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Renal > General pathology & physiology > Flashcards

General pathology & physiology Flashcards

1
Q

homeostatic mechanism that protects from salt and volume wasting by the macula densa sensing NaCl concentration in the filtrate leaving the loop of Henle. If the [NaCl] is high, it signals the afferent arteriole to constrict, decreasing GFR.

A

tubuloglomerular feedback

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2
Q

referred to as the “diluting segment of the nephron” since it is impermeable to water but reabsorbs NaCl, producing dilute urine

A

DCT and thick ascending limb

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3
Q

location where final adjustments to electrolyte composition are made, under the influence of aldosterone; AVP (ADH) modulates the water permeability of this portion of the nephron

A

collecting duct system

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4
Q
  1. concentration of NaCl in the interstitium by active transport in the TAL (no water permeability)
  2. water is extracted from the filtrate in the collecting duct, under the influence of ADH
  3. urea is concentrated in the filtrate, since the cortical & outer medullary ducts have low permeability to urea
  4. urea diffuses out of the inner medullary collecting duct, since it is permeable
  5. urea is trapped by countercurrent exchange in the vasa recta
  6. urea in the medullary interstitium attracts water from the tubular fluid, concentrating the NaCl within the tubule (thin descending limb)
  7. NaCl diffuses out of the thin ascending limb, contributing to the hypertonicity of the medullary interstitium
A

passive countercurrent multiplier hypothesis

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5
Q

Major Prerenal Causes of Acute Renal Failure

A
  1. volume depletion (GI, renal, third space losses)
  2. CHF or valvular heart disease
  3. hepatorenal syndrome is advanced cirrhosis
  4. bilateral renal stenosis (after ANG II inhibitor)
  5. drugs that interfere with autoregulation (NSAIDs)
  6. Shock due to fluid loss, sepsis, cardiac failure (progressing to ATN)
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6
Q

Major Causes of Intrinsic Renal Disease w/ ARF

A 
Glomerular Disease
Tubulointerstitial disease (ATN, postischemic, drug toxicity, intratubular obstruction)
Vascular Disease (vasculitis, atherothrombi to the kidney)
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7
Q

Major Postrenal Causes of ARF

A

Prostatic disease in men
pelvic or retroperitoneal malignancy
these are conditions that cause urinary obstruction

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8
Q

Hematuria
mild to moderate proteinuria
HTN
Due to glomerular injury

A

nephritic syndrome

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9
Q 
>3.5 g/day proteinuria
hypoalbuminemia
edema
hyperlipidemia
lipiduria
due to glomerular injury
A

nephrotic syndrome

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10
Q

manifests as polyuria and electrolyte abnormalities

A

renal tubular defects

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11
Q

acute nephritis
proteinuria
acute renal failure

A

rapidly progressing glomerulonephritis

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12
Q

uremia progressing for years

A

chronic renal failure

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13
Q

subepithelial accumulation of Ig deposits causing diffuse thickening of the glomerular capillary wall
Causes nephrotic syndrome in adults
85% idiopathic but remainder caused by SLE, NSAIDs, infections, malignancy

A

Membranous nephropathy

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14
Q

What underlies most glomerular injury?

A

immune mechanisms

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15
Q

elevation of BUN and creatinine in the blood

A

azotemia

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16
Q

characterized by failure of renal excretory function with a host of metabolic and endocrine alterations resulting from renal damage, including secondary involvement of the GI system, peripheral nerves and heart

A

uremia

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17
Q

oliguria or anuria with recent onset of azotemia; can result from glomerular, interstitial or vascular injury or acute tubular injury

A

acute renal failure

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18
Q

dominant features are polyuria, nocturia and electrolyte disorders

A

renal tubular defects

Ex: cystinuria, RTA, lead nephropathy

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19
Q

constituents of the GBM

A

type IV collagen, laminin, proteoglycans (mostly heparan sulfate), fibronectin, entactin

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20
Q

contractile, phagocytic cells, capable of proliferation capable of laying down both matrix and collagen, also secrete biologically active mediators. These cells support the glomerular tuft and are between capillaries (p910R)

A

mesangial cells

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21
Q

accumulations of proliferating parietal cells and infiltrating leukocytes, from immune or inflammatory injury; response is elicited by fibrin leaking into the urinary space (fibrin deposition is stimulated by macrophage procoagulant activity)

A

crescent formation

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22
Q

thickening of basement membrane due to increased synthesis of its protein components

