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 Pathology Review Notes  



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  #1

This thread may be used to post personal review notes for Pathology.


Regards!




  #2

guess I'll be the first to post in this thread smiling face

Renal Path
-Type II Rapidly Progressive (cresentic) GN associated with SLE and Henoch-Schlura purpura
Type III - Wegner's granulamoutousisisis(sp?) and microscopic polyangitis

-IgA nephropathy (berger's Disease) - assocaited with Celiac Disease; intermitentn hematuria

-Alports syndrome - XD, can be AD or AR; foamy change in tubular epithelial cells,

-Nephrotic Syndrome --» see Oval Fat bodies which are sloughed tubular cells containing abundant lipid

-membranous GN - granular deposits are of IgG and C3

-minimal change disease - fusion of foot procesess are due to injury induced by T-cell derived cytokines

-RCC
--» see painless hematuria in an adult, think neoplasm.
--» usually unilateral, doesn't destory all of kindney, no sig loss of
renal fxn, HTN due to Inc. renin secretion.
1) Clear Cell Ca --» MC, presents with painless hematuria in 6th or 7th
decades. 80% show sporadic loss of VHL gene
--» germ line mutation of VHL loss occurs in 4th decade of life, assoc w/
von Hippel Lindua syndrome (which is associ with other tumors)
2) Papillary variant of RCC --» MET on chr7

-Hemolytic-Uremic Syndrome (HUS)
1)MCC of acute renal failure in children, occurs after ingestion of meat
infected with E.COli o157:h7
2) may see microangiopathic hemolytic anemia


-Adult Polycystic Kidney Disease (APKD)
MC C/x are HTN and infection, Inc. risk of RCC, AD (= adult onset of the
dz), cysts are 1-4cm, replace kidney, can see cysts in liver and pancreas
as well, assoc with berry aneurysm, non-smooth kidney surface

-Juvenille Polycystic Kidney Disease (JKPD)
AR, occurs in neonates or prenatal, cysts involve liver, kidneys have
smooth surface.


-Hypercalcicuira
doesn't have to be linked to Hypercalcemia, T/x = thiazide diuretics

-Acute drug-induced intersititial nephritis
1) caused by ampicillin (PCN?), see eosinophils in urine

-ATN -
due to ischemia
1) accompanied by rupture of basement membrane (tubulorrhexis?)
2) 3 phases; (a) initiating phase, lasts 1 day (b) maintenance phase -
progrossive oliguria and increasing BUN levels with salt and h20 overload
(c) recovery phase - inc. urinary output and hypokalemia then restoration
of of tubular fxn.

-Renal Papillary Necrosis
4. Analgesic nephopathy - chr usage of acetaminophen and aspirin


-Simple cysts
common in adults, may be multiple, but not as numerous as those in
APKD, no renal failure, may become as large as 10cm, can hemorrhage
into cyst

-Chronic Pyelonephritis
due to reflux nephropathy
1)coarse and irregular scarring from asc. infxn.
2)blunting and deformity of the calyces

-Prerenal Azotemia
= basically due to Dec. C.O. ==» Dec. RBF, etc[/b]


  #3

Hi all.
1)AFP-----Hepatoma,testicular germ cell tumor(non-seminomatous)
2)hCG-----H.mole,choriocarcinoma
3)Calcitonin----Medullary thyroid ca:
4)CEA----Ca: lung,pancreas,breast,stomach,colon.
5)CA-125-----Ovarian ca:
6)CA19-9-----Pancreatic tumor.
7)Placental alkaline phosphatase-----Seminoma.
8)Prostate acid phosphatase & PSA------Prostate ca:
9)S-100------Melanoma,neural tumors.
10)


  #4

Along with unusual inheritence and nephritic syn. Alports can present with:
DEAFNESS AND BLINDNESS! :cry:


  #5

HYPERTENSION: Defined as systolic blood pressure greater than 160mm, or diastolic blood pressure greater than 90mm, or both.
Subtypes:
1) BENIGN HYPERTENSION: Asymptomatic.
2) MALIGNANT HYPERTENSION: Rapidly progressing to end-organ failure.

MORPHOLOGY: Blood vessels show fibrinoid necrosis or concentric hyperplasia of smooth muscle-cells -- onion-skin changes).

