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209 Cards in this Set
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Nephritic syndrome
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due to glomerular disease
acute onset of hematuria mild to moderate proteinuria hypertension "classic presentation of acute post-streptococcal glomerulonephritis" |
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Rapidly progressive glomerulonephritis - RPGN
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a nephritic syndrome
rapid decline in GRF Half are associated with underlying disease: SLE, Goodpasture's, Wegner's granulomatosis. Half are idiopathic |
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Nephrotic syndrome
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Due to glomerular disease
Heavy proteinuria >3.5g/day Hypoalbuminemia Severe edema Hyperlipidemia Lipiduria |
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Acute renal failure
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oliguria or anuria
recent onset azotemia Can result from any renal disease: glomerular, vascular, tubular, or interstitial |
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Chronic renal failure
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prolonged symptoms and signs of uremia, end result of all chronic renal parenchymal diseases
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Nephrolithiasis
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severe spasms of pain
hematuria Most often calcium oxalate, then triple stones (magnesium ammonium phosphate), then uric acid (gout), then cystine |
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Alport syndrome
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Mutation in collagen IV genes - leading to dysfunctional GBM
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Filtration barrier in the glomerulus consists of:
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1. Fenestrated endothelium
2. Anionic acidic proteoglygans in GBM 3 Filtration slits - space between podocyte foot processes. Footprocesses connected by nephrin, podocine. |
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Mutations of nephrin and podocin cause:
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proteinuria
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JGA responsible for:
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renin secretion
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4 histologic changes seen in glomerulopathies
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1. hypercellularity
2. basement membrane thickening 3. hyalinosis 4. sclerosis |
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Minimal change disease
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Nephrotic disease of children
Low weight proteins lost No hematuria, HTN, or loss of renal fxn on EM: effacement of foot processes Responds to steroids - likely immune related |
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Primary Focal segmental glomerulosclerosis
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Nephrotic range proteinuria, hematuria, HTN
Often idiopathic Mutation in podocin or nephrin |
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Secondary focal segmental glomerulosclerosis
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Nephrotic range proteinuria, hematuria, HTN
Caused by: HIV, IVDA, reflux nephropathy, reduction of renal parenchyma, |
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focal, diffuse, segmental, global
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focal - part of the kidney
diffuse - most/all of the kidney segmental - part of the glomerulus Global - all of the glomerulus |
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Membranous glomerulopaty
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Cause of nephrotic syndrome.
Thickened GBM (wire loops) Deposits of Ig and complement Idiopathic: unidentified renal antigen Secondary: SLE, infection, drugs, heavy metals, malignancy |
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SLE nephrotic syndrome
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Immune complex deposition
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Diffuse and nodular glomerulosclerosis
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Seen often in DM
Thickening of GBM |
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Amyloidosis
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causes nephrotic syndrome
mesangial regions expanded Congo red stain - turns pink/orange, apple green with polarized. |
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Red cell casts
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ALWAYS pathogenic
usually associated with nephritic syndromes and indictes glomerular damage |
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Granular casts
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aggregates of plasma proteins
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Post streptococcal glomerulonephritis (proliferative)
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Immune complex nephritis 5-30 days after group A strep
Acute nephritic syndrome |
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IgA nephropathy
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Focal proliferative GN
Gross hematuria - nephritic IgA accumulates in mesangium |
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Rapidly Progressive Glomerulonephritis RPGN
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Accumulation of cells in Bowman's space (crescents), which eventually undergo sclerosis.
