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RENAL Flashcards

0
Q

What are the embryologic sources of renal system?

A

Pro nephrons degenerates 4 week
Mesonephros male genital contribution
Metanephros uerteric bud until collector tubes // metanephric mesenchyme (mesoderm) until distal convoluted tubule

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1
Q

What’s POTTER sequence ?

A 
Pulmonary hypoplasia 
Oligohydramnios (trigger) 
Twisted face
Twisted skin 
Extremity defects 
Renal failure (in utero)
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2
Q

Genetic defects related whit Horseshoe kidney ?

A

ANEUPLOID DEFECTS

down, Edwards, Patau, turner…

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3
Q

What’s the clearance Ecuation?

A

Cx = UxV/Px

Cx GFR: net tubular secretion of X.
Cx = GFR: no net secretion or reabsorption.

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4
Q

What’s the GFR Ecuation?

A

GFR = Uinulin × V/Pinulin

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5
Q

What are the effective renal plasma flow And renal blood flow?

A

eRPF = UPAH × V/PPAH = CPAH.
RBF = RPF/(1 − Hct).

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6
Q

What’s filtration fraction and filtered load?

A 
Filtration fraction (FF) = GFR/RPF. 
Normal FF = 20%.

Filtered load (mg/min) = GFR (mL/min)× plasma concentration (mg/mL).

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7
Q

Actions of NSAIDs and ACE inhibitors in bowman capsule

A

NSAIDs ⬇️GFR ⬇️RPF ↔️FF (afferent 🚫)

ACE inhibitors ⬇️GFR ⬆️RPF ⬇️FF (efferent ✅)

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8
Q

Calculation of reabsorption and secretion rate(4)

A

Filtered load = GFR × Px.
Excretion rate = V × Ux.
Reabsorption = filtered – excreted.
Secretion = excreted – filtered.

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9
Q

How is the glucose clearance?

A

∼ 200 mg/dL, glucosuria begins (threshold)

∼ 375 mg/dL, all transporters are fully saturated (Tm).

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10
Q

What’s Hartnup disease?

A

neutral aminoaciduria and  absorption from the gut Ž  tryptophan for conversion to niacin Ž pellagra-like symptoms.
Treat with high-protein diet and nicotinic acid.

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11
Q

Which drugs acts in the 4 diferents nephrons segments?

A

EARLY PCT
ACE inhibitors 🚫Na/H exchange
ACETAZOLAMIDE 🚫carbonic anidrase

THICK ASCENDING LOOP
Loop diuretics 🚫NA,K,Cl co-transporter

EARLY DCT
Thiazides diuretics 🚫NA,Cl co transporter
⬆️Ca/Na exchanger PTH

COLLECTING TUBULE
Amiloride triamterene 🚫 Na channels
Espironolactone 🚫aldosterone receptores

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12
Q

Whats the fundación of ALDOSTERONE in Collecting Tubule? (1,3. 2,2.)

A

✅ In principal cells:⬆️  apical K+ conductance,  ⬆️Na+/K+ pump,  ⬆️ENaC channels Ž⏩lumen negativity Ž ⏩K+ loss.

✅In α-intercalated cells: ⬆️ H+ ATPase activity⏩⬆️ Ž  HCO3−/Cl− exchanger activity.

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13
Q

Whats the función of ADH in Collecting tubule?

A

✅ADH—acts at V2 receptor⏩ Ž insertion of aquaporin H2O channels on apical side.

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14
Q

Explain renal tubular defects (FaBio Guarnizo Loca)

A

FANCONI 🚫PCT ⬆️excretion a.a. , glucose, HCO3–, and PO43– metabolic acidosis
BARTTER Affects Na+/K+/2Cl– cotransporter.metabolic alkalosis ⬆️U Ca
GITELMAN Affects NaCl reabsortion DCT Hypokalemia , hypomagnesemia, hypocalsuria ,metabolic alkalosis.
LIDDLE ⬆️Na reabsortion ⬆️TA hypokalemia metabolic alkalosis ⬇️aldosterone tto Amiloride

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15
Q

What’s Syndrome of apparent mineralocorticoid excess?

A

Hereditary deficiency of 11β-hydroxysteroid dehydrogenase
TOO MUCCH CORTISOL
⬆️mineralocorticoid activity
⬆️TA,hypokalemia,metabolic alkalosis.

