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renal mak Flashcards

1
Q

nephrotic syndrome characteristics

A

edema, intial normal GFR, >3.5g/d proteinuria, lipiduria

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2
Q

if these foot processes which were there are now effaced, why then do we get so much leakage of protein

A

effacement changes the BM, making it more permeable to allow proteins to leak across

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3
Q

the major EM finding on a renal biopsy of a 5y/o w/ nephrotic syndrome who responded to corticotherapy is

A

fusion of foot processes (minimal change glomerulopathy)

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4
Q
  1. 10yo Girl was brough by her parents to their family physician. History revealed that the child had a sore throat for about 10d prior to the office visit. Initial laboratory tests ordered by the family physician revealed an elevated BUN and creatinine. A microscopic urinalysis showed hematuria w/ dysmorphic RBC’s. The light microscopic appearance of the renal biopsy showed hypercellularity, w/ PMN’s present, and there were subepithelial electron dense “humps” seen by electron microscopy. What additional laboratory finding is most likely to be present in this setting:
A

c. Elevated anti-streptolysin O titer

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5
Q

focal seqmental glomerulosclerosis of the kidney characteristics

A

b. It is not as common as minimal change disease in children
c. There is effacement of podocytes plus segmental scarring
d. It tends to recur after transplantation
e. Less than half of patients have some response to corticosteroids

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6
Q

light microscopic findings on renal biopsy suggests the worst immediate prognosis

A

d. Glomerular crescents (proliferation of parietal epithelium)

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7
Q

Major clinical feature associated w/ the renal biopsy finding on immunofluorescence microscopy of mesangial IgA deposistion in a 35yo man following a “flulike” illness is: (IgA nephropathy)

A

hematuria

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8
Q

Hyaline arteriolosclerosis of the kidney is most likely to be associated with which of the following conditions

A

Renal artery stenosis in the opposite kidney

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9
Q

The microscopic findings at autopsy of hyalinized glomeruli, interstitial fibrosis and focal tubular atrophy, and arteriolar thickening in a 75yo woman w/ normal renal function most strongly suggests:

A

d. Benign nephrosclerosis

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10
Q

Nephritic Sx Pathogenesis

A

inflammatory rupture of glomerular capillaries w/ bleeding into the urinary space

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11
Q

Nephritic Sx Clinical

A

mild to mod proteinuria and edema

  • *gross hematuria**
  • red cell casts*
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12
Q

Nephritic Sx Diseases

A
  1. Acute Proliferative
  2. Nonstrep Acute
  3. Rapidly Progressive (RPGN)

Glomerulonephritis

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13
Q

Acute Proliferative

A

1-4 weeks post GAS (kids)

immune complex mediated–> coarse IF

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14
Q

Acute Proliferative Morph

A

LM: proliferation w/ neutrophils and monocyte infiltration

IF: Granular deposits

EM: “humps” in epithelial side of BM

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15
Q

Acute Proliferative clinical

A

kids 6-10yo, 1-2 weeks post sore throat

hematuria, oliguria, periorbital edema, HTN, mild proteinuria and red cell casts

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16
Q

Nonstrep Acute

A

same as Acute, just after another disease

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17
Q

RPGN

A

severe, death w/in weeks if untreated

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18
Q

RPGN path

A

ruptures in GBM triggers Crescent formation

immunologically mediated

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19
Q

Crescent

A

proliferation of parietal epithelia cells lining Bowman’s capsule due to infiltration by monocytes and macrophages

