How can you distinguish glomerular from extraglomerular hematuria?
GLOMERULAR DISEASES
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
Q.148. How can you distinguish glomerular from
extraglomerular hematuria?
A. Glomerular
vs. extraglomerular hematuria:
|
“Extraglomerular” |
“Glomerular” |
Color (macroscopic): |
Red or
pink. |
Red, smoky brown, or "Coca-Cola“. |
Clots |
May be
present. |
Absent. |
Proteinuria |
usually
absent. |
May be
present |
RBCs morphology |
Normal. |
Dysmorphic |
RBCs
casts. |
Absent
. |
May be
present. |
Q. 149.What
is the Hallmark of S.L.E. ?
- Auto-A.B. production of: A.N.A.
& Anti-DNA, incr. Anti-DNA. titre correlate well é clinical
activity.
-
Anti-S.m. A.B. (25% of cases): V. specific to L. nephritis & greatly ass.
é C.N.S. , R. disease., more cutaneous
mnf. &, cardiopulmonary
mnf. & Worse prognosis.
Q.150. What are the renal manifestations of SLE? 👓
A. Renal
Manifestation of SLE:
1)
Proteinuria: 100 %, N.S.: (45-65%).
2)
Hematuria:
Microhematuria: 80 %.
RBCs casts: 10 %.
Macrohematuria 1 %.
3) Cellular casts: (30%).
4) Reduced renal
perfusion: (40-80%):
🠞 RBGN:
10-20%.
🠞AKI: 1%
5) Hypertension: (15-50%).
6) Hyperkalemia: 15 %.
Tubular abnormalities:
(a.Sm.tc.)(60-80%).
Q.151. Mention the major criteria for diagnosis?
- { 4 of Eleven criteria are necessary for Dg.x. of S.L.E. } :
1) Malar
rash.
2) Photosensitivity.
3) Discoid
Lupus.
4) Dermal mamifestation.
5) Oral/nasal ulcers.
6) C.N.S. mamifestation.
7) Serositis (Pleural/Pericardial).
8) Renal mnf. (Persistent Prot. ½ g./d.).
9) Cytopenias.
10)
Arthritis (Non-defomitive).
11)Im/m.
markers:
[ANA-Anti-DNA-
Anti-Sm.].
Q.152. What is Full House in S.L.E. ? What’s its significance?
A. Full House=After booker hands =Christmas Tree
in S.L.E. = Pres. of [Ig.: G+A+M+ C3+ C1q.] altogether in I.F.
study of R. biopsy, of a lupus ptn..
- Full House & C1q
staining
Strongly suggestive of “Lupus Nephritis”.
IF-anti IgG:
The immunofluorescence profile is “full house”, meaning
that IgG, IgA, IgM C3 &
C1q are usually present. This image displays mesangial and
granular loop staining for IgG.
IF-anti-IgA:
Both mesangium & capillary loops are stained. Note the intensity is less
than with anti-IgG.
IF-anti-IgM: Again both
mesangium & capillary loop staining is observed, however there is slightly
more within the mesangium. Note the intensity is also less than that seen with
anti-IgG.
IF-anti-C 1 q: Staining here’s
v. similar to tht sn é anti-IgG.
Often the intensity rivals tht of anti-IgG.
IF-anti-C3:
C3 is the most
common complement observed in SLE, with C1q almost as common.
Q.153. Give the new classification of
S.L.E.?
i.Minimal mesangial (N. in L.M.).
ii.Mesangial proliferation.
iii.Focal (<50%) proliferative.
iv.Diffuse (>50%) proliferative.
v.Membranous Lupus.
vi.Advanced Sclerosis.
Q. 154. How can you monitor “Lupus Activity”? What are the signs & symptoms of Lupus Flare?
A. - “Parameters of activity”:
(1)
Active urinary sediment (Dysmorphic RBCs. & RBCs casts).
(2)
Hypocomplementemia .
(3)
Anti-DNA titer.
(4)
High E.S.R.
(5)
High C.R.P.
(6)
Circulating im/m. complexes.
(7)
Cytokine & IL. Level.
(8)
Systemic mnf. (fever, fatigue, asthenia).
(9)
Activity features in biopsy: [fibrinoid
necrosis.- Leukocytic
infiltration- Wireloop
deposits.
*** Sn.s & Sm.s of Lupus
Flare: Ptn shd be aware of
one or more of these Sm.s:
v Persistent fatigue out of proportion é
expected.
v Persistent weakness.
v Aching all over.
v Fever, wch may be slight
to high (check your °C yourself).
v Persistent loss of appetite.
v Involuntary wt loss.
v Increasing hair loss.
v Recurring nose bleeds.
v Sore é roof of mouth,
wch burns é spicy foods.
v Unexplained skin rash anywhere on the
body.
v Hives.
v Sores on the skin
v Painful joint(s)
v Swollen joint(s)
v Stiffness of joints é waking up in the
morning
v Chest pain wch incr. é breathing
v Shortness of breath
v Coughing up blood.
v Persistent unusual headache.
v Nausea or vomiting.
v Recurring or persistent abd. pain.
v Persistent, incr. swelling of feet & legs
v Puffy eyelids.
v Blood in the urine.
N.B. : “Silent Lupus” :
{ptn. Clinically Normal + “Proliferative” les. é R. Biopsy.}.
Q.155. What
are the serological parameters of clinical
implications in S.L.E.?
Anti-Sm.
A.B.: (25%
of cases)
very specific to “Lupus nephritis” & greatly
ass. é CNS, R. disease, more cutaneous mnf. &, cardiopulmonary mnf. & Worse prognosis.
Maternal
(anti-Ro): Cardiac anomalies in newly born.
Anti-Ro Unique
dermal form of Lupus é Psoriaform of Lupus.
C3/C4 start
decline before clinical
flare, CH50 is better thn isolated C3 & C4.
C3/CH50 may
dcr. without clinical activity, é
sev. dermatologic involvement.
Q.156. Which group of drugs can induce Lupus?
A.
Drug-induced lupus:
[Hydralazine-
Procainamide-Penicillamine-Diltiazem-INH-Methyl dopa]use for > one m. or longer:
can induce Lupus.
Q.157. How
to manage?
A. History of drug intake and presence of (Anti-histone
auto-A.B.), help in Dg.x. of drug-induced Lupus, which. can be reversed by stoppage
the offending drug. The "gold standard" in Dg.X. is spontaneous
resolution of the disease é 1-7 m.
after the offending drug has been discontinued. Addition of NSAID
& antimal-arials will help in clearance of constitutional & musculoskeletal Sm.s rapidly. Steroids
cn help in quick resolution of serositis.“Cytotoxic
therapy” only needed in “Hydralazine
-induced” vasculitis.
Q.158. Which
type of therapy is allowed for pregnant
lupus?
A. {Steroid therapy. + Aza} , can be safely used é relative safety.
Q.159. What
prognostic features denoting good response?
A. Reversal of :{1. Inflammatory
response (see criteria of activity above). 2. Im/m. deposits. 3. Glomerular segmental scarring.
4. Interstitial fibrosis.}
..occ. within 6 m. denotes a favorable prognosis.
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