A

diabetic glomerulosclerosis

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23
Q

histologic alterations of glomerulopathies

A

hypercellularity
basement membrane thickening
hyalinosis and sclerosis

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24
Q

accumulation of extracellular collagenous matrix, confined to the mesangial areas or involving the capillary loops or both

A

sclerosis

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25
Q

Primary glomerulopathies that present with nephrotic syndrome

A

membranous glomerulopathy
minimal-change disease
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis type I

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26
Q

Primary glomerulopathy that presents with nephritic syndrome

A

postinfectious glomerulonephritis

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27
Q

Note about GFR prediction of ESRD (p916R)

A

Once renal disease causes GFR to decrease to 30-50% of normal, progression to ESRF proceeds at a relatively constant rate, independent of the original stimulus

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28
Q

IgA deposition in the mesangium, sometimes with IgG and C3 in a child age 3-8yr
purpuric skin lesions on arms, legs & buttocks
nephritic or nephrotic syndrome
subepidermal hemorrhages
may have recurrent hematuria for years

A

Henoch-Schonlein Purpura

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29
Q

Thickened capillary loops and glomerular cell proliferation => double-contour appearance => tram-track appearance
50% progress to chronic renal failure in 10 years
Glomeruli appear lobular due to mesangial cell proliferation.
Type I: Ag/Ab complex deposition and complement activation with subENDOthelial deposits
Type II: (dense deposit disease) alternative complement pathway activation with C3 deposits on either side of the GBM

A

Membranoproliferative Glomerulonephritis

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30
Q

visceral epithelial damage (effacement or detachment) in affected glomerular segments and due to cytokine or mutation of proteins of slit diaphragm
sclerosis of some but not all glomeruli and only a portion of the capillary tuft is involved
non-selective proteinuria, hematuria, reduced GFR, HTN
progresses to chronic renal failure in 20%

A

Focal Segmental Glomerulosclerosis

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31
Q

accounts for 20% of steroid-resistant nephrotic syndrome in children with mutation of a protein of the slit diaphragm

A

FSGS with mutation of NPHS2 (encodes podocin)

32
Q

most common cause of glomerulonephritis worldwide and major cause of recurrent hematuria
Increased secretion of mucosal IgA in response to ingested or inhaled antigens
Present with gross hematuria following respiratory, GI or urinary infection
IgA deposition in the mesangium and activation of alternate complement pathway

A

IgA Nephropathy = Berger disease

33
Q

Hematuria progressing to chronic renal failure
Symptoms at age 5-20 yr with RF at 20-50 yr in men
Nerve deafness
lens dislocation
cataracts
corneal dystrophy
Defective assembly of Type IV collagen in the GBM (85% are X-linked with mutations in alpha5 chain & autosomal forms are in alpha3 & alpha4)
Lab: increased IgA & red cell casts
GBM thinning and interstitial cells are stuffed with fats & mucopolysaccharides

A

Alport Syndrome = hereditary nephritis

34
Q

asymptomatic hematuria with diffuse thinning of the basement membrane
normal renal function
NO involvement of hearing or eyes
associated with mutations in alpha3 and alpha4 chains of type IV collagen

A

Thin Basement Membrane Lesion = Benign Familial Hematuria

35
Q

Common end stage of poststrep GN, RPGN, membranous GN, FSGS, MPGN, IgA nephropathy
kidneys are symmetrically contracted with diffuse granular surfaces and thinned cortex
Clinical: HTN, uremia, pericarditis, uremic gastroenteritis, secondary hyperparathyroidism, nephrocalcinosis, renal osteodystrophy
must do dialysis or renal transplant

A

Chronic Glomerulonephritis

36
Q

Nonenzymatic glycation of proteins of the GBM
Hemodynamic changes resulting in increased GFR, increased GC pressure and glomerular hypertrophy
Glomerular disease leading to ESRF
Glomerular disease leading to proteinuria with or without nephrotic syndrome
Includes: hyalinizing arteriolar sclerosis, increased susceptibility to pyelonephritis and papillary necrosis
See: basement membrane thickening, diffuse mesangial sclerosis, NODULAR glomerulosclerosis

A

Diabetic nephropathy

37
Q

Congo red + fibrillary protein deposit in the mesangium
proteinuria severe enough to cause nephrotic syndrome
eventually obliterate the glomerulus completely
Ig light chain most common
Dialysis-associated protein deposit: alphabeta2m (beta2 microglobulin which cannot be filtered by the dialysis membrane deposits in synovium, joints, tendon sheaths) -> presents as carpal tunnel