contain fibrin

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20
Q

Type I RPGN

A

Anti-GBM antibody, linear IF

Goodpasture’s Sx

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21
Q

Goodpasture’s Syndrome

A

anti-GBM ab also xreact with pulmonary alveolar BM

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22
Q

Type II RPGN

A

immune complex deposition granular IF

lupus, post infections, Henroch Scheloin

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23
Q

Type III RPGN

A

NO anti-GBM or immune complexes

circulating ANCA

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24
Q

RPGN gross

A

large, pale kidneys with cortical petechial hemes

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25
RPGN clinical
**hematuria, RBC, proteinuria, htn , edema**
26
Nephrotic Syndrome
increased BM permeability leading to loss of plasma protein
27
Nephrotic Syndrome clinical
**severe proteinuria >3.5g/day**, hyperlipidemia, edema
28
Nephrotic Syndrome diseases
Membranous nephropathy, minimal-change disease, Focal Segmental Glomerulosclerosis, Membranoproliferative Glomerulonephritis
29
Membranous Nephropathy
idiopathic, autoimmune **immune complex mediated** with diffuse thickening of glomerular capillary wall
30
Membranous Nephropathy EM
- deposits btwn GBM and epithelial cells - spikes protruding from GBM - **spikes and domes**
31
Membranous Nephropathy clinical
INITIAL **mild proteinuria, hematuria, mild HTN** --> severe goes to sclerosis, inc Creatinine, HTN worse
32
Minimal Change disease
**kids in 2-6 following RI** selective to albumin
33
Minimal change disease
**no immune complexes seen**, but responds to steroids **effacement of foot processes of visceral epithelial cells on EM**
34
Focal Segmental Glomerulosclerosis (FSGS)
idiopathic, adaptive response to loss of renal tissue **poor steroid response**
35
FSGS path
visceral epithelial damage w/ **hyalinosis and sclerosis**
36
FSGS light microscopy
focal sclerosing, segmental, **affected capillary loops collapse**
37
FSGS EM
effacement of foot processes, detachment of epithelial cells and denudation of GM
38
MPGN Type I
immune complexes in glomerulus w/ activation of **both** complement pathways *secondary is always Type I*
39
MPGN Type II
*dense deposit disease* **alternative** complement only (C3 only)
40
MPGN LM
proliferation of mesangial cells and capillary endothelium **tramtrack splitting*
41
MPGN Type I EM
subdendothelial deposits
42
MPGN Type II EM
ribbonlike dense material in GM
43
MPGN clinical
nephrotic syndrome + hematuria bad reoccurrence
44
Berger's Disease | IgA nephropathy
**hematuria** in young adult, following UTI, lasts several days, slow progression to CRF
45
Alport Syndrome
X-linked recessive abnormal a5 collagen IV mutation **Hematuria and Red casts with Nerve Deafness and Eye Disorders**
46
Alport syndrome morph
GMB thinning initially late: GBM alternating thick and thin, splitting and layering of lamina densa
47
Thin BM Lesion | Benign Familial Hematuria
thinning of GMB, asymptomatic, no big deal
48
Chronic Glomerulonephritis
contracted kidneys with granular, thinned cortex leading to atrophy of the tubules
49
End Stage Renal disease
sclerosis, fibrosis, inflammation, hylanized sclerotic vessels, atrophy of tubules
50
Henoch Schonlein Purpura
3-8yo following URI w/ IgA deposited in the glomerular mesangium
51
DM nephropathy clinical
nonnephrotic proteinuria, nephrotic syndrome, CRF
52
AMyloidosis
deposits in mesangium and capillary walls presents with nephrotic syndrome
53
Nephrosclerosis pathogenesis
medial and intimal thickening due to hemodynamic changes, aging, and genetics hyaline deposition in arterioles
54
when does Nephrosclerosis cause renal insufficiency
AA, severe HTN, underlying disease (**DM**)
55
Malignant HTN gross morph
"flea bitten" appearance of kidney from petechial hemes on cortical surface w/ associated edema
56
Malignant HTN histo morph
fibronoid necrosis of arterioles with eosinophilic granules
57
Malignant HTN hyperplastic arteriolitis
onion-skinning appearance due to proliferation of **concentrically** arranged SM cells and collagen
58
Renal artery stenosis
**UNILATERAL** constriction decreases intrarenal circulation/blood pressure
59
Renal artery stenosis pathway
JGA cells rls renin--> angiotensin II (**htn**) --> aldosterone (**hypernatremia and hyperH2O**)
60
Kidney embryo germ layer
intermediate mesoderm at Day 22
61
Kidney embryo derivation
mesoderm-->intermediate mesoderm-> lateral urogenital ridge--> nephrogenic cords--> meso: mesonephric duct (Wolffian) meta: kidney/uretric bud
