and Phosphate

Deafness is common in hereditary forms (same channels as in kidney)

Treatment –
K-Citrate (citrate becomes HCO3-), 1-2 meq/L/d

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81
Q

Type 4 – Hypoaldostronemia RTA?

A

no aldosterone 🡪 less Na/Katpase 🡪 No lumen electronegativity 🡪 no excretion of K+ from principle cells🡪 no excretion of H+ by A-intercalated

Usually comes with renal failure (partly blamed for aldosterone resistance)

Common in Diabetes Mellitus (because of hyporeninemia)

Treatment –
Treat hyperkalemia
Sometimes mineralocorticoids (mimic aldosterone)

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82
Q

lactic acidosis pathophysiology?

A

●Increased pyruvate production.

●Reduced entry of pyruvate into mitochondria, where it is oxidized to carbon dioxide and water or converted to glucose precursors.

●A shift of the cellular cytoplasmic redox state such that NADH accumulates and NAD+ falls. This drives the pyruvate/lactate ratio toward lactate.

generally defined as a serum lactate concentration above 4 mmol/L

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83
Q

lactic acidosis anion gap?

A

lactate === Addition of non-carbonic non Cl- acids
🡪 HCO3- utilization 🡪 AG increase
over 17 with K added / over 12 without K added

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84
Q

metabolic acidosis investigation?

A
  1. check for metabolic acidosis (HCO3- low and Pco2 low in correlation)
  2. Check Lactate, Ketoacids
  3. Check Osmollar Gap= Measured osmolarity – Calculated Osmolarity

Calculated = 2Na+ + urea +glucose (millimol)
>25 milliosmol – Suggests methanol or ethylene glycol intoxication

measured osmolarity done by LAB-
low freezing point, higher boiling point (anionic bonds are stronger than H bonds)

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85
Q

Metabolic Acidosis: Symptoms?

A

Tachypnea, dyspnea

Low blood pressure (reduced cardiac contractility, vasodilation)

Reduced response to cathecholamines

lethargy to coma

Chronic acidemia:
Bone disorders
Anorexia, Vomiting

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86
Q

Metabolic Acidosis- Treatment?

A 
Treat Cause
not organic-  pH < 7.2 
organic acidemia treat when pH < 7.1
↓
consider giving NaHCO3- 
practically the only way to give HCO3-== Be sure patient is capable of coping with Na+ and fluid overload
↓
consider dialysis if cant (HF ,PHT...)
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87
Q

Metabolic Alkalosis Maintenance Etiology?

A

Decreased HCO3- excretion by the kidneys:

EBV Depletion- Na+/ H2O reabsorption, with it more HCO3- than usual tmax (26 to 33-34)

Chloride depletion (vomitting)- electrical balancing requires HCO3- reabsorption

Hypokalemia

Hyperaldostronism

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88
Q

Metabolic Alkalosis Etiology?

A
  1. Loss of H+ or Chloride

-Gastrointestinal loss
Vomiting (urine Cl < 20 meq/L)
Naso-gastric tube
Chloride losing diarrhea (rare)

-Renal loss
Loop or thiazide diuretics (urine Cl < 20 meq/L)
Hereditary (Barter, Gittelman) 
Mineralocorticoid excess
Post chronic hypercapnea
Non-reabsorpable anions

-Skin Loss
Burns
Cystic Fibrosis

  1. Administration of HCO3

Massive blood transfusion
Administration of NaHCO3
Milk –alkali Syndrome

  1. H+ shift into the cells

Hypokalemia

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89
Q

Metabolic Alkalosis Symptoms?

A

Asymptomatic
Or

Weakness, muscle cramps (related to hypovolemia)

Polyuria polydipsia and muscle weakness (hypokalemia)

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90
Q

Metabolic Alkalosis Treatment?

A

Stop the reason

If EBV↓ Cl↓ – Give Normal Saline NaCl 0.9%

If Fluid overload – give CA2 inhibitors (Acetazolamide) or NH4Cl

If Minralocorticoid excess – block and correct.

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91
Q

PTH- FGF23- calcitriol relationship ?

A

PTH induce secretion of FGF23 and VIT D
both negative feedbacking on PTH.

VIT D induce secretion of FGF23
it negative feedbacking on VIT D

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92
Q

negative endocrine feedback loops? (with minerals)

A 
PTH and VIT-D
induce Ca+2 deposition to bone at low lvls
secretion of Ca+2 from bone at high lvls
inhibit excretion of Ca from kidney
Ca inhibit PTH and VIT-D secretion

VIT-D
inhibit excretion of P from kidney
induce absorption from intestine of Ca+2 and P

FGF23 induce secretion of P from kidney

P induce PTH and FGF23 secretion

high lvls of P forming complexeswith Ca+2 in the serum
thus inducing hypocalcemia

thus
PTH and VIT D generally elevates Ca+2 in serum
VIT-D elevates P in serum

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93
Q

plasma calcium level?

A

8.8 to 10.3 mg/dL
2.2 to 2.6 mmol/L thus 4.4 to 5.2 mEq/L
50% ionized and free- the only one relevant

10% in complexes
40% bound to proteins

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94
Q

Calcium shifts with normal albumin?

A

low albumin does not influence on free ionized Ca+2 lvls

acidemia (opposite with alkalemia)
more H+ bound to albumin 🡪 less Ca+2 bound to albumin 🡪 [Ca] Ionized ↑

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95
Q

pleiotropy definition?

A

includes all of a drug’s actions other than those for which the agent was specifically developed.

adverse effects + additional beneficial effects (usually standard reference)

96
Q

Vitamin D mechanism of Ca+2 absorption in the small intestines?

A

VIT-D bind VDR 🡪 dimerization with another VDR or RXR 🡪 bind DNA at VDRE 🡪 gene transcription (PTH and distranscription of CaSR)

TRPV6 -Luminal transport, exp. dependent on VIT-d

high [Ca+2] is toxic to cells 🡪 buffering system needed 🡪 Calbinding-D9k

PMCA - plasma membrane Ca ATPase- basolateral transport

97
Q

Vitamin D mechanism of Ca+2 reabsorption in the kidney?

A

TRPV5 -Luminal transport, exp. dependent on VIT-d

high [Ca+2] is toxic to cells 🡪 buffering system needed 🡪 CABP

NCX1 (antiporter)- basolateral transport

98
Q

Hypercalcemia etiology?