A

Amyloidosis

38
Q 
Wire loop lesions suggest active disease
ANA to DNA
female
presents age 20-30 yr typically
failure of self-tolerance
presents as diffuse proliferative glomerulonephritis in 35-60%
A

SLE

39
Q

Characterized by 3 Clinical stages:
1. ischemic event (36 hrs)
2. maintenance stage: 40-400 ml/day urine output, salt and water overload, increased BUN, hyperkalemic metabolic acidosis, uremia with dialysis initiation
3. Recovery: urine output increasing up to 3L/day, hypokalemia, vulnerability to infection
Morph: flattened epithelium with evidence of regeneration and mitotic figures; loss of prox tubule brush borders
hyaline and pigmented granular casts in distal and collecting tubules

A

Acute Tubular Necrosis

40
Q

Organisms that cause acute pyelonephritis

A 
E coli
Proteus
Klebsiella
Enterobacter
staph (in immunocompetent)
polyomavirus, CMV and adenovirus in immunocompromised
41
Q

causes pyelonephritis in kidney allografts
viral infection of tubule epithelial cell
nuclear enlargement with inclusions

A

polyomavirus

42
Q

tubulointerstitial inflammation, renal scarring, and dilated deformed calyces
Most frequently caused by vesicouretal reflux diagnosed when investigating childhood HTN

A

chronic pyelonephritis

43
Q

Drugs that can cause acute interstitial nephritis

A

PCNs, rifampin, diuretics (thiazide), NSAIDs, allopurinol, cimetidine
see fever, rash, and renal abnormalities ~15 days after exposure

44
Q

papillary necrosis followed by cortical tubulointerstitial nephritis; associated with phenacetin mixed with aspirin, caffeine, acetaminophen, codeine
Glutathione is depleted with ROS generation

A

analgesic nephropathy

45
Q

hyperuricemia causing acute uric acid nephropathy: precipitation of uric acid crystals in collecting ducts
seen in chemotherapy patients with leukemia lymphoma: uric acid released from apoptotic tumor cells as they are broken down
leads to obstruction and acute renal failure, chronic urate nephropathy and nephrolithiasis

A

urate nephropathy

46
Q

pink to blue amorphous masses fill and distend tubular lumens as a complication of a tumor
hypercalcemia, hyperuricemia, obstruction of ureters
Can erode the tubules and cause granulomatous reaction
light chain casts

A

Light-chain Cast Nephropathy = Myeloma Kidney

47
Q

vascular insult causes endothelial injury, platelet deposition, increased vascular permeability leading to fibrinoid necrosis with intravascular thrombosis
small pinpoint petechial hemorrhages on cortical surface from rupture of arterioles or glomerular capillaries
“flea-bitten kidney”
BP: systolic > 200 mm Hg and diastolic > 120 mm Hg
hyperplastic arteriopathy (onion-skinning)
Hematuria, proteinuria, papilledema, encephalopathy, cardiovascular abnormalities, eventual renal failure

A

malignant accelerated nephrosclerosis

48
Q

Manifests clinically with bruit, ELEVATED PLASMA RENIN
Male > female
most commonly caused by atheromatous plaque at the origin of the renal artery

A

unilateral renal artery stenosis

49
Q

Seen most frequently after obstetrical emergency such as abruptio placentae, septic shock, or extensive surgery
Fatal if bilateral and symmetric; if patchy survival is possible
Ischemic necrosis
may cause sudden anuric and uremic death

A

Diffuse Cortical Necrosis

50
Q

sporadic disorder caused by abnormality in metanephric differentiation and characterized by persistence of abnormal structures: cartilage, undifferentiated mesenchyme, immature collecting ductules and abnormal lobar organization
Most cases are associated with ureteropelvic obstruction, ureteral agenesis or atresia
unilateral or bilateral & almost always cystic dysplasia
If unilateral, the other kidney has normal function.