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16
Q

What’s the action of ANP BNP?

A

relaxes vascular smooth muscle via cGMP⏩ ⬆️GFR ⬇️renin

⬆️Na+ filtration with no compensatory Na+ reabsorption

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17
Q

What’s the function of juxtaglomerular aparatus?

A

JG cells secret RENIN ( B1 receptors ⏩renin) BBs⏩ ⬇️renin

MACULA DENSA sense ⬇️NaCl ⏩adenosine⏩vasoconstriction

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18
Q

Action of PTH to ⬆️ Ca reabsortion

A

✅1α-hydroxylase

Convert 25-OH D3⏩1,25-(OH)2 D3

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19
Q

Action of ATII

A

Efferent constriction ⏩⬆️GFR and ⬆️FF but with compensatory Na+ reabsorption

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20
Q

Which situations cause hyperkalemia? DO LAβS.

A

Digitalis (blocks Na+/K+ ATPase)
HyperOsmolarity
Lysis of cells (e.g., crush injury, rhabdomyolysis, cancer)
Acidosis
β-blocker ⬇️Na+/K+ ATPase
High blood Sugar (insulin deficiency)

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21
Q

What’s the predicted PCO2 from Metabolic Acidosis

A

Pco2 =1.5[HCO3–]+8±2

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22
Q

Types of renal tubular acidosis (3)

A

Distal (type 1), urine pH > 5.5 Hypokalemia ⬇️H secretion
Proximal (type 2), urine pH

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23
Q

Ethology of urine Casts (6)

A

RBC casts glomerulonephritis malignant hypertension
WBC casts acute pyelonephritis transplant resection
Fatty casts (“oval fat bodies”) Nephrotic Syndrome
Granular (“muddy brown”) Acute Tubular Necrosis
Waxy casts CRF
Hyaline casts Non specific

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24
Q

What are the Nephritic syndromes (5)

Which is a GBM Damage

A
  • Acute poststreptococcal glomerulonephritis
  • Rapidly progressive glomerulonephritis
    • IgA nephropathy (Berger disease)
    • Alport syndrome
    • Membranoproliferative glomerulonephritis
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25
Q

What are the Nephrotic Syndromes (5)?

Which is Podocyte Disruption

A
  • Focal segmental glomerulosclerosis (1° or 2°)
  • Minimal change disease (1° or 2°)
    • Membranous nephropathy (1° or 2°)
    • Amyloidosis (2°)
    • Diabetic glomerulonephropathy (2°)
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26
Q

What are the Nephritic - Nephrotic Syndromes(2)

Which is a severe GBM damage

A

• Diffuse proliferative glomerulonephritis
• Membranoproliferative glomerulonephritis

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27
Q

Lab findings in Acute poststreptococcal glomerulonephritis(4)

A

Cola-colored urine
IF—(“starry sky”) granular appearance (“lumpy-bumpy”)
⬆️ anti-DNase B titers
⬇️complement levels

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28
Q

Microscopic findings in Rapidly progressive (crescentic) glomerulonephritis (RPGN) and cells , type of hypersensitivity

A

LM and IF—crescent moon shape
glomerular parietal cells, monocytes, macrophages.
Type II hypersensitivity

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29
Q

What diseases can provoke RPGN (3)

A

ƒGoodpasture syndrome—type II linear IF HEMATURIA/HEMOPTYSIS

IMMUNE -COMPLEX : postestreptococal , SLE, Ig A, Henoch-shonlein
ƒ
Granulomatosis with polyangiitis (Wegener) ƒ PR3-ANCA/c-ANCA. Microscopic polyangiitis MPO-ANCA/p-ANCA.

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30
Q

How is seen in LM and IF the Diffuse proliferative glomerulonephritis (DPGN)

A

Due to LES
LM—“wire looping”
IF—granular

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31
Q

How is seen Ig A nephropaty (Berger Disease)

A

IF—IgA-based IC deposits in mesangium proliferation

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32
Q

How is seen Alport Syndrome?

A

Mutation type IV collagen
thinning and splitting of glomerular basement membrane
can’t see, can’t pee, can’t hear

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33
Q

How is seen Membrano­ proliferative glomerulonephritis (MPGN)

A

Type I—subendothelial immune complex “tram-track” GBM splitting caused by mesangial ingrowth.