A

90%:

  • 1° hyperparathyroidism 🡪 most common
  • malignancy-related (PTHrP)

10%:

  • vitamin D-related: intoxication, sarcoid, etc.
  • high bone turnover: hyperthyroid, immobility

-associated with renal failure:
tertiary hyperparathyroidism
aluminum and adynamic bone disease
milk-alkali syndrome

99
Q

Primary hyperparathyroidism ETIOLOGY?

A

solitary adenoma

parathyroid hyperplasia

multiple endocrine neoplasia (MEN)
MEN1; MENIN tumor suppressor
MEN2A, MEN2B; RET proto-oncogene

Familial hypocalciuric hypercalcemia (FHH) – CaSR mutations (Primary hyperparathyroidism mimicking)

100
Q

Hypercalcemia of malignancy etiology?

A

humoral; tumor secretes PTHrP-
squamous cell carcinoma
renal tumors

direct bone marrow invasion – bone resorption and local destruction by cytokines

1,25(OH)2D - lymphoma

101
Q

Hypercalcemia symptoms?

A

moans- psychiatric
groans- abdominal
bone
stones- renal

102
Q

Treatment of hypercalcemia?

A

+ renal failure 🡪 dialysis

aggressive IV rehydration 🡪 loop diuretic

osteoclasts inhibition 🡪 bisphosphonate +- calcitonin

lymphoma / leukemia 🡪 steroids

refractory 🡪 gallium or denosumab

103
Q

Hypocalcemia sings?

A

Trousseau sign- facial nerve tapping induced spasm

Chvostek’s sign- hypoxia induced arm flexors contraction (extensors too but weaker 🡪 we see flexetion)
pathophysiology-
NA channels open at lower membrane voltage in presence of Ca+2 🡪 Na basal current is higher 🡪 AP threshold is lower

104
Q

Hypocalcemia on ECG?

A

long QT -> polymorphic VT

105
Q

Treatment of hypocalcemia?

A

symptomatic or Ca+2 <1.9mmol/L

control immediately 🡪 IV 10% Ca-glucoronate
10-20 ml over a period of 10-15 minutes
(glucoronate because than we can give in peripheral vein)

control over days/weeks: VIT-D
if PTH deficient 🡪 VIT-D analogue (active)
if PTH intact 🡪 Cholecalciferol or ergocalciferol

106
Q

hypophosphatemia Clinical findings?

A 
-neuromuscular
weakness, paralysis
confusion, hallucinations
ataxia
seizures
coma
rhabdomyolysis
  • respiratory failure, cardiac dysfunction
  • hemolysis, defective leukocytes and platelets
  • chronic: osteomalacia, rickets
107
Q

hypophosphatemia Mechanisms: Decreased intestinal absorption?

A

Inadequate intake

Antacids containing aluminum or magnesium

Steatorrhea and chronic diarrhea

Vitamin D deficiency or resistance

108
Q

phosphate intestinal absorption mechanism?

A

VIT-D bind VDR 🡪 dimerization with another VDR or RXR 🡪 bind DNA at VDRE 🡪 gene transcription 🡪
sodium phosphate cotransporter 2B 🡪 Luminal transport

high Pi diet = passive paracellular

109
Q

Increased urinary excretion of phosphate etiology?

A

PTH:
Primary hyperparathyroidism
Vitamin D deficiency (2° hyperparathyroidism)
PTHrP-dependent

independent of PTH:
Primary renal phosphate wasting
Fanconi syndrome (proximal tubule defect)
Hereditary hypophosphatemic rickets
Oncogenic osteomalacia (FGF23↑)
Other - osmotic diuresis, acetazolamide, acute volume expansion

110
Q

refeeding syndrome?

A

starvation 🡪 carbohydrates↓ 🡪 insulin ↓ 🡪 fat and protein catabolised to produce energy 🡪 intracellular loss of electrolytes, mainly phosphate 🡪 intracellular phosphate stores can be depleted despite normal serum phosphate concentrations 🡪 start to feed 🡪 sudden shift from fat to carbohydrate metabolism 🡪 insulin↑ 🡪 cellular uptake of phosphate🡪 hypophosphatemia, hypomagnesemia, hypokalemia, B1↓

111
Q

hungry bone syndrome?

A

hypocalcemia (< 2.1 mmol/L) postparathyroidectomy in patients with hyperparathyroidism, which usually resolves in 2-4 days.

hypophosphatemia, hypomagnesemia, hyperkalemia can be seen

can be seen in osteoblastic metastases too

112
Q

Symptoms of hyperphosphatemia?

A

Increased cardiovascular calcifications and associated morbidity and mortality
(which means none)

113
Q

hyperphosphatemia mediated vascular calcification mechanism?

A

vascular smooth muscle cells (VSMCs):
osteogenic/chondrogenic conversion in the vascular wall
🡪 dramatic loss of mineralization inhibitors
🡪production of calcifying matrix vesicles
🡪extracellular matrix (ECM) degradation
🡪apoptosis and release of apoptotic bodies, which, in turn, form the initial nidus for vascular calcification.

114
Q

hyperphosphatemia etiology?

A

Renal failure (decreased filtration)

Massive acute phosphate load:

  • Tumor lysis syndrome
  • Rhabdomyolysis
  • Crush injury
  • Hyperthermia
  • Fulminant hepatitis
  • Hemolysis
  • Exogenous administration

Primary increase in proximal phosphate reabsorption

  • Primary hypoparathyroidism
  • Parathyroid suppression (2° hypo-para)
  • Pseudohypoparathyroidism
  • Familial tumoral calcinosis (FGF23 mute)
  • Heparin therapy
115
Q

phosphate excretion?

A

acts as in creatinine clearance 🡪 immediate reduction of elevation of GFR does not cause change in serum [Pi]

116
Q

PTH Mechanism of hypophosphatemia?

A

PTH1R- PTH interaction 🡪 PKA (maybe C) activation 🡪 NHERF1 phosphorylation 🡪 NPT2a/c endocytosis

117
Q

Treatment of hyperphosphatemia?

A

Dietary restrictions

Phosphate binders-
Revela / sevelamer carbonate
lanthanum

(Dialysis- at tumor lysis syndrome)

118
Q

סוגי המטוריה?

A

גלויה (מקרוסקופית) או נסתרת (מיקרוסקופית)

ממקור עליון (הכליה) או תחתון

מבודדת או יחד עם פרוטאינוריה

לא אמיתית (מיוגלובין, המוגלובין)

119
Q

hematuria DD?

A 
זהום(שלפוחית, ערמונית, שופכה, כליה)
טראומה 
מציסטה
מחלת אבנים
מחלה גידולית
מחלה דלקתית גלומרולארית (לרוב עם פרוטאינוריה)או אינטרסטיציאלית 
אוטם כלייתי
120
Q

hematuria treatment?

