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Step 1 > Renal > Flashcards

Renal Flashcards

1
Q

Congenital hepatic fibrosis (and portal HTN) + hepatic cysts

A

associated with AR Polycystic Kidney Disease

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2
Q

Renal Failure, HTN, +/- Potter Sequence

A

ARPKD

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3
Q

Cysts in Liver and Kidney

A

ARPKD

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4
Q

Hypertension, Hematuria, and progressive Renal Failure in a young adult

A

ADPKD. HTN due to Renin

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5
Q

Conditions associated with ADPKD

A

Berry Aneurysm
MVP
Hepatic Cysts

so cysts in Brain, Liver, and Kidney

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6
Q

Inherited defect leading to bilateral enlarged kidneys with cysts in renal cortex and medulla

A

AR and AD PKD

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7
Q

Cysts and shrunken kidneys

A

Medullary Cystic Kidney Disease (ADPKD is enlarged kidneys). Cysts are in the medullary collecting ducts

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8
Q

Azotemia

A

“Increased nitrogenous waste products” =
Increased BUN and Creatinine.
Seen in Acute Renal Failure (along with oliguria)

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9
Q

Oliguria

A

Low urine production. Seen in ARF

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10
Q

Hematuria and Proteinuria + Flank Pain

A

Renal Papillary Necrosis

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11
Q

Causes of Renal Papillary Necrosis

A

Sickle cell (disease or trait),
Analgesics (aspirin/nsaids),
Acute pyelonephritis,
Diabetes Mellitus.

Papillary Necrosis is SAAD.
Can be triggered by infection or immune stimulus, or a sequelae of AIN

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12
Q

Basics of Nephrotic Syndrome (4 changes)

A
  1. Hypoalbuminemia = Pitting Edema
  2. Hypogammaglobulinemia = Infection risk
  3. Hypercoagulable state = loss of Antithrombin III (in urine)
  4. Hyperlipidemia/cholesterolemia = Fatty casts/frothy urine
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13
Q

Protein loss in MCD

A

Selective proteinuria

  • loss of albumin (LMW protein)
  • very minimal loss of bulky proteins –> so no Immunoglobulin loss
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14
Q

Treatment for MCD

A

Excellent response to Corticosteroids

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15
Q

Trigger for MCD

A

Can be triggered by recent infection (URI) or immune stimulus (vaccine or bee sting/insect bite)

rarely can be 2dary to Hodgkin lymphoma (cytokine mediated)

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16
Q

Imaging in MCD

A

LM - normal glomeruli
IF - negative (since no complex deposition)
EM - podocyte effacement

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17
Q

Nephrotic syndrome in Hispanic or African American

A

Focal Segmental Glomerulosclerosis

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18
Q

Nephrotic Syndrome in HIV pt, Sickle Cell Disease, or Heroin user

A

Focal Segmental Glomerulosclerosis

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19
Q

5 groups that get FSGS

A

Hispanic, Blacks, Heroin user, HIV pt, Sickle Cell

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20
Q

Effacement of podocytes (on EM)

A

MCD and Focal Segmental Glomerulosclerosis

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21
Q

Presents like MCD but no response to steroids and probs not in a child

A

FSGS (effacement of podocytes)

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22
Q

Nephrotic syndrome in Caucasian

A

Membraneous Nephropathy

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23
Q

Nephrotic syndrome in Hepatitis B or C, SLE, or drugs (NSAIDS)

A

Membraneous Nephropathy

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24
Q

4 associations with Membraneous Nephropathy

A

SLE, Hep B/C, Drugs (NSAID), Caucasian

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25
Q

C3 nephritic factor

A

Auto-Ab that stabilizes C3 convertase = increased complement and decreased serum C3

Type 2 MembranoProliferativeGlomeruloNephritis

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26
Q

Type 1 MPGN

A

Hep B/C infection. Tram track appearance. Subendothelial immune complex deposits with Granular IF.

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27
Q

Mesangial expansion + GBM thickening

A

Diabetic Glomeruolonephropathy

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28
Q

Nonenzymatic glycosylation of vascular BM –> Hyaline arteriolosclerosis

A

1st renal change in Diabetes Mellitus.