Type II—intramembranous IC deposits; “dense deposits.”

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34
Q

Why in Nephrotic syndrome there is an hypercuagulative and immunodeficiency state?

A

Antithrombin (AT) III loss in urine

loss of immunoglobulins in urine

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35
Q

Principal features of Focal segmental glomerulosclerosis (2)

A

EM—effacement of foot process like minimal change disease.
Collapsing glomerulopathy
Proliferation and hypertrophy of epithelial cells

MCC of nephrotic syndrome in African Americans and Hispanics.

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36
Q

Principal features of Minimal change disease (lipoid nephrosis)

A

EM—effacement (fusion) of foot processes
MCC of nephrotic syndrome in children
GOOD RESPONSE TO ABs

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37
Q

What’s the principal features of Membranus Nephropaty?

A

EM—“spike and dome” appearance with subepithelial deposits.
MCC of 1° nephrotic syndrome in Caucasian adults.

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38
Q

How is seen Amyloidosis?

A

LM—Congo red stain shows apple-green birefringence under polarized light.

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39
Q

How is the GFR and permeability in Diabetic Glomerulonephropaty?

A

GMB thickening
⬆️ Permeability
⬆️ GFR

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40
Q

How is seen calcium stones?

A

⬆️pH calcium Phosphate
⬇️pH calcium oxalate

RADIOPAQUE!!!!
Hypercalciuria
Normocalcemia
TTO hydratation, tyazides, citrate

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41
Q

Cause of Ammonium, magnesium, phosphate stones

A

⬆️pH

infection with urease ⊕ bugs (e.g., Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella)

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42
Q

What are the RADIOLUCENT stones?(2)

A

Utica acid

Cystine Cistinuria Children Sodium cyanide nitroprusside test ⊕

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43
Q

What are the most common renal cancers in children and adults?

A

ADULTS Renal cell carcinoma from PCT cells

CHILDREN Wilms tumor (nephroblastoma) from embryonic glomerular

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44
Q

What are the associations for transitional cell carcinoma? Pee SAC

A

Phenacetin
Smoking
Aniline dyes
Cyclophosphamide

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45
Q

Risk factors of Squamous cell carcinoma of the bladder (4)

A

Schistosoma haematobium infection (Middle East)
chronic cystitis
smoking
chronic nephrolithiasis

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46
Q

What is the characteristic microscopic change of chronic Pyelonephritis?

A

thyroidization of kidney

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47
Q

Disease related whit diffuse cortical necrosis (2)

A

Obstetric catastrophes

Septic shock

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48
Q

Keys findings in Acute Tubular Necrosis

A

⬆️FENa>1

Granular “muddy brown” casts

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49
Q

Stages of Acute tubular necrosis and its etiology

A
  1. Inciting event
  2. Maintenance phase—oliguric; lasts 1–3 weeks; risk of hyperkalemia, metabolic acidosis, uremia
  3. Recovery phase risk of Hypokalemia

ISCHEMIC
NEPHROTOXIC

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50
Q

What’s Renal Osteodystrophy?

A

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia Ž 2° hyperparathyroidism.

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51
Q

Contraindications of use of mannitol

A

Anuria

Heart Failure

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52
Q

What are Loop diuretics?(4)

A

Furosemide
Bumetanide
Torsemide

Ethacrynic acid

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53
Q

What are the toxicity symptoms of Loop diuretics OH DANG!

A 
Ototoxicity, 
Hypokalemia, 
Dehydration, 
Allergy (sulfa), 
Nephritis (interstitial), 
Gout.
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54
Q

What are the toxicity symptoms of Thiazides diuretics?(4)

A

⬆️ Glycemic
⬆️ Lipidemia
⬆️ Uricemia
⬆️ Calcemia

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55
Q

How can identify diuretics by urine labs ? (5)

A 
⬇️ Na : Osmotic 
⬇️ K : potassium sparing 
⬆️ HCO3 : carbonic anhydrise inhibitor 
⬆️ Ca : loop diuretic 
⬇️ Ca : thiazide
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56
Q

What are potassium sparing diuretics? (3)

A

Spironolactone
Eplerenone
Triamterene
Amiloride

57
Q

What diuretics cause acidemia? (2)

A

Carbonic anhydrise inhibitors

K sparing

58
Q

What diuretics cause alkalemia?