A

על פי הגורם:

אנטיביוטיקה
ריסוק או הוצאת אבנים
הוצאת גדול או טפול אחר (קרינה, כימותרפיה, ביולוגי)
טפול בבעיה הנפרולוגית

121
Q

glomerular proliferative disease pathopisiology?

A 
ריבוי תאי דלקת 
או 
ריבוי תאים כיליתיים מקוריים:
תוך קפילריים
חוץ קפילריים – קופסית על שם באומן
 ↓
Crescent – סהרון
יורכב מהמונוציטים 
או
מתאי האפיתל הפריאטליים המצפים את קופסית באופן בחלקה הפנימי, המשכיים לפודוציטים בקוטב הוסקולארי ולתאי האפיתל הטובולריים בקוטב היורינארי.
122
Q

Sclerosis definition (in kidney)?

A

עלייה בכמות החומר החוץ תאי עם מבנה והרכב זהים לממברנת הבסיס הגלומרולרית ולחומר המזנגיאלי התקין

123
Q

Fibrosis definition?

A

שקיעה של קולגן מסוג 1+3 כתוצאה מהגלדה של תהליך דלקתי

124
Q

The Major Glomerulopathies?

A

תסמונת נפריטית:
גלומרולונפריטיס חריפה
גלומרולונפריטיס תת חריפה – RPGN
גלומרולונפריטיס כרונית

תסמונת נפרוטית

פגיעות אסמפטומטיות – פרוטאינוריה והמטוריה

125
Q

?תסמונת נפרוטית הגדרה

A

בהגדרה (עפ”י אפ-טו-דייט ולא לפי מה שבא למרצה באותו רגע!):
פרוטאינוריה מעל 3.5 גרם ל-1.73 מטר רבוע/יום
היפואלבומינמיה- (אלבומין< 3.5 גרם/דצ”ל)
בצקת

חלק עם פרוטאנוריה קשה ולא יפתחו את התסמונת
חלק עם פרוטאנוריה אפילו פחותה, ויפתחו את כל התסמונת

סימנים נוספים-
היפרליפידמיה
נטייה לקרישיות יתר

126
Q

הפרשת חלבון תקינה בשתן?

A

150 מ”ג ביום
Ig 20%
אלבומין 40%
Tamm Hors fall 40%- tubular secretion only
role in prevention of infection and stones

127
Q

Proteinuria stages?

A

150-300mg/24h- microalbuminuria
<300mg/24h- proteinuria
<3-3.5gr/24h- nephrotic proteinuria

over 0.5gr demands treatment
over 1gr demands biopsy

128
Q

nephrotic syndrome diagnosis?

A

שתן:
1. מראה- קצפי

  1. urine dipsticks- only albumin
  2. sulfosalycilic acid- a must if dipstick came negative, checks for any kind of protein, makes sample murky
  3. יחס אלבומין או פרוטאין / קראטינין בשתן- אצל רופאי ילדים באופן קבוע, כשאי אפשר לעשות איסוף 24 שעות
  4. איסוף שתן ל – 24 שעות. הגולד סטאנדרט

False positive:
שתן מרוכז.
אנטיביוטיקה.
חומר ניגוד.

129
Q

Peripheral edema cycle?

A

oncotic pressure↓ 🡪 fluids move to ECF 🡪 low intravascular pressure 🡪 RAAS activation, ADH secretion and ANP inhibition 🡪 fluids reabsorption 🡪 exacerbation of edema

130
Q

nephrotic syndrome: hypercoagulation pathophysiology?

A
  • urinary loss of antithrombin 3 🡪 reduction in activation of proteins C+S
  • urinary loss of proteins C+S
  • fibrinogen production in liver ↑
  • platelets activation ↑
    thus: DVT, RVT ,PE are all up
131
Q

other influences of nephrotic syndrome?

A

VIT-D def.

thyroxin def.

anemia- transferrin def.

infection- IgG urinary loss, ‘whipping edema’

132
Q

Nephrotic syndrome DD Of primary diseases?

A

children-
Minimal change disease 80%
Focal segmental glomerulosclerosis

adults-
1st. focal segmental glumerulosclerosis
2nd. membranous nephropathy 20-30%
minimal change 20%
mesangiocapillary GN
immunotactoid glomerulopathy
133
Q

Nephrotic syndrome DD Of systemic diseases?

A

diabetes

amyloidosis

MM, light chain disease

SLE- membranous

HBV,HCV,HIV- membranous, MPGN

lymphomas- MCD
solid neoplasms- membranous

drugs (heroine, gold, penicillin)

134
Q

Minimal change disease clinical findings?

A

nephrotic syndrome

albumin loss due to GBM electrical negativity loss

no urine precipitations

microscopic hematuria 20-30%- this is why it is
called minimal change

rarely: renal insufficiency, Hypertension

135
Q

Minimal change disease pathological findings?

A

EM- podocyte feet diffuse effacement and detachment

Light microscopy- normal glomeruli

Tubular epithelial cell protein- resorption droplets

Immunofluorescence microscopy- negative

136
Q

Minimal change disease etiology?

A

idiopathic mostly

drugs- Rifampicin (TB), NSAIDS

Hodgkin lymphoma

HIV, viral

137
Q

Minimal change disease treatment?

A

30-40% self limiting in children
steroids
90% children / 50% adults

reflaming or refractory- cytotoxicity:
cyclophosphamide, calcineurin

138
Q

Focal and segmental glomerulosclerosis clinical findings?

A

nephrotic syndrome

More often non selective proteinuria

if idiopathic:
1/3 will have hematuria, reduced GFR (renal failure), hypertension

139
Q

Focal and segmental glomerulosclerosis pathology?

A

IF- focal segmental IgM and C3 (nonspecific, ‘trapping’)

EM- in affected glomeruli
increased mesangial matrix
focal detachment of visceral epithelial cells
diffuse effacement of foot processes

Hypertrophy and proliferation of glomerular visceral epithelial cells (podocytes)- HIV, collapsing variant

Secondary event reflecting scarring

140
Q

Focal and segmental glomerulosclerosis etiology?

A

primary: idiopathic
can reappear in kidney transplants, responds to plasmapheresis in some

secondary: over usage
- single kidney
-acquired glomerular injury (<50%):
surgery, reflux, CRD
- over weight (higher demand of kidneys)
-HIV, heroin addiction, sickle cell disease

141
Q

Focal and segmental glomerulosclerosis treatment?