Loss of negative charge barrier of glomerulus
–> Increased permeability

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29
Q

Mesangial sclerosis aka eosinophilic nodular glomerusclerosis

A

Kimmelstiel-Wilson nodules

–> Diabetic Glomerulonephropathy

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30
Q

Nonenzymatic glycosylation of Efferent Arteriole

A

Increased GFR! (because thickening blows outflow) –> Mesangial Expansion

ACE inhibitors help by blocking AGII = decrease vasoconstriction of EA

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31
Q

Ovoid/Spherical Hyaline Masses in Glomerular Mesangium

A

Kimmelstiel-Wilson. indicates IRREVERSIBLE damage.

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32
Q

Most common location of Amyloidosis

A

Kidney. Deposits in mesangium = nephrotic

Associated with chronic conditions = Multiple myeloma, Rheumatoid arthritis, TB

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33
Q

Oliguria, Azotemia, Salt retention with periorbital edema and HTN, rbc casts

A

Nephritic Syndrome (glomerular bleeding)

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34
Q

Hypercellular, inflamed glomeruli

A

Nephritic Syndrome

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35
Q

Subepithelial deposits on EM, granular IF

A

Membraneous Nephropathy (nephrotic)–> Spike and Dome

PSGN (nephritic)–> Lumpy Bumpy due to IgM, IgG, C3 deposition
so decreased complement levels/decreased serum C3

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36
Q

Nephritic Syndrome after URI

A

within 5 days: IgA Nephropathy

2-3 weeks later: Strep Pyogenes (GAS) Impetigo

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37
Q

Composition of RPGN Crescents (bowmans space)

A

Fibrin and Macrophages!! (not collagen)

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38
Q

RPGN IF:

A

Goodpasure = Linear (Anti-GBM and alveolar BM) –> Ab against collagen in these BM’s

Wegener (granulomatosis with polyangiitis) & Microscopic Polyangitis
–> Pauci-immune. so negative IF. Do ANCA

PSGN and Diffuse Proliferative (SLE): Granular

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39
Q

Episodic hematuria with rbc cast after gastroenteritis/mucosal infection. Presents during childhood

A

IgA Nephropathy (Berger not Buerger)

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40
Q

IgA Nephropathy imaging

A

LM: Mesangial proliferation

IF/EM: IgA immune complex deposition in mesangium

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41
Q

Renal pathology of Henoch-Schonlein purpura

A

IgA Nephropathy (because its an IgA mediated Type 3 hypersensitivity)

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42
Q

Can’t see, can’t pee, can’t hear a buzzing bee

A

Alport Syndrome

43
Q

Thinning and splitting of GBM; Defective Type IV Collegen; X-linked

A

Alport Syndrome

44
Q

Isolated hematuria, sensory hearing loss, Retinopathy/lens dislocation (eye problems)

A

Alport Syndrome.

So lens dislocation don’t automatically pick Marfan

45
Q

Dysuria, urinary frequency, suprapubic pain, urgency, without any systemic signs(fever/chills)

A

UTI: Cystitis –> infection of bladder

46
Q

UTI: Cystitis infectious agents

A

E coli, Staph Saprophyticus, Kelbsiella Pneumoniae, Proteus mirabilis (alkaline urine with ammonia scent), Enterococcus faecalis

47
Q

Sterile pyuria: definition and dx

A

Pyuria (>10 wbcs and leukocyte esterase) with negative urine culture. Suggests Urethritis –> Chlamydia or Neisseria gonorrhoeae. clinical sign = dysuria

UTI generally has positive bacterial culture

48
Q

Colicky pain + hematuria + unilateral flank pain

A

Nephrolithiasis

49
Q

Risk factors for kidney stone

A

High concentration of solute in urinary filtrate

Low urine volume

50
Q

Most common causes of chronic renal failure

A

Diabetes Mellitus
Hypertension
Glomerular Disease

51
Q

Uremia (chronic renal failure) definition

A

Clinical manifestations of Azotemia (increased nitrogenous waste products in blood)

52
Q

Uremia features

A 
Nausea
Anorexia 
Pericarditis
Platelet Dysf(x) - adhesion and aggregation
Encephalopathy with Asterixis 
Urea crystal deposition in the skin
53
Q

Clinical features of Chronic Renal Failure: MADHHUNGER

A 
Metabolic 
Acidosis
Dyslipidemia
Hyperkalemia
Hypocalemia
Uremia
Na/H20 retention = HTN/pulm edema/HF
Growth retardation
EPO deficiency = Anemia
Renal Osteodytrophy

Renal Osteodystrophy

  • -> from secondary Hyperparathyroidism (increase PTH resorbs bond to increase Ca)
  • ->from Osteomalacia:
54
Q