A

Loop diuretics

Thiazides

59
Q

What are the toxicity symptoms of ACE inhibitors? CATCHH

A 
Cough
Angioedema 
Teratogen 
⬆️Creatinine ( ⬇️GFR)
Hyperkalemia
Hypotension.
60
Q

Mechanism of action of Aliskiren

A

Direct renin inhibitor

61
Q

How is seen in LM biopsy of kidney in HTA and chronic Diabetes?

A

Homogenous deposition of eosinophilic (pink) hyalin material in the intima and media of small arteries and arterioles HYALINE ATHEROSCLEROSIS

62
Q

In the embryonic stage what is the structure which communicates the yolk sac and urogenital sinus?

A

ALLANTOIS!!!!!!

63
Q

What are the congenital situations in allantois problems?

A

PATENT URACHUS complete failure of obliteration
URACHAL SINUS failure of close distal
URACHAL CYST failure of central obliteration

64
Q

What’s the most common pathologic cause of unilateral fetal hydro nephrosis ?

A

Narrowing of ureteropelvic junction

65
Q

What’s the most common cause of bilateral fetal hydro nephrosis in boys?

A

Posterior urethral valves

66
Q

Which substance is needed to calculate GFR (2)

A

INULINE or CREATININE!!!!!!!!

67
Q

Which elements are seen in Fluorescent microscopy in RPGN?

A

Linear IgG a and C3

68
Q

Clinical symptoms of goodpasteur, reumatic heart disease, granulomatosis and polyangiitis.

A

goodpasteur HEMOMPTISIS OLIGURIA
reumatic heart disease JOINT PAIN AND CARDIAC MURMUR
granulomatosis and polyangiitis. NASAL ULCER HEMATURIA

69
Q

What’s the most important feature to develop in Order to start a Pielonephritis?

A

Anatomic or Functional Vescicoureteral Reflux

70
Q

Does the the testicular vessels enter the true pelvis?

71
Q

What’s selective proteinuria?

A

Albumin loss with minimal loss of the more bulky proteins ( IgG macroglobulin)

72
Q

What components are most selective in Glomerulus ?

A

Diaphragms between foot process

GBM

73
Q

What happen is there is too much acyclovir in the system?

A

Acyclovir can undergo on crystallization, crystaluria , renal tubular damage in the collecting duct.

74
Q

What is the effect of lithium in the nephron?

A

Nephrogenic diabetes insipidus

Antagonist of ADH

75
Q

How mucho is the mínimum Urine production by a healthy kidney ?

76
Q

What are kimmelsteil-Wilson nodules?

A

Diagnosis for nodular glomerulosclerosis in diabetic nephropathy
Whit glomerular basement thickening and increased mesangial matrix deposition

77
Q

What’s the normal anion GAP and how is calculated?

A

8-12

Anion GAP = Na-[Cl + HCO3]

Differentiate METABOLIC ACIDOSIS

78
Q

What diseases are related whit focal segmental glomerulonephritis ?(3)

A

HIV
Heroin abuse
Severe obesity

79
Q

What type situations are related whit membranous glomerulonephritis ?(4)

A 
TUMORS 
Solid tumors lung
Breast
Prostate 
Colon

SISTEMIC DISEASES SLE DM2

INFECTIONS hepatitis B. C malaria syphilis

DRUGS Gold penicilamine NSAIDs

80
Q

What type of bacteria is linked whit staghorn stone? (2)

A

Proteus

Urease ➕

81
Q

What are staphylococcal antibodies?

A

Anti DNAasa B
Anti hialuronidase
ASO

82
Q

How is PSGN IF and EM seen?

A

IF. Granular deposits of. Ig G, Ig M and C3 in GMB mesangium

EM Subepithelial Humps

83
Q

What type of of deposits are characteristic in type 1 glomerulonephritis ?

A

Sub endothelial C1q

84
Q

What type of deposits are found in LES whit poor prognosis?

A

Ig E deposits

85
Q

What blood and serum findings are common in renal cell carcinoma?