A

50% end stage renal disease within 10 years

long period steroids- 70% reaction, in those:
cytotoxicity- 50% reaction

renal failure or hypertension- worse prognosis (da)

142
Q

Membranous Glomerulopathy etiology?

A

Primary (idiopathic ) 80%

Secondary 20%:
SLE 15%
penicillamine, captopril, NSAID, gold
Chronic hepatitis B,C, syphilis, schistosomiasis, malaria
diabetes mellitus, MCTD, GRAVE, PBC
carcinoma
143
Q

Membranous Glomerulopathy Clinical findings?

A

non selective Nephrotic syndrome

macroscopic hematuria- 50%
hypertension 10-30%

144
Q

Membranous Glomerulopathy pathology?

A

Uniform thickening of capillary wall BM (no
increased cells/proliferation)- “spikes and
holes”

IF- peripheral (capillary, not in mesangium) granular deposits of IgG and C 3

EM- subepithelial deposits surrounded
by new basement like material;
fusion of foot processes

ANTI PLA2R (IgG4, fixed intrinsic) 80% OF CASES

145
Q

Membranous Glomerulopathy treatment?

A

40% self limited
40% reflaming- give cytotoxicity
20%- ESRD

146
Q

Membranous Glomerulopathy: diabetes pathophysiology?

A

glycosuria (not only glucose) 🡪 glucose and Na reuptake 🡪 ANP ↑ 🡪 Afferent vasodilation 🡪 glomeruli hypertension 🡪 secondary damage🡪 give ACEi for Efferent vasodilation

147
Q

Nephrotic Syndrome - Therapy?

A 
Treat underlying disorder
Low sodium, normal protein diet
Diuretics
ACE inhibitors
Statins
Consider anticoagulation (PE, DVT)
vitamin D
148
Q

Nephritic syndrome- definition?

A

oliguria: <400ml/day

glomerular hematuria: red cell casts, dysmorphic RBC, sometimes microscopic
“pee looks like coke
non nephrotic proteinuria (<3.5gr/day)

hypertension

peripheral edema

149
Q

Nephritic syndrome: low GFR pathophysiology?

A
  • mesangial proliferation + capillary block by inflammation cells
  • disequilibrium of vasoconstrictors>vasodilators
150
Q

RPGN -Rapidly Progressive G.N Pathology?

A

crescents!!!- proliferation of podocytes, monocytes and macrophages present,
fibrin

Glomeruli may show focal necrosis, diffuse or
focal endothelial or mesangial proliferation

IF depends on type:
Immune complex GN 45% (grannular pattern)
Pauci immune GN 45%
Anti GBM 10%

EM rupture in GBM, in some cases
subepithelial deposits; NOT HELPFUL

151
Q

Nephritic syndrome DD (שאלה במבחן)?

A

anti-GBM-
IgA nephropathy/ burger’s diseases

Pauci-immune GN-
Idiopathic
Granulomatosis with polyangiitis (GPA)
Microscopic polyarteritis nodosa (PAN)

immune complex GN- 
Idiopathic
Postinfectious
SLE
Henoch Schonlein purpura
Cryo
SBE
shunt
NON RPGN-
malignant HTN
HUS/TTP
interstitial nephritis
SRC
emboli
152
Q

Immune complex GN characteristics?

A

low or normal C3

anti-GBM negative

IF: granular IgG and C3

153
Q

PAUCI – IMMUNE GN general characteristics?

A

normal C3
anti-GBM negative

IF: NORMAL

AntiNeutrophil Cytoplasmic Antibody (ANCA):

cANCA- Wegener’s granulomatosis / granulomatosis with polyangiitis

pANCA- microscopic polyangiitis

154
Q

Anti GBM GN characteristics?

A

normal C3

anti-GBM possitive 90%

IF: linear IgG and C3

Goodpasture syndrome (50-70%, lung involvement):
Antibodies against noncollagenous domain of alpha 3 chain of collagen IV

cresents!

155
Q

nephritic syndrome treatment?

A

PSGN- self limited

steroids (IV)

cytotoxicity- cyclophosphamide, Imuran

MMF (Mycophenolate mofetil)- for T cells

rituximab- B cells

HTN balancing

156
Q

MAP (mean arterial pressure) calculation?

A

2/3 DP +1/3 SP or DP + 1/3 PP

<60mmHg

157
Q

new blood pressure stages?

A 
(not that good with healthy young):
normal <120 <80
elevated blood pressure 120-129 <80
stage 1 HTN 130-139 80-89
stage 2 HTN >=140 >=90
158
Q

israeli blood pressure stages?

A 
best <120 <80
normal 120-129 80-84
borderline 130-139 85-89
stage 1 HTN 140-159  90-99
stage 2 HTN 160-179 
stage 3 HTN >=180 >=110
159
Q

Ambulatory Blood Pressure Monitoring?

A

better prognostic tool
HTN ≥130/80 24/h
day HTN / HomeBPM ≥135/85
night HTN ≥120/70 (‘dipping’, normal)

160
Q

Malignant hypertension pathology?

A

וסקוליטיס נמקית דיפוסית
קרישים בארטריולות
משקעי פיברין בדפנות הארטריולות.

161
Q

Malignant hypertension definition?

A

> 180/120

קצב העליה חשוב יותר מהערך עצמו- יל”ד חדש (רעלת היריון, גלומרולונפריטיס חדה)

162
Q

Malignant hypertension categories?

A

Hypertensive urgency- asymptomatic
community care

Hypertensive emergency- symptomatic (organ damage)
hospitalization, urgent IV

163
Q

primary blood pressure risk factors?

A

age- systolic elevates, diastolic elevated mid-age and reduced in elders

family history- 2X %

race- blacks

Obesity
low nephron count
high Na intake
high methanol intake 
low physical activity
psychosocial pressure
164
Q

secondary HTN risk factors?

A

drugs- oral contraceptives, NSAIDS, Tricyclics, SSRI, steroids, ErythroStymulatingAgents ,cyclosporine , amphetamines…

CRF/ ARI

primary hyperaldosteronism- HTN, hypokalemia, metabolic alkalosis

reno-vascular HTN-
Fibromuscular dysplasia- renal artery spiraling
>1% of patients with mild HTN
10-45% AT HIGH HTN
10-14% of coronary atherosclerosis (elders)
24-35% of peripheral arterial disease

ObstructiveSleepApnea

other: 
pheochromocytoma,  Cushing's , hypo/hyperthyroidism (mild diastolic,  mild systolic in accordance)
hypo/hyperparathyroidism
Aortic coarctation 
acromegaly 
hypercalcemia
165
Q

מתי יש לחשוד ביתר לחץ דם רנו-וסקולרי?