Hypocalcemia in Chronic Renal Failure

A

Hypocalcemia

  • -> decreased 1-alpha hydroxylation of Vit D by PCT cell
  • ->Hyperphosphatemia (can’t excrete) binds up Ca
55
Q

Calcium oxalate/phosphate stones

A

most common
Hypercaliuria most common cause
Exclude hypercalcemia
Seen with Crohns as well

Tx with Hydrochlorothiazide (calcium sparing diuretic)

56
Q

Ammonium Magnesium Phosphate stone

A

Infection with Urease + organisms (klebs, proteus)

Alkaline urine leads to formation

57
Q

Thyroidization of Kidney

A

Chronic Pyelonephritis

58
Q

Renal hamartoma seen in Tuberous Sclerosis

A

Angiomyolipoma

59
Q

Hematuria, palpable mass, flank pain (malignant tumor)

A

Renal Cell Carcinoma

60
Q

Paraneoplastic syndromes of RCC

A

EPo, renin PTHrP, ACTH

61
Q

RCC invasion path

A

Renal vein -> IVC -> hematogenous spread (bone and lung)

62
Q

Mechanism of L-sided Varcocele in RCC

A

Left Spermatic vein drains into Renal Vein. Block draining = varicocele
R spermatic vein goes directly into IVC so no issues

63
Q

Loss of Von-Hippel-Lindau tumor suppressor (increased IGF-1)

A

RCC

64
Q

Sporadic vs Hereditary RCC tumor

A

Sporadic: single tumor in Adult male smoker
Herediatry: bilat, younger adult. VHL!

65
Q

Auto Dominant disease
Inactivation of tumor suppressor
Hemangioblastoma of Cerebellum + Renal Cell Carcinoma

A

VHL

66
Q

Golden yellow mass in kidney

A

RCC tumor

67
Q

Why does clear cell carcinoma appear clear

A

high lipid content and glycogen in cytoplasm

68
Q

Hypercalcemia from RCC

A

Paraneoplastic syndrome: EPO beta

69
Q

consequence of albuminuria

A

EDEMA

loss of intravascular protein = fluid shift into the interstitium = edema

70
Q

Patchy necrosis of tubular epithelium and loss of basement membrane

A

ATN

71
Q

Inciting events for Minimal change disease

A

URI, bee sting, immunization

72
Q

Hypertension….seen with Nephritic or Nephrotic?

A

Nephritic

73
Q

Hypoalbuminemia….Nephritic or Nephrotic?

A

Nephrotic. Leads to edema

74
Q

Podocyte damage: Nephritic or Nephrotic? Results in?

A

Nephrotic.

Results in charge barrier disruption = massive proteinuria

75
Q

Hypercoaguble state: Nephritic or Nephrotic?

A

Nephrotic…loss of ATIII

76
Q

Increased risk of infection: Nephritic or Nephrotic?

A

Nephrotic…loss of Immunoglobulins

77
Q

Protein in urine is principally albumin, minimal amounts of IgG and alpha2 macroglobulin

A

MCD: selective proteinuria. Lose charge barrier (i.e. that was provided by anions such as heparan sulfate and proteoglycans) so albumin is lost

78
Q

What tx do you give to Diabetic with early signs of nephropathy, e.g. albuminuria?

A

ACE Inhibitor decreases albumin excretion

79
Q

Pathology from Malignant Hypertension

A

Fibrinoid Necrosis: localized destruction of the vascular wall with a circumferential ring of pink surrounding lumen
Hyperplastic arteriolosclerosis: concentric thickening due to laminated layers of smooth muscle cells (onion skin)

80
Q

glassy material in subendothelial space that stains with PAS

A

hyaline (arteriolosclerosis)

81
Q

Liver response to albuminuria

A

Increase albumin production (renal loss exceeding hepatic synthesis). Increase synth of lipoproteins–> contributes to increase TG, cholesterol, VLDL LDL etc seen in nephrotic syndrome

82
Q

Hydrostatic pressure of capillaries as a result of protein/albuminuria

A

Decreases. Since decreased oncotic pressure, fluid moves into interstitium (edema

83
Q

Why do you get sodium and water retention after proteinuria?

A

The loss of albumin/oncotic pressure = edema. Less fluid in the vascular system = decreased renal perfusion pressure = renin release (aldosterone and adh)

84
Q

Lowest osmolality in the nephron?