A

⬆️ EPO ( eritrocytosis )

⬆️ PTH ( hypercalcemia )

86
Q

Histologic characteristics of goodpasteur syndrome?

A

IF linear deposits

LM crescent formation

87
Q

How is seen membranoproliferative glomerulosclerosis ?

A

LM basement membrane splitting

Lobular aparence whit proliferative messangial cells

88
Q

What is found in focal segmental glomerulosclerosis ?

89
Q

Side effects of somatic diuretic therapy (3)

A

Dilutional Hyponatremy
Metabolic acidosis
Hypercalemia

90
Q

What are the causes of stress ,urge and overflow incontinence ?

A

Stress🔹urethral sphincter disfunction (cough, laugh )
Urge 🔹detrusor overactivity
Overflow🔹 impair detrusor contractility , obstruction

91
Q

What type of renal cells suffer hyperplasia after arterial renal stenosis?

A

Yuxtaglomerular apparatus

92
Q

What nephron son is impermeable to water?

A

Ascending loop

early distal consulate tubule

93
Q

Effect of the ADH on the urea?

A

Increase the Urea absorption in the collecting tubules

94
Q

What structure has to be transpassing in suprapubic cystostomy?

A

Anterior abdominal aponeurosis

95
Q

How tiazides cause Hypokalemia? If tiazides block Na/Cl cotransporters in PCT ?

A

Leads to hypovolemia activating renine-angiotensin- aldosterone
Enhancing Na/K antiporter

96
Q

What’s chlortalidone?

A

TIAZIDE!!!

97
Q

What a.a. Are not absorbed in cystinuria? COLA

A 
COLA
Cysteine
Ornithine
Lysine
Arginine
98
Q

Difference between metabolic alkalosis saline responsive and saline un-responsive?

A

Saline Responsibe vomit,nasogastric suction, thiazide/loop diuretic

Saline Un-Responsibe HYPERALDOSTERONISM

99
Q

Which electrolyte messured in urine is important to evaluate cause of metabolic alkalosis?

A

CHLORIDE IN URINE

100
Q

What kind of pathological bladder have patients whit SCLEROSIS MULTIPLE?

A 
Spastic bladder (hypertrophic)
Urge incontinence
101
Q

Where originates the clear cell carcinoma?

A

PROXIMAL TUBULAR EPITHELIAL CELLS!!!!

102
Q

Where the quantity of potassium is change. In Hyperkalemic or hypokalemic states ?

A

COLLECTING DUCT!!!

In the others remain the same

103
Q

Where is the hight osmolarity?

A

In the junction of the descending and ascending limbs of Henle

104
Q

Which substance increase the absorption of urea in collecting duct ( which normally is impermeable to urea)?

105
Q

Which type of cells proliferate and which substance is in the capsule bowman space in RPGN?

A

PARIETAL CELLS macrophages fiblobalsts

FIBRIN

106
Q

Drug used in ganciclovir-resistant CMV, and can cause hypocalcemia and hypomagnesemia ?

A

FOSCARNET!!!!!

⬆️risk of SEIZURES!!!

107
Q

Features in digital rectal examination in prostate cancer?

A

Nodules or asymmetric induration

108
Q

How much increase of serum creatinine is normal (tolerable) after beginning ACE inhibitors?

109
Q

Which agents can cause tubular necrosis? (5)

A 
Aminoglycosides 
Radiocontrast media
Cisplatin
Amphotericin B
Foscarnet
110
Q

Common drug which cause interstitial nephritis?

A

METHICILLIN!!!

111
Q

What is Nesetitide?

A

BNP analog

112
Q

How are the coagulation studies in thrombocytopenic thrombotic purpura and hemolytic uremic syndrome?

A

BT ⬆️
aPTT↔️
PT↔️

113
Q

What means livedo Reticularis?

A

Micro-embolism

114
Q

Effect in the kidney whit chronic use of NSAIDs ? (2)

And what serum cell is elevated?

A

Chronic interstitial nephritis
Ischemic papillary necrosis

HIGH SERUM EOSINOPHILIC COUNT !!!!!

115
Q

What’s oxybutinin?

A

Anti Muscharinic agent used in urge in continence

116
Q

What nephrogenic disease is related whit palpable purpura?