A
  • התחלה של יל”ד חמור לאחר גיל 55.
  • עליה של 50% קריאטינין אחרי מעכבי אנגיוטנסין.
  • מחלה טרשתית מפושטת
  • כליה אטרופית (ללא הסבר טוב אחר)
  • הפרש גדלים בין הכליות של מעל 1.5 ס”מ
  • כליה קטנה חד צדדית (<9 ס”מ)- 75% חסימה של כלי גדול
  • אירועים חוזרים של בצקת ריאות
  • אוושה סיסטולית-דיאסטולית בטנית חד צדדית – רגישות כ-40%, ספציפיות 99%!
166
Q

מתי לחשוד באלדוסטרוניזם ראשוני?

A

היפוקלמיה לא מוסברת <50%
היפרנתרמיה קלה
יתר לחץ דם עמיד לטיפול בנוכחות אינסידנטלומה.

167
Q

HTN treatment management?

A

life style- all

drugs-

stage 1- after life style changes fail or organ damage

stage 2- consider 2 drugs
(careful with elders or diabetes- orthostatism)

<80y- lower to 130/80
>80y / fragile patient- moderate reduction

168
Q

HTN drugs: compelling indications?

A

reduction of HTN it-self is more important than which drug to give

most- 7-13 mmHg systolic and 4-8mmHg diastolic reduction

systolic heart failure-
ACEi or ARB, BB, diuretic, spironolactone

post MI-
ACEi, BB, ARB, diuretic, spironolactone

proteinuric CKD-
ACEi or ARB

AP-
BB, CCB,

A.fib / A. flutter-
BB, NON-dihydropyridine CCB

169
Q

HTN drugs: comorbid conditions?

A

BPH- alpha blocker

essential tumor- BB

hyperthyroidism- BB

migraine- BB, CCB

osteoporosis- thiazides

Raynaud’s syndrome- dihydropyridine CCB

170
Q

HTN drugs: Contra indications?

A

Angioedema- ACEi

pregnancy- ACEi, ARB, renin inhibitor
will give- Labetalol, nifedipine, methyl-dopa

2nd/ 3rd heart block- BB, non-dihydropyridine CCB

may have adverse affects on comorbidities-
GOUT- diuretics
hyperkalemia- spironolactone , ACEi/ARB
hyponatremia- thiazides

171
Q

HTN primary treatment?

A

thiazides, CCB-DHP, ACEi, ARB

BLACKS- thiazides, CCB-DHP
proteinuric CKD- ACEi or ARB

172
Q

HTN combined therapy?

A

better than MAX dose of one drug
CCB-DHP- ACEi/ARB
thiazides- ACEi/ARB (not as good)

no ACEi AND ARB!!

173
Q

HTN therapy at night?

A

15% lower than day

Non-dipping= <10% reduction of night blood tension

move one drug to be taken at evening

174
Q

resistant HTN?

A

resistant after combination of 3 drugs (diuretics too) at <50% max dose
or
(15%) controlled with 4 drugs

175
Q

Pseudo-resistant HTN?

A

1st- drug non compliance
2nd- low salt life style non compliance

small cuff of Blood pressure checker
white coat (do ABPM)
176
Q

Urgent dialysis indications (test) ?

A

עודף נוזלים – בצקת ריאות

פריקרדיטיס (טמפונדות)

אנצפלופטיה אורמית-
שקיעה במצב הכרה
פרכוס

היפרקלמיה

חמצת מטבולית לא ניתנת לטיפול:
-כשסודיום-ביקרבונט לא יכול להינתן עקב עודף נוזלים

דמם לא נשלט בחולה אורמי (פגיעה בטסיות)

היפרקלצמיה קשה

הרעלות (Lithium)

177
Q

איך נבדיל בין אי-ספיקת כליות כרונית ואקוטית?

A

osteoporosis
anemia- EPO

US- small, cortex-medulla border attenuation

Amyloidosis- kidneys can be larger

178
Q

ARF categorization?

A

Pre renal
Renal
Post Renal- will start here, will help determine if urology patient

179
Q

POST RENAL- ARF diagnosis?

A 
אנמנזה:
מחלת אבנים
פרוסטטזים
גידול
שתן- כיליה שניה עובדת, לא עובדת, חסימה חד"צ
בדיקה פיזיקלית:
מישוש + ניקוש
רגישות מותנית
פרוסטטה- גושים, הגדלה
קטטר- שארית, גדולה בעיה בצינור שופכה

הדמיה:
US –
תחילה גודל כליה (כרוני/אקוטי), שנית הדרונפרוזיס
C.T.- פרוטוקול אבנים (IntraVenous Pyelogram)
צסטוסקיפיה + בדיקה רטרוגרדית (גולד סטנדרט)

180
Q

POST RENAL - ARF treatment?

A

קטטר (בייחוד בבעיות בצינור שופכה)

נפרוסטומיה- באים מהעור

181
Q

PRE RENAL ARF definition?

A

הכליה מתפקדת כיאות אך אינה מקבלת די דם כדי לסננו

182
Q

PRE RENAL ARF etiology?

A
  1. היפו-וולמיה

דימום: GI, בטני, חיצוני, (נבדוק דימום רקטלי)
שוק
לבבי : אינפרקציה, הפרעת קצב, בעיה מסתמית חריפה, טמפונדה (פריקרדיטיס)
MASSIVE PE
ANAPHYLAXIS
ספטי (שכיח במיוחד במאושפזים)
נוירוגני (נדיר)

איבוד מים:
זיעה
בטן פתוחה - פרפורציה ושטיפות, 3-4 ליטר ביום
כוויות

איבוד מים + מלח:
מעי - הקאות, שלשול

  1. מדור שלישי
    מיימת
    בצקות
  2. איבוד בשתן :
    DI, הגיע לניתוח, מונשם מורדם ולא שותה, איבוד מים
183
Q

PRE RENAL – ARF diagnosis?

A

אנמנזה:
בהתאם לנ”ל

בדיקה פיזיקאלית: 
ל"ד (ירוד) + אורטוסטטיזים (יש פיצוי בשכיבה)
טורגור ירוד (למשוך את העור)
ריריות יבשות
בצקות + מיימת
שיפשוף פריקרדיאלי 
Pulsus Pardoxus          
מיעוט/ריבוי שתן

מעבדה:

Urea/ creatinine (Plasma) > 20
(יוראה משמשת לריכוז השתן, מה שהכליה יכולה ורוצה)

Na (plasma) ↓ 🡪
(if adequate) Na (urine)< L/mmol10-20

U/P creatinine > 40 (if adequate function)

Fractional excretion of Na < 1% (FENA)
Na(U) \Na(P) x creatinine(P) \creatinine(U) x 100

urine osmolarity = Specific gravity > 1.030

184
Q

PRE RENAL – ARF treatment?