May follow: goodpasture, immune complex GN, Pauci-immune (ANCA), wegener's, polyarteritis nodosa |
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Goodpasture Syndrome
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Lung and Kidney
anti-GBM - antibody to type IV collagen. Pulmonary hemorrhage and acute GN, crescents usually seen in young males |
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Wegener granulomatosis
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Lung and Kidney (only 2 of these diseases)
Acute GN c-ANCA positive. Fibrinoid necrosis, hypercellularity, crescent formation |
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Alport syndrome
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Deafness, eye conditions,
Mutation COL4A5 Lamellated lamina densa - basket weave. |
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Thin basement membrane/Benign familial heaturia
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glomerular hematuria, proteinuria
GBM thinning |
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Fabry disease
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lysosomal storage disease
x-linked recessive Can cause renal failure over time |
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Diseases that present both nephrotic and nephritic
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SLE, membranoproliferative GN
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Membranoproliferative GN
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Presents with nephrotic and/or nephritic
Type I more common Type II less common, more serious, recurs in transplant Lobular glomeruli, mesangial and endothelial proliferation "TRAM TRACK" apparearance, because of double layer GBM with mesangium in the middle. |
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Causes of acute kidney injury:
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Ischemic, toxic injury, acute tubulointerstitial nephritic (drug hypersensitivity), urinary obstruction
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2 pathways to pyelonephritis
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ascending from lower UTI
or hematogenous |
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Factors favoring UTI
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Female gender
catheterization urinary obstruction vesicoureteral reflux Diabetes, immunosuppression/deficiency |
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Morphology of pyelonephritis
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Starts in medulla and travels outward where the most damage occurs.
Suppuritive inflammation + tubular necrosis. Glomeruli spared at first. Abscess may occur |
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Papillary necrosis
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acute pyelonephritis seen in:
diabetes analgesic nephropathy alcoholism sickle cell disease |
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Polyoma virus nephropathy
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Seen in transplant patients
Latent infection in many people,activated by immune suppression causes 1-5% of transplant failures Interstitial inflammatory response |
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Pyonephritis
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Complete urinary obstruction allows infection to turn kidney into a sac of pus
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Patterns of chronic pyelonephritis
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1. Obstructive - bacterial infection recurs because of obstruction
2. Reflux - urinary infections and reflux up the ureters |
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Presentation of chronic pyelonephritis
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may be insidious
slow onset of polyuria and nocturia due to inability to concentrate. Gradual onset of renal insufficiency and HTN |
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Morphology of chronic pyelonephritis
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Grossly scarred and contracted kidneys
Tubules are atrophic Lymphocytes in interstitium |
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Xanthogranulomatous pyelonephritis
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mimics RCC
Macrophages, giant cells, granuloma E coli, Staph, Proteus |
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Benign nephrosclerosis
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Very common (75% of men over 60)
associated with benign hypertension Rarely impairs renal function |
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Malignant hypertension adn accelerated nephrosclerosis
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Hyperplastic arteriolitis ONION SKINNING of arterioles
Gross: flea bitten kidney vasculature of kidney becomes permeable to fibrinogen and plasma proteins. Fibrinoid necrosis of arterioles. |
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Vasculitis
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Polyarteritis nodosa (p-ANCA)
Wegener granulomatosis (c-ANCA) Necrotizing glomerulonephritis |
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HUS/TTP
hemolytic uremic syndrome/thrombotic thrombocytopenic purpura |
causes thrombi in glomeruli
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Benign renal tumors
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renal papillary adenoma
angiomyolipoma oncocytoma |
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Renal adenoma
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Benign, common
arise from tubular epithelium usually papillary |
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Angiomyolipoma
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Benign, renal
Consists of vessels, SM, and fat associated with tuberous sclerosis, skin abnormalities |
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Oncocytoma
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Benign, renal
Epithelial tumor Arise from collecting ducts - eosinophilic due to mitochondria |
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Renal Cell Carcinoma RCC
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Malignant
Male preponderance arises from tubular epithelium Presents with pain, mass, hematuria Tobacco, obesity, HTN, estrogen therapy are risk factors |
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Genetic associations with RCC
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Von Hippel-Lindau syndrome (VHL)
Hereditary clear cell carcinoma Hereditary papillary carcinoma |
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Types of RCC
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1. Clear cell (most common)
2. Papillary 3. Chromophobe |
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Clear cell carcinoma
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Type of RCC
70-80% of RCC Loss of part of short arm of chromosome 3 |