Renal Flashcards
1
Q
Congenital hepatic fibrosis (and portal HTN) + hepatic cysts
A
associated with AR Polycystic Kidney Disease
2
Q
Renal Failure, HTN, +/- Potter Sequence
A
ARPKD
3
Q
Cysts in Liver and Kidney
A
ARPKD
4
Q
Hypertension, Hematuria, and progressive Renal Failure in a young adult
A
ADPKD. HTN due to Renin
5
Q
Conditions associated with ADPKD
A
Berry Aneurysm
MVP
Hepatic Cysts
so cysts in Brain, Liver, and Kidney
6
Q
Inherited defect leading to bilateral enlarged kidneys with cysts in renal cortex and medulla
A
AR and AD PKD
7
Q
Cysts and shrunken kidneys
A
Medullary Cystic Kidney Disease (ADPKD is enlarged kidneys). Cysts are in the medullary collecting ducts
8
Q
Azotemia
A
“Increased nitrogenous waste products” =
Increased BUN and Creatinine.
Seen in Acute Renal Failure (along with oliguria)
9
Q
Oliguria
A
Low urine production. Seen in ARF
10
Q
Hematuria and Proteinuria + Flank Pain
A
Renal Papillary Necrosis
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
12
Q
Basics of Nephrotic Syndrome (4 changes)
A
- Hypoalbuminemia = Pitting Edema
- Hypogammaglobulinemia = Infection risk
- Hypercoagulable state = loss of Antithrombin III (in urine)
- Hyperlipidemia/cholesterolemia = Fatty casts/frothy urine
13
Q
Protein loss in MCD
A
Selective proteinuria
- loss of albumin (LMW protein)
- very minimal loss of bulky proteins –> so no Immunoglobulin loss
14
Q
Treatment for MCD
A
Excellent response to Corticosteroids
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)
16
Q
Imaging in MCD
A
LM - normal glomeruli
IF - negative (since no complex deposition)
EM - podocyte effacement
17
Q
Nephrotic syndrome in Hispanic or African American
A
Focal Segmental Glomerulosclerosis
18
Q
Nephrotic Syndrome in HIV pt, Sickle Cell Disease, or Heroin user
A
Focal Segmental Glomerulosclerosis
19
Q
5 groups that get FSGS
A
Hispanic, Blacks, Heroin user, HIV pt, Sickle Cell
20
Q
Effacement of podocytes (on EM)
A
MCD and Focal Segmental Glomerulosclerosis
21
Q
Presents like MCD but no response to steroids and probs not in a child
A
FSGS (effacement of podocytes)
22
Q
Nephrotic syndrome in Caucasian
A
Membraneous Nephropathy
23
Q
Nephrotic syndrome in Hepatitis B or C, SLE, or drugs (NSAIDS)
A
Membraneous Nephropathy
24
Q
4 associations with Membraneous Nephropathy
A
SLE, Hep B/C, Drugs (NSAID), Caucasian
25
C3 nephritic factor
Auto-Ab that stabilizes C3 convertase = increased complement and decreased serum C3
Type 2 MembranoProliferativeGlomeruloNephritis
26
Type 1 MPGN
Hep B/C infection. Tram track appearance. Subendothelial immune complex deposits with Granular IF.
27
Mesangial expansion + GBM thickening
Diabetic Glomeruolonephropathy
28
Nonenzymatic glycosylation of vascular BM --> Hyaline arteriolosclerosis
1st renal change in Diabetes Mellitus.
Loss of negative charge barrier of glomerulus
--> Increased permeability
29
Mesangial sclerosis aka eosinophilic nodular glomerusclerosis
Kimmelstiel-Wilson nodules
| --> Diabetic Glomerulonephropathy
30
Nonenzymatic glycosylation of Efferent Arteriole
Increased GFR! (because thickening blows outflow) --> Mesangial Expansion
ACE inhibitors help by blocking AGII = decrease vasoconstriction of EA
31
Ovoid/Spherical Hyaline Masses in Glomerular Mesangium
Kimmelstiel-Wilson. indicates IRREVERSIBLE damage.
32
Most common location of Amyloidosis
Kidney. Deposits in mesangium = nephrotic
Associated with chronic conditions = Multiple myeloma, Rheumatoid arthritis, TB
33
Oliguria, Azotemia, Salt retention with periorbital edema and HTN, rbc casts
Nephritic Syndrome (glomerular bleeding)
34
Hypercellular, inflamed glomeruli
Nephritic Syndrome
35
Subepithelial deposits on EM, granular IF
Membraneous Nephropathy (nephrotic)--> Spike and Dome
| PSGN (nephritic)--> Lumpy Bumpy due to IgM, IgG, C3 deposition
so decreased complement levels/decreased serum C3
36
Nephritic Syndrome after URI
within 5 days: IgA Nephropathy
| 2-3 weeks later: Strep Pyogenes (GAS) Impetigo
37
Composition of RPGN Crescents (bowmans space)
Fibrin and Macrophages!! (not collagen)
38
RPGN IF:
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
39
Episodic hematuria with rbc cast after gastroenteritis/mucosal infection. Presents during childhood
IgA Nephropathy (Berger not Buerger)
40
IgA Nephropathy imaging
LM: Mesangial proliferation
| IF/EM: IgA immune complex deposition in mesangium
41
Renal pathology of Henoch-Schonlein purpura
IgA Nephropathy (because its an IgA mediated Type 3 hypersensitivity)
42
Can't see, can't pee, can't hear a buzzing bee
Alport Syndrome
43
Thinning and splitting of GBM; Defective Type IV Collegen; X-linked
Alport Syndrome
44
Isolated hematuria, sensory hearing loss, Retinopathy/lens dislocation (eye problems)
Alport Syndrome.
So lens dislocation don't automatically pick Marfan
45
Dysuria, urinary frequency, suprapubic pain, urgency, without any systemic signs(fever/chills)
UTI: Cystitis --> infection of bladder
46
UTI: Cystitis infectious agents
E coli, Staph Saprophyticus, Kelbsiella Pneumoniae, Proteus mirabilis (alkaline urine with ammonia scent), Enterococcus faecalis
47
Sterile pyuria: definition and dx
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
Colicky pain + hematuria + unilateral flank pain
Nephrolithiasis
49
Risk factors for kidney stone
High concentration of solute in urinary filtrate
| Low urine volume
50
Most common causes of chronic renal failure
Diabetes Mellitus
Hypertension
Glomerular Disease
51
Uremia (chronic renal failure) definition
Clinical manifestations of Azotemia (increased nitrogenous waste products in blood)
52
Uremia features
```
Nausea
Anorexia
Pericarditis
Platelet Dysf(x) - adhesion and aggregation
Encephalopathy with Asterixis
Urea crystal deposition in the skin
```
53
Clinical features of Chronic Renal Failure: MADHHUNGER
```
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
Hypocalcemia in Chronic Renal Failure
Hypocalcemia
- -> decreased 1-alpha hydroxylation of Vit D by PCT cell
- ->Hyperphosphatemia (can't excrete) binds up Ca
55
Calcium oxalate/phosphate stones
most common
Hypercaliuria most common cause
Exclude hypercalcemia
Seen with Crohns as well
Tx with Hydrochlorothiazide (calcium sparing diuretic)
56
Ammonium Magnesium Phosphate stone
Infection with Urease + organisms (klebs, proteus)
| Alkaline urine leads to formation
57
Thyroidization of Kidney
Chronic Pyelonephritis
58
Renal hamartoma seen in Tuberous Sclerosis
Angiomyolipoma
59
Hematuria, palpable mass, flank pain (malignant tumor)
Renal Cell Carcinoma
60
Paraneoplastic syndromes of RCC
EPo, renin PTHrP, ACTH
61
RCC invasion path
Renal vein -> IVC -> hematogenous spread (bone and lung)
62
Mechanism of L-sided Varcocele in RCC
Left Spermatic vein drains into Renal Vein. Block draining = varicocele
R spermatic vein goes directly into IVC so no issues
63
Loss of Von-Hippel-Lindau tumor suppressor (increased IGF-1)
RCC
64
Sporadic vs Hereditary RCC tumor
Sporadic: single tumor in Adult male smoker
Herediatry: bilat, younger adult. VHL!
65
Auto Dominant disease
Inactivation of tumor suppressor
Hemangioblastoma of Cerebellum + Renal Cell Carcinoma
VHL
66
Golden yellow mass in kidney
RCC tumor
67
Why does clear cell carcinoma appear clear
high lipid content and glycogen in cytoplasm
68
Hypercalcemia from RCC
Paraneoplastic syndrome: EPO beta
69
consequence of albuminuria
EDEMA
loss of intravascular protein = fluid shift into the interstitium = edema
70
Patchy necrosis of tubular epithelium and loss of basement membrane
ATN
71
Inciting events for Minimal change disease
URI, bee sting, immunization
72
Hypertension....seen with Nephritic or Nephrotic?
Nephritic
73
Hypoalbuminemia....Nephritic or Nephrotic?
Nephrotic. Leads to edema
74
Podocyte damage: Nephritic or Nephrotic? Results in?
Nephrotic.
| Results in charge barrier disruption = massive proteinuria
75
Hypercoaguble state: Nephritic or Nephrotic?
Nephrotic...loss of ATIII
76
Increased risk of infection: Nephritic or Nephrotic?
Nephrotic...loss of Immunoglobulins
77
Protein in urine is principally albumin, minimal amounts of IgG and alpha2 macroglobulin
MCD: selective proteinuria. Lose charge barrier (i.e. that was provided by anions such as heparan sulfate and proteoglycans) so albumin is lost
78
What tx do you give to Diabetic with early signs of nephropathy, e.g. albuminuria?
ACE Inhibitor decreases albumin excretion
79
Pathology from Malignant Hypertension
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
glassy material in subendothelial space that stains with PAS
hyaline (arteriolosclerosis)
81
Liver response to albuminuria
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
Hydrostatic pressure of capillaries as a result of protein/albuminuria
Decreases. Since decreased oncotic pressure, fluid moves into interstitium (edema
83
Why do you get sodium and water retention after proteinuria?
The loss of albumin/oncotic pressure = edema. Less fluid in the vascular system = decreased renal perfusion pressure = renin release (aldosterone and adh)
84
Lowest osmolality in the nephron?
DCT. even in dehydrated state (not PCT)
85
effect of ACE-I on FF
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
conditions causing Hypercalciuria as a result of Hypercalcemia
1 Hyperparathyroidism (stones/bones/groans), sarcoidosis, malignancy (PTHrP)
87
ADH (V1 and V2 receptors)
V1: Vasoconstriction and PG release
V2: ADH release
88
In a patient with renal colic and disturbed ion levels, what could Peptic Ulcer disease signify?
GROANS of hypercalcemia/hyperPTHism
89
what is osteitis fibrosa cystica
manifestation of Hyperparathyroidism. path = subperiosteal resorption with cystic degeneration --> one of the mech for hypercalcemia in this condition.
90
So hemangioblastoma ass. with VHL (and RCC). what is it?
NEURO TUMOR: Cerebellum. can produce ECTOPIC EPO = secondary polycythemia
91
Presentation:
| RCC vs Renal Oncocytoma(benign epithelial tumor with large eosinophilic cells/abundant mitochondria)
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
Transitional Cell Carcinoma (90% of the tumors in Renal Pelvis)
Often papillary. Painless hematuria.
Smoking, Aniline Dyes (benzidine), Cyclophosphamide
93
Mesonephros vs Metanephros
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
Last to canalize in kidney aka most common site of obstruction (hydronephrosis)
Ureteropelvic j(x)`
95
Causes of Potter Seq (Pulmonary Hypoplasia, Oligohydramnios, Twisted facies i.e. Low set ears, Twisted skin, Extremity Defects, Renal fucked)
ARPKD
Posterior Urethral Valve
Bilat Renal Agenesis
Any major obstruction
96
Horseshoe kidney ass. and f(x)
F(x) normally
Ass. with Ureteropelvic j(x) obstruction, hydronephrosis, renal stones, infection, chromosomal aneuploidies (Down, Turner, Patau), renal cancer sometimes
97
Licorice (glychheretic acid) blocks:
11beta-hydroxysteroid dehydrogenase = syndrome of apparent mineralocorticoid excess
-->hypertension, metab alkalosis, hypokalemia
98
PTH effects
Decrease Phosphate reab in PCT
Increase Ca reab in DCT
(vs Vit D increases Ca and Phosphate reab from gut)
99
what kind of incontinence do MS patients develop and why?
Urge Incontinence: Loss of CNS inhibition of detrusor contraction in bladder
-->Spastic bladder/hypertonicity/UNINHIBITED BLADDER CONTRACTION DOG
100
Pelvic floor strengthening (kegel) targets:
LEVATOR ANI (not EUS) because this decreases Stress Incontinence
=Iliococcygeus, Pubococcygeus, Puborectalis
101
What kind of incontinence do Diabetcs have?
Diabetic NEUROPATHY = Overflow incontinence --> affects detrusor innervation (impaired contractility)
PVR = Post-void residual testing can confirm incomplete bladder emptying
102
So Diabetic vs MS Incontinence
MS: Lose Inhibition to Detrusor (UMN damage) = Urge
DM: Lose Innervation to Detrusor (periph) = Overflow
103
Hx of Smoking and exposure to rubber, plastics, aromatic amine-containing dyes i.e. Benzidine, textiles, leather, aniline dyes, cyclophosphamide
Transitional Cell Carcinoma (painless hematuria)