A

נוזלים, דם לפי צורך

פתרון הבעיה

185
Q

RENAL - ARF etiology?

A

פגיעה גלומורולית
פגיעה אנטרסטיציאלית
פגיעה טובולורית

כלי דם גדולים:
חסימה עורקית
חסימה ורדית

כלי דם קטנים:
HUS , TTP
cholesterol emboli

186
Q

renal artery blockage diagnosis?

A

atherosclerosis, ParoxymalAF

Pain, hypertension

US doppler
CT angio
MRA
angiography (treat too)

187
Q

renal vein blockage diagnosis?

A

same as artery but:

hypercoagulative patients

flank pain

hematuria, proteinuria

irreversible damage

188
Q

RENAL ARF- acute tubular necrosis Pathophysiology?

A

מדולה :
אספקת חמצן נמוכה
צריכת חמצן גבוהה

הטובולים - הראשונים לסבול

189
Q

RENAL ARF- acute tubular necrosis etiology?

A

same as pre-renal ARF

טוקסינים אנדוגנים-
המוגלובין, מיוגלובין

טוקסינים אקסוגניים-
חומר ניגוד
אמינוגליקוזידים
ציטוטוקסיקה/ כמוטרפיה
NSAID’s
190
Q

rhabdomyolysis etiology?

A 
טראומה
פרכוס
שכיבה ממושכת
מכת חום
מחלה וירלית קשה
חסר CPT- carnitine palmitoyltransferase
191
Q

acute tubular necrosis diagnosis?

A 
אנמנזה:
סיבות לאיסכמיה כנ"ל
המוליזה – מחלות רקע, שתן קולה
חשיפה לחומר ניגוד-
CT 
אנגיוגרפיה 
צינטור לב
תרופות (כימו וכו)

קליניקה:
אוליגוריאה (ניתן בזהירות פוסיד, גרם ל24 שעות)
ללא אוליגוריה

מעבדה : (שתן)
Na >20
FENA > 1%
Specific Gravity ↓
hematuria 
Muddy Broad Brown Casts
plasma:
rhabdomyolysis- CPK↑ + myoglobin↑
Pi↑ K↑
hemolysis- bilirubin↑ + LDH↑
uric acid↑
192
Q

ATN treatment?

A

נוזלים

הבססת שתן ע”פ צורך (מוריד קריסטליזציה של מיוגלובין בטובולי)

משתנים- עד גרם ביממה, במידה ואוליגורי

דיאליזה

193
Q

A.I.N definition?

A

תהליך דלקתי באינטרסטיציום המתפתח באופן מהיר והגורם לאי ספיקת כליות חריפה.

15% ממקרי אי ספיקת כליות חריפה.

194
Q

A.I.N etiology?

A

תרופות (70-80%)

פנצילינים (הכי רווח)- ללא קשר למינון לעיתים תגובה אלרגית הכוללת: חום פריחה וארטרלגיה.

NSAID- גם פגיעה גלומרולרית ואז פרוטאינוריה.
דיורטיקה
צפאלוספורינים

זהום (הכל, 15%)

אוטואימוני:
דחייה חריפה של כליה מושתלת.
ואסקוליטיס
S.L.E.
סארקואידוזיס
T.I.N.U. SYND.

גידול- לימפופרוליפראטביות

מטאבולי

אידיופאטי- 8%

195
Q

A.I.N diagnosis?

A

אנמנזה: חום, פריחה, ארטראלגיה ב1/3 מהמקרים
תרופות חשודות, מעורבות איברים אחרים.

בדיקה פיזיקלית: פריחה, עיניים.

שתן: אאוזנופלוריה (הכי חשוב), כדוריות לבנות, מעט חלבון ויתכנו מעט גלילים גרנולאריים.

ספירת דם: אאוזינופליה לעיתים. אנמיה.

ביופסיה- גולד סטנדרט

196
Q

Renal Biopsy indications?

A

No improvement after withdrawal

drug, infection

197
Q

renal biopsy Contraindications?

A 
Bleeding diathesis 
Solitary kidney (not absolute)
No cooperation
End-stage renal disease (most important)
Uncontrolled hypertension 
Patient refusal 
Sepsis
198
Q

A.I.N- treatment?

A

הפסקת תרופות חשודות.

יתכן וטיפול בסטרואידים מקצר משך מחלה ורמות קראטינין אך לא פרוגנוזה

ב NSAIDS אין כנראה יתרון לסטרואידים

במחלות אוטואימוניות לשקול ציטוטוקסיקה

199
Q

CKD definition?

A 
פגיעה בתפקוד הכליה למשך 3 חודשים ויותר:
אלבומינוריה
משקע שתן פעיל
ממצאים בהדמיה (כליות קטנות, היפראקואיות, פוליציסטיות וכו)
ביופסיית כליה
כליה מושתלת (בלי קשר לתפקודה)
ירידת GFR
200
Q

גורמי סיכון במחלה כלייתית כרונית: קרדיווסקולארי?

A

מחלה כלייתית כרונית מהווה בעצמה גורם סיכון קרדיווסקולארי משמעותי ולכן נקפיד יתרה על איזון גומרים קרדיווסקולאריים אחרים:

היפרליפידמיה, נרצה להגיע ל:
LDL< 100gr%, 70gr% is better

עישון

יל”ד-
עם פרוטאינוריה מעל 0.5 גרם ליום- עד 130/80
ללא -עד 140/90

פרוטאינוריה- פחות מ 1 גרם ליממה או ירידה של 50-60% לפחות (מתחת ל 3.5 גרם ליממה).
טיפול במחלת יסוד, ACE/ARB, הגבלת חלבון
כלכלה דלת מלח-
2.3 גרם נתרן ליום
מעל גיל 51 עם רקע של סכרת ו/או יל”ד ו/או אי ספיקת כליות= עד 1.5 גרם ליום.

201
Q

סיבוכים במחלה כלייתית כרונית?