PATHOGENESIS:
ESSENTIAL HYPERTENSION: Primary hypertension in which there is no single identifiable cause. In majority of cases,Renin from kidney is a major player.
Renin converts Angiotensinogen ------> Angiotensin I
ACE converts Angiotensin I ------> Angiotensin II
Angiotensin II effects:
1) Vasoconstriction.
2) Stimulate secrete of aldosterone from adrenal glands ------> K+ excretion and Na+ retention, fluid retention in kidney ------> higher blood volume.

SECONDARY HYPERTENSION: Hypertension secondary to a disease. Minority of cases....
-Renal Ischemia: Anything causing ischemia to the kidney (vascular stenosis or atherosclerosis of Renal Artery or arterioles) will release renin and probably result in hypertension.
-Fibromuscular Dysplasia of Renal Artery is a congenital disorder, with progressive concentric thickening of the Renal Artery. Occurs in young females.
-Cushing's Syndrome: Primary hypersecretion of cortisol.
-Conn's Syndrome: Primary hypersecretion of aldosterone.
-Pheochromocytoma: Adrenal medullary tumor.
-Norepinephrine is secreted in spurts, so patient will have wildly fluctuating, paroxysmal elevations in blood pressure.
-Thyrotoxicosis

RISK FACTORS: Similar as those for atherosclerosis and CAD.
Genetics: often found to be familial
Diet
Stressful lifestyle
Obesity

CLINICAL MANIFESTATIONS: Often asymptomatic
Early on: Headache, nosebleeds, tinnitus, dizziness, fainting, visual impairment.
Later: End-stage hypertension results in stroke, heart failure (from compensatory hypertrophy), renal failure


  #6

a few points to ponder

1. sjogrens syndrome has a high chances of developing malignant lymphoma

2. embroynal ca. ha high afp levels, and is not radiosenstive



  #7

3. ifon absorbed in the duedonum

4. folatein jejunum and b12 in the illeum



  #8

5. in sickle cell anaemia, the splleen enlarged till 20 yrs of age, but becomes non functional by 2 yrs of age, and reduces to thumb size by 20 yrs of age.and hence autosplenectomy, give pneumovax after 2 yrs of age, not before that, but spherocytosis, spleen always enlarged and hence doing a splenectomy, reduces the symptoms


  #9

SLE

INCREASED---
AB against DS-DNA
INR,ESR,CD3
WCBCs,Lymphocytes

DECREASED----
PLATELETTES
C3,C4

NORMAL

C-REACTIVEPROTEIN


  #10

Cytoskeletal Abnormalities:
A.Cytoskeleton = 1.Microtubules 2.ThinFilaments(Actin)3.Thick Myosin Filament4.Intermediate Filament
B.Abnormalities=
1.Microtubles : a.assembly of microtubles=> Mitotic spindles(cell division );Inhibited by Vinca alkaloids & Colchicin hence antiproliferativeb.Defect leads to Immotile cillia syndrome
c.Colchicin in acute attacks of gout, as it inhibits leucocyte migretion in response to urate crystal deposition, by inhibiting microtubule
2.Thin filaments: leucocyte movement and phagocytosis. Phalloidin(toxin in Amanita phalloides) bind to actin.
3.Intermediate Fillaments:
a.Keratin (epithelial cell).....Mallory bodies(ubiquinated Keratin in hepatocytes in ALD)
b.Neuro filaments(neuronal cells)......Neurofibrillary tangles(Alzhiemer's, also CJD)Lewy Bodies(in Substantia nigra in PD)
c.Desmin(muscle cell)
d.Vimentin(connective tissues)
e.Glial filaments(astrocytes)


Edited by focususmle on Jun 29, 07 - 06:25




  #11

nod thank you nod
Also, increased CA19-9 is indicated for cholangioCA.


Edited by precious on Dec 04, 2007 - 4:45 AM

  #12

Thanks & CA-153 for breast CA
CD117 & CD34 for GI Stromal tumor


  #13

p.s. CD117&CD34 are for immunohistochemistry not serum marker.


  #14

black,35,x-ray-hilar nodes-swell along with uveitis nad parotid enlargement and lacrimal gland involvement------

sarcoidosis.



hey remember---its diagnosis of exclusion.



what if we get the hand x-ray??grin






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