62
Ureteric bud
Day 32 forms 1-3m collectuing tubules and ducts, major and minor calyces, renal pelvis, ureters
63
metanephric blastema
glomeruli, tubules, bowman's space
64
Final kidney
T12-L3 rt lower than lt **week 12** but placenta still does waste
65
hydronephrosis
dilation of the calyces and and pelvis due to obstruction of urine flow by aberrant/accessory renal arteries
66
horseshoe kidney
inferior mesenteric artery disrupts kidney ascent leading to fused lower poles
67
Wilms tumor
nephroblastoma 11p13, more likely in horseshoe kidney
68
multicystic dysplastic kidney
Nephrons fail to develop and ureteric bud fails to branch so collecting ducts never form
69
Autosomal Recessive Polycystic Kidney Disease
Cysts form from **collecting ducts**
70
Autosomal DominantPolycystic Kidney Disease
Cysts form from **all segments** of the nephron
71
Renal agenesis
Failure of kidney development (bilateral renal agenesis) due to the failure of formation of the ureteric bud **Potter Syndrome**
72
Potter Syndrome
anuria, oligohydroamnios, pulm hypoplasia craniofacial abnormalities, noncompatible with life
73
WAGR syndrome
aniridia, hemihypertrophy, wilms tumor
74
Ureteropelvic junction obstruction
**Most common site of obstruction** Presents prenatally as hydronephrosis; may present as a palpable abdominal mass. Evaluate with US, VCUG
75
HUS
Endothelial injury (Shiga like toxin)→ platelet activation and thrombosis
76
TTP
Platelet aggregation from very large multimers of vWF due to deficiency of ADAMST13
77
HUS sx
kids Severe oliguria, and hematuria, Microangiopathichemolytic anemia, Thrombocytopenia
78
TTP sx
adults Pentad of fever, neurologic symptoms, microangiopathichemolytic anemia, thrombocytopenia, renal failure
79
TTP/HUS acute kidney effects
Cortical necrosis, subcapsular petechiae, thickened walls
80
TTP/HUS chronic kidney effects
scarring of cortex, tramtracking, thickening of everything
81
cholesterol emboli
Arterial seeding of fragmented atherosclerotic plaque to small arterioles •Clear clefts of cholesterol seen embolizedto small vessels
82
Sickle-cell Disease Nephropathy
Hematuria, Proteinuria, Diminished concentrating ability
83
Diffuse Cortical Necrosis
Follows catastrophic conditions such as abruptioplacentae, septic shock Massive ischemic (coagulative) necrosis
84
HH EQUATION
pH=pKa + log (A-)/(HA)
85
respiratory acidosis cause
respiratory distress, no breathing
86
respiratory alkalosis cause
hyperventilating
87
how to look at ABG
1. Look at pH. 2. Look at PCO2 3. What is the primary disorder (respiratory or metabolic) 4. Calculate anion gap 5. Look for compensation 6. Look for clues to mixed disorders – multiple problems can coexist.
88
Anion Gap
4-12 normal high: ketone, lactic acid, ethylene glycol poisoning
89
Anion Gap equation
Na - (Cl + HCO3)
90
Metabolic Acidosis
pH less than 7.4 HCO3 less than 24
91
Metabolic Acidosis Respiratory Compensation
PCO2 less than 40
92
Respiratory Acidosis
pCO2 greater than 40
93
Respiratory Acidosis Metabolic Compensation
HCO3 greater than 24
94
Metabolic Alkalosis
pH >7.40, HCo3 greater than 24
95
Metabolic Alkalosis Respiratory Compensation
PCO2 greater than 40
96
Respiratory Alkalosis
pH >7.40, PCO2 less than 40
97
Respiratory Alkalosis Metabolic Compensation
HCO3 less than 24
98
Mixed Disorder Clues
1. pH is normal but PCO2 or HCO3- is abnormal 2. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap. 3. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder
99
Mixed Disorders rule of thumb
- When the PCO2 is elevated and the [HCO3-] reduced, respiratory acidosis and metabolic acidosis coexist. - When the PCO2 is reduced and the [HCO3-] elevated, respiratory alkalosis and metabolic alkalosis coexist
100
diarrhea/renal failure acid base disorder
non anion gap metabolic acidosis
101
Metabolic Acidosis diseases
Lactic acidosis, ketoacidosis, loss of bicarb, ingested toxins **anion gap**
102
Metabolic Alkalosis
vomiting, diuretic, increased mineralcorticoid effect, increased intake of alkali
103
Respiratory Acidosis
CNS depressant, neuromuscular disorders, obstructive lung disease
104
Respiratory Alkalosis
Hyperventilation (anxiety, CNS infection) Salicylates!! SIRS Pulmonary disease (acute PE and acute flair of asthma). Hypoxia
105
Chronic Kidney disease definition
GFR 3 months.
106
CKD sx
Usually none. Fatigue. Nocturia. Swelling. Confusion.
107
drug to preven protein excretion
ACEI
108
metabolic acidosis tx
sodium bicarb
109
calcium acetate MOA
binds phosphate to keep it under

DT III (2 decks)

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