A

קרדיווסקולארי

זיהומים
בעיקר בדרכי הנשימה, המין והשתן- חיסונים לפני דיאליזה

ממאירויות (ציסטות בכליות שלא עובדות)

אנמיה

מחלות עצם

עודף נוזלים- 
הגבלת השתייה, מתן משתנים והגבלת מלח
היפרקלמיה- 
kayexalate, ACEi/ARB, spironolactone.
חמצת מטאבולית- דיאטה דלת חלבון, סודיוםביקרבונט, דיאליזה
202
Q

סיבוכים במחלה כלייתית כרונית: אנמיה?

A

חסר ברזל במחלת כליות כרונית מתקדמת?
סטורציית טרנספרין < 20%
פריטין < 100 נ”ג/מ”ל
-במטופלי דיאליזה: <200נ”ג/מ”ל

ניתן ESA-
נביא להמוגלובין של 10-12 גרם %.
מקובל גם במטופלי מרפאת פרה דיאליזה

203
Q

זרחן באי ספיקת כליות?

A

עיקר ההפרשה דרך הכליות- 5400מ”ג בשבוע
דיאליזה- מחצית מכך= יש לטפל בתצורות נוספות

היפרפאראתיירודיזם משני לרמות הזרחן הגבוהות:
גירוי ישיר
היפוקלצמיה משנית להיפרפוספטמיה
ירידה בייצור ויטמין D פעיל
עמידות בלוטת PT לפעילות ויטמין D
  • שקיעת קומפלקסים זרחן-סידן בדפנות כלי הדם
  • קלסיפיקציה של כלי דם עקב רמות סידן גבוהות
  • פגיעה באנדותל
  • יצירת רדיקאליים חופשיים
204
Q

מחלות עצם במטופלי אי ספיקת כליות?

A

Osteitis fibrosa cystica
Adynamic bone disease
Osteomalacia
Mixed uremic osteodystrophy

parameters of differentiation:
turnover rate (OS, OB)
mineralization
bone volume

205
Q

Osteitis Fibrosa Cystica?

A 
due to high PTH 🡪
high turnover rate (OS, OB)
high bone volume
איזורי ספיגת עצם מוגברת
עצם חלשה ולא יציבה
206
Q

Adynamic Bone Disease?

A 
due to low PTH 🡪
low turnover rate (OS, OB)
low bone volume
מגיל מבוגר ,סוכרת
נטייה לשברים מרובים 
נטייה רמות סידן גבוהות
207
Q

Osteomalacia?

A

mainly due to VIT-D.diff
low turnover rate (OS, OB)
higher bone volume with abnormal mineralization

208
Q

CKD treatment?

A
  1. Pi-
    need protein in diet↑ 🡪 Pi ↑ (E-101…) 🡪 restriction is problematic 🡪 Pi binders
    most common:
    Calcium Carbonate
    Calcium Acetate
    (מינון מוגבל עקב סיכון מוגבר להסתיידויות כלי דם)

Sevelamer Carbonate-
in CKD 3 and above

Lantanum-
liver excretion
ph>3 🡪 vast GI activity

  1. ויטמין D פעיל-
    המינון מוגבל בשל הופעת היפרפוספטמיה ו/או היפרקלצמיה כתוצאה מהטיפול.
    לדיכוי הפרשת PTH
    קיים גם במתן לוריד
  2. Vitamin D Receptor Agonist Zemplar
    הפעלת של רצפטור לויטמין די רק בפאראתיירואיד
    ADVANCED CKD not responsive to alfa D3
    קיים גם במתן לוריד
  3. Mimpra
    Ca sensing receptor (CaSR) ACTIVATOR 🡪 PTH ↓
    המינון מוגבל ע”י היפוקלצמיה או רמת הורמון פאראתיירואיד

preperation for Renal replacement therapy

209
Q

גישה לכלי דם לצורך דיאליזה?

A

צנתר מרכזי -
וריד הצוואר, וריד המפשעה, הווריד התת בריחי
יושב בתוך חדר ימין, דרך הקוואה העליונה, פתח יציאה דרך תעלה תת עורית יחסית ארוכה:
מניעת זיהומים
פיברוזיס הקבע את הצנתר ומקשה על הוצאתו
זמין לשימוש מיידי

Arteiovenous Fistula
יכול לקחת כמה חודשי הכנה

Arteiovenous Graft
עורקים וורידים לא תקינים, דקירה דרך השתל עצמו.

דיאליזה פריטונאלית שבה הפריטונאום משמש כממברנה חדירה חלקית
לאחר פרק זמן שנקבע מראש מרוקנים את הנוזל מן הבטן ומחליפים אותו בנוזל חדש

210
Q

עקרונות פעולה של המודיאליזה?

A

שאיבת הדם באופן אקטיבי

Convective transport-
גרירת המומסים עם גרדיאנט המים

Diffusive transport-
מעבר דרך ממברנה חצי חדירה

סליל הדיאליזה-
שמירת גרדיאנט מומסים ע”י הזרמת דיאלזט ודם בכיוונים מנוגדים.
ניתן לשנות הרכב דיאליזט לצרכינו

211
Q

סיבוכי המודיאליזה?

A

ירידת לחץ דם (שוק)
זיהום בצנתר
חסימת שאנט

בין דיאליזה אחת למשניה:
צבירת נוזלים
היפרקלמיה

212
Q

גישה לביצוע דיאליזה צפקית?

A

tenckhoff catheter

subcutaneous cuff + deep cuff (muscle)

213
Q

דיאליזה צפקית- עקרונות פעולה?

A

כ-40% מהאולטרה-פילטרציה.
תעלות אקוופורינים מסוג 1 - מעבר מים בהתאם למפל אוסמוטי, הנוצר ע”י הוספה של דיאליזאט היפרטוני.
60% מעבר פרה-צלולרי.

דיפוזיה וקונבקציה.

דיאליזאט: דומה להמודיאליזה אבל
dextrose
ריכוזים שונים שלו ימשכו כמות מים שונה תוך זמן שונה

נחכה כשבועיים שלושה עד שיש רקמה מסביב לצינור למניעת דלף

214
Q

סוגי דיאליזה צפקית?

A

CAPD (continuous ambulatory PD)
לרוב 3 שחלופים במהלך שעות היום ושחלוף אחד ארוך בשעות הלילה

CCPD (continuous Cycler Assisted PD)
המכשיר מבצע את השחלופים בעצמו במהלך הלילה. לקראת הבוקר המכשיר ממלא את הבטן בתמיסת הicodextrin
שיכולה להישאר 12-14 שעות

IPD (intermittent PD)
פחות שחלופים

215
Q

דיאליזה צפקית- סיבוכים?