A

DCT. even in dehydrated state (not PCT)

85
Q

effect of ACE-I on FF

A

FF= GFR/RPF. ACE-I block AGII mediated vasoconstriction of EA. This causes decreased gfr and increased RPF = Decreased FF (i.e. increased serum creatinine)

86
Q

conditions causing Hypercalciuria as a result of Hypercalcemia

A

1 Hyperparathyroidism (stones/bones/groans), sarcoidosis, malignancy (PTHrP)

87
Q

ADH (V1 and V2 receptors)

A

V1: Vasoconstriction and PG release
V2: ADH release

88
Q

In a patient with renal colic and disturbed ion levels, what could Peptic Ulcer disease signify?

A

GROANS of hypercalcemia/hyperPTHism

89
Q

what is osteitis fibrosa cystica

A

manifestation of Hyperparathyroidism. path = subperiosteal resorption with cystic degeneration –> one of the mech for hypercalcemia in this condition.

90
Q

So hemangioblastoma ass. with VHL (and RCC). what is it?

A

NEURO TUMOR: Cerebellum. can produce ECTOPIC EPO = secondary polycythemia

91
Q

Presentation:

RCC vs Renal Oncocytoma(benign epithelial tumor with large eosinophilic cells/abundant mitochondria)

A

RCC:
Hematuria, Secondary Polycythemia, Flank Pain, FEVER and WEIGHT LOSS. Esp in Smokers and Obese, esp in men 50-70.
PCT AND THICK ASCENDING LIMB ORIGIN

Oncocytoma (very rare though):
PAINLESS hematuria, Flank Pain, Abdominal Mass. COLLECTING DUCT ORIGIN

92
Q

Transitional Cell Carcinoma (90% of the tumors in Renal Pelvis)

A

Often papillary. Painless hematuria.

Smoking, Aniline Dyes (benzidine), Cyclophosphamide

93
Q

Mesonephros vs Metanephros

A

MESOnephros: interim kidney in 1st trimester, becomes MALE GENITAL SYSTEM. : MESO Is in ME

METAnephros: Permanent.
—>Ureteric Bud: caudal end. Produces URETEr, Pelvis, Calyces, COLLECTING DUCT, canalized by wk 10

—>Metanephric Mesenchyme: Formation of GLOMERULUS PCT LOH and DCT (induced by interaction with Ureteric Bud)

–>Last to canalize = Ureteropelvic j(x) = most common site of obstruction (hydronephrosis) in fetus

94
Q

Last to canalize in kidney aka most common site of obstruction (hydronephrosis)

A

Ureteropelvic j(x)`

95
Q

Causes of Potter Seq (Pulmonary Hypoplasia, Oligohydramnios, Twisted facies i.e. Low set ears, Twisted skin, Extremity Defects, Renal fucked)

A

ARPKD
Posterior Urethral Valve
Bilat Renal Agenesis
Any major obstruction

96
Q

Horseshoe kidney ass. and f(x)

A

F(x) normally
Ass. with Ureteropelvic j(x) obstruction, hydronephrosis, renal stones, infection, chromosomal aneuploidies (Down, Turner, Patau), renal cancer sometimes

97
Q

Licorice (glychheretic acid) blocks:

A

11beta-hydroxysteroid dehydrogenase = syndrome of apparent mineralocorticoid excess

–>hypertension, metab alkalosis, hypokalemia

98
Q

PTH effects

A

Decrease Phosphate reab in PCT
Increase Ca reab in DCT

(vs Vit D increases Ca and Phosphate reab from gut)

99
Q

what kind of incontinence do MS patients develop and why?

A

Urge Incontinence: Loss of CNS inhibition of detrusor contraction in bladder

–>Spastic bladder/hypertonicity/UNINHIBITED BLADDER CONTRACTION DOG

100
Q

Pelvic floor strengthening (kegel) targets:

A

LEVATOR ANI (not EUS) because this decreases Stress Incontinence

=Iliococcygeus, Pubococcygeus, Puborectalis

101
Q

What kind of incontinence do Diabetcs have?

A

Diabetic NEUROPATHY = Overflow incontinence –> affects detrusor innervation (impaired contractility)

PVR = Post-void residual testing can confirm incomplete bladder emptying

102
Q

So Diabetic vs MS Incontinence

A

MS: Lose Inhibition to Detrusor (UMN damage) = Urge
DM: Lose Innervation to Detrusor (periph) = Overflow

103
Q

Hx of Smoking and exposure to rubber, plastics, aromatic amine-containing dyes i.e. Benzidine, textiles, leather, aniline dyes, cyclophosphamide

A

Transitional Cell Carcinoma (painless hematuria)

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