A

Henoch-Schonlein purpura. Ig A immune complex

117
Q

Specific urine finding in minimal change disease in the nephrotic syndrome and what is its cause?

A

Selective loss of ALBUMIN!!!!

Direct damage of podocytes by IL-13!!!!

118
Q

What is the WHO classification for renal disease of lupus?

A

Class I. Normal
Class II mesangial lupus nephritis
Class III focal proliferative glomerulonephritis
Class IV. Diffuse proliferative glomerulonephritis
Class V. Membranous glomerulonephritis

119
Q

Which arteries supply blood to the ureter?

A

Renal artery PROXIMAL!!!!!

superior Vesical artery DISTAL!!!!

120
Q

What type of patient suffers of fibromuscular dysplasia of the renal artery?

A

Women 20-30 years “strings and beads”

121
Q

What’s the most common cause of glomerulonephritis?

A

Ig A nephropaty (Berger disease)

5 DAYS AFTER FLULIKE SYMPTOMS

+ extrarenal symptoms ( abdominal paín, Arthralgias ,purpurik skin lesion) is call HONOCH- SCHONLEIN purpura

122
Q

How is seen the renal biopsy in Alport syndrome?

A

Lamellated basement membrane

Whit irregular thinning and thickening

123
Q

Which a.a. Generates CHO3 in the kidney in acidemia?

A

Glutamine ⏩ glutamate ⏩ ammonium ➕ HCO3

124
Q

What are the micturition centers?(3)

A

SACRAL parasympathetic bladder contraction S2-S4

PONTINE RETICULAR FORMATION relaxation external urethral sphincter

CEREBRAL CORTEX 🚫inhibits sacral

125
Q

Where the acute tubular necrosis ocurrs?

A

PROXIMAL TUBULES!!!!!

126
Q

When renal papillary necrosis ocurrs?(3)

A 
Urinary obstruction /infection
Interstitial nephritis (NSAIDs)
Microvascular disease
127
Q

What are the acid buffers used in the collecting duct to enhance the H+ excretion? (2)

A

HPO4 orthophosphoric acid➡️H2PO4 phosphoric acid

NH3 ammoniac ➡️ NH4 ammonium

128
Q

Which renal cell carcinoma is associated whit VHL?

A

Von hippel-Lindau disease chromosome 3q

Renal cell carcinoma

129
Q

What kind of crystals have pseudogout?

A

Rhomboidal
CALCIUM PYROPHOSPHATE !!!

Blue parallel
Yellow perpendicular

130
Q

Antigen implicated with membranous nephropathy ?

A

Phospholipase A2 receptor

131
Q

What are the histological findings in acute tubular necrosis?

A

Proximal tubular cell ballooning and vacuolar degeneration

132
Q

The finding of oxalate crystals are related whit what kind of poisoning?

A

Ethylene glycol poisoning

133
Q

In hepatorenal syndrome how is the renal flow?

A

RENAL VASOCONSTRICTION!!!!

134
Q

What is RASBURICASE?

A

Recombinant version of ureteres oxidase
Take Uric acid and transform to ALLANTOIN (10 times more soluble in urine)

Used in tumor Lysis Syndrome

135
Q

Important clinical presentation in acute interstitial nephritis by beta-lactamics?(3)

A

Fever
Rash
Acute renal failure

⬆️eosinophils
⬆️IgE

136
Q

Drugs which cause tubular vacuolization?

A

CALCINEURIN INHIBITORS

Tacrolimus
Cyclosporine

137
Q

Why patients with membranous nephropathy are on risk of thrombotic situations?

A

URINARY LOSS OF ANTITHROMBIN III !!!!

138
Q

What’s nutcracker effect ?

A

Left varicocele by compression of left renal vein by superior mesenteric artery.

140
Q

How ADH increase the osmotic concentration at the medullary interstisium?

A

increasing the absortion of Urea at the medullary segment of the collecting tube

141
Q

What are the High anion gap metabolic acidosis? CATMUDPILES

Normal 10-14

A 
Carbon monoxide/cyanide
Alcohol
Toluene 
Methanol
Uremia
Diabetic ketoacidosis 
Propylene glycol/ Paraldehyde
Isoniazid/Iron
Lactic acidosis
Ethylene glycol (antifreeze)
Salicylates

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