A

זיהומים: מוצא צנתר, תעלה, פריטוניטיס

בעיות טכניות בזרימה/דלף (עצירות- לחץ/ סתימה של החרירים)

אובדן חלבון- שיאכלו כי פינוי זרחן טוב יחסית

ספיגת סוכר – סוכרת, דיסליפידמיה (ספיגת הדקסטרוז)

בקעים- עליית תוך בטני

הרס פריטונאום: AGEs
עקב הדקסטרוז

216
Q

types of RRT and indications?

A

hemodynamic instability-
1st CRRT / SLEDD (keep blood pressure)
2nd PeritonealDialysis
3rd Interminant hemodialysis

Fluid overload-
1st CRRT / SLEDD
2nd Interminant hemodialysis
3rd PeritonealDialysis

acute intracranial injury / hypertension-
1st CRRT / PD
2nd ProlongedIterminantRRT
3rd Interminant hemodialysis

life threatening conditions-
1st IHD
2nd ProlongedIterminantRRT
3rd CRRT
4rd  PD

CRRT vs IRRT
Better in hemodynamically unstable patients
Better at fluid control / removal (no nephron damage)

217
Q

CRRT characteristics?

A

disadvantages:
Requires anticoagulation
Difficult mobilization

Higher flexibility
Large cumulative dose
Planned fluid removal
Hemodynamic stability
No large solutes changes – for Neuro patients
218
Q

Intermittent renal replacement therapy characteristics?

A

Higher solutes removal rate
Intermittent = easier mobilization

disadvantages:
High fluids shifts – hemodynamic instability
Rapid solutes shifts

219
Q

direct / indirect presentation (graft)?

A

direct-
התאים של התורם עצמו מציגים לתאים של המקבל (דנדריטיים)

indirect-
לאחר מספר ימים
מעבר לתאים של המקבל המציגים את האנטיגנים בבלוטות הלימפה.

220
Q

Adaptive (Acquired) Immunity (t cell) activation?

A
  1. TCR-MHC2- ANTIGEN presentation
  2. CD28-CD80/86 (CTELA4 inhibitory)
    3.cytokines-
    from APC IL12
    autocrine singnaling (IL-2)
221
Q

detection of anti HLA antibodies?

A

ELISA- innate immune activation and membrane poring thus stain enter cells

Flow bead- florescent conjugated anti-IgG to HLA antibodies to HLA antigens on beads

222
Q

donor antibody / cross match scenarios?

A

Antibody negative 🡪 Cross Match negative 🡪 proceed

Antibody negative 🡪 Cross Match positive 🡪 proceed ( antibodies not to HLA)

Antibody positive (low count antibodies) 🡪 Cross Match negative 🡪 proceed

Antibody positive 🡪 Cross Match positive 🡪 do not proceed

223
Q

purpose of induction therapy?

A

deplete or modulate T-cell responses at time of antigen presentation

allow reduction of other components such CNI or corticosteroids

224
Q

glucocorticoids role at traslplantation?

A

induction + maintenance + treatment of rejection

inhibit dendritic cell function
inhibit NF-kB pathway
inhibit cytokines production
inhibit innate and addaptive immunity

225
Q

depleting agents role at transplantation?

A

thymoglobulin (polyclonal) / OKT-3 (monoclonal) / Alemtuzumab (anti CD52):

T-cell lysis and/or clearance of circulating lymphocytes

ADVERSE EFFECT:
Cytokine storm syndrome- massive cell lysis
thrombophlebitis (avoid- give in large vein)
thrombocytopenia, leukopenia
CMV
anaphylaxis
Post transplantation lymphoproliferative.d- (EBV Ab positve donor)

226
Q

IL-2 RA?

A

binds CD25 antigen at surface of activated T lymphocytes
non depleting - no risk of cancer or infection

ADVERESE:
insomnia, tremor, headache

227
Q

rituximab role in transplantation?

A

induction with ABO incompatible

228
Q

Maintenance Immunosuppression?

A

Usually in addition to steroids

calcineurin inhibitors-
mTOR inhibitors
antiproliferative agents

229
Q

Calcineurin Inhibitors?

A

Ciclosporin A, Tacrolimus

T-cell activation 🡪 incearse Ca 🡪 calmodulin binding 🡪 Inncrease IL-2 🡪 proliferation

calcineurin inhibit Ca-calmodulin binding

ADDVERSE:
Diabetes, hyperlipidemia, hypertension
interactions with other drugs (CYP3A4)

During diarrhea- absorption is increased (P-Glycoprotein, MDR-1= epithel excretion dysfunction)

230
Q

mTOR Inhibitors

A

Sirolimus, Everolimus

cell growth inhibition (cytoskeletal and protein synthesis)

231
Q

antiproliferative agents (Antimetabolites)?

A

azathioprine-
purine analogue

was largely replaced by:

Mycophenolate-
inosine monophosphate dehydrogenase inhibitor (IMPDH)
- inhibition of DE NOVO synthesis

232
Q

transplantation drugs combinations?

A

prednisone, PROGRAF, MYCOPHENOLATE

prednisone, PROGRAF, mTOR INHIBITOR

prednisone, mTOR INHIBITOR, MYCOPHENOLATE

PROGRAF, MYCOPHENOLATE
נדיר בארץ שנותנים רק קלצינאורין אינהיבטור ומיקופנולט, בעולם מקובל

233
Q

HyperAcute GRAFT rejection?

A

very rare
minutes to hours
Anti ABO, Anti HLA

no effective treatment

234
Q

Acute GRAFT rejection?

A

cellular, T cell mediated= anti donor immune reaction, graft T cell infiltration
weeks to years

Renal: interstitial and tubular infiltration (blood vessels too)

treatment:
biopsy before steroids if able
bad biopsy or non effective treatment 🡪 depleting agents

235
Q

?Antibodies Mediated Rejection

A

שכיח בחולים מרוגשים מראש, גם כאשר ההצלבה הייתה שלילית מראש

PMNs + lympocytes in PTC +- endothelial arteritis
usually no tubulitis

donor specific anti HLA 1 or 2
+- thrombi duo to coagulation activation

C4d deposition in immunofluorescent stain

236
Q

treatment of Antibodies Mediated Rejection?

A

antibody removal/ neutralization-
rituximab (splenectomy) , plasmapheresis, IVIg

anti plasma cells- bortezomib

if needed (by biopsy):
depleting agents for cell mediated rejection
conversion to tacrolimus based regims

237
Q

chronic rejection?

A

month to years
anti HLA antibodies against donor cells

no treatment

מבואות (8 decks)

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