A

multicystic renal dysplasia

51
Q

AD hereditary disorder characterized by multiple expanding cysts of both kidneys, ultimately destroying the renal parenchyma and causing renal failure
Requires mutation of both alleles.
Universally bilateral
Function retained until 4th or 5th decade, since only parts of the nephrons are initially involved
Mutations of PKD1 in 85%

A

polycystic kidney disease

PKD1 encodes polycystin-1 which has been localized to the distal nephron
PKD2 encodes polycystin-2 which is in all segments of the nephron and in other tissues
Polycystin-1 and polycystin-2 are in the primary cilium which is a mechanosensor that monitors changes in fluid flow & shear stress

52
Q

inheritance of PKD that is perinatal, neonatal, infantile, juvenile and associated with hepatic lesions

A

ARPKD

53
Q

gene mutation associated with ARPKD

A

PKHD1 which encodes for fibrocystin which is localized to the primary cilium of tubular cells and highly expressed in adult and fetal kidney, liver, and pancreas

54
Q

Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction of outflow or urine.
Renal calyces dilate and high pressure in the pelvis is transmitted to the collecting ducts into the cortex, causing renal atrophy
-impaired tubular concentrating ability initially followed later by fall in GFR

A

hydronephrosis

55
Q

can cause obstruction of urinary flow or produce ulceration & bleeding

A

renal calculi

56
Q

4 types of renal calculi

A
  1. calcium oxalate
  2. magnesium ammonium phosphate (staghorn = triple)
  3. uric acid
  4. cystine
57
Q

Most common type of renal cell carcinoma
somatic mutations in VHL gene
(loss, hypermethylation, or inactivated/mutated)

A

clear cell carcinoma
other types of carcinoma associated with VHL:
papillary(10-15%) and chromophobe (5%)

58
Q

What does VHL gene encode?

A

Protein that targets other proteins for degradation, especially HIF-1.
Remember the role of HIF in renal cell carcinoma. The patient in the case had polycythemia due to elevated HIF.

59
Q

risk factors for renal cell carcinoma

A 
tobacco
obesity (female)
HTN
unopposed estrogen therapy
asbestos exposure
petroleum products
heavy metals
chronic renal failure
acquired cystic disease (dialysis)
tuberous sclerosis
60
Q

pediatric renal tumor
presents age 2-5 yr with most by age 10
WAGR syndrome: Aniridia, Genital abnormalities, mental Retardation
WT1 deletion is “first hit” but tumor develops after second hit
Morph: tightly-packed blue cells (blasts)
Presentation: hematuria, pain in abdomen after trauma, HTN

A

Wilms tumor

Denys-Drash -> gonadal dysgenesis associated with WT1 mutation

61
Q

vesical inflammatory reaction related to chronic bacterial infection with E coli or Proteus
most common in transplant patients (immunosuppression)
macrophages stuffed with particulate and membranous debris of bacterial origin

A

Malacoplakia

62
Q

occurs more frequently in countries with urinary schistosomiasis
nearly always associated with chronic bladder irritation and infection

A

squamous cells carcinoma of the bladder

63
Q

risk factors for adenocarcinoma of the bladder

A 
cigarette smoking
industrial exposure to arylamines
schistosoma haematobium infection
long-term use of analgesics
cyclophosphamide
bladder irradiation
64
Q

benign sexually transmitted tumor caused by HPV 6 & 11

related to the common wart

A

Condyloma acuminatum

65
Q

50% are from HPV (esp 16 and 18)

-cigarette smoking increases risk

A

squamous cell carcinoma of the penis

66
Q

Where do most adenocarcinomas of the prostate arise?

A

70% arise in the peripheral zone in a posterior location where it may be palpable on rectal exam

67
Q

What part of the kidney do lymphatics drain?

A

Lymphatics drain the interstitial fluid of the cortex. They may contain high concentrations of EPO. Lymphatics do not drain the medulla, because that would impair the ability to concentrate urine.

68
Q

Describe the mesangial cells

A

They comprise a network of contractile cells which secrete EC matrix. The network is continuous with the smooth muscle cells of the afferent arteriole, efferent arteriole and extend to the extraglomerular mesangial cells which are part of the JGA.

69
Q

specialized smooth muscle cells that produce, store and release renin

A

granular cells

70
Q

Features of the cells of the TAL

A

tall interdigitations and numerous mitochondria within extensively invaginated basolateral membrane. The TAL terminates at the macula densa.

71
Q

Included in the distal tubule

A

macula densa, connecting tubule, initial collecting tubule. Early distal tubule = DCT; late distal tubule = initial collecting tubule

72
Q

Where is the first location of intercalated cells?

A

connecting tubule. The connecting tubule has connecting tubule cells and intercalated cells.

73
Q

What do connecting tubule cells release?

A

kallikrein

74
Q

Are the cells of the Initial collecting tubule and the cortical collecting tubule identical?

A

Yes. They are composed of intercalated and principal cells.

75
Q

What do alpha-intercalated cells secrete?

A

They secrete H+ and absorb K+

76
Q

What do principal cells absorb?

A

Principal cells absorb NaCl and secrete K+

Renal (8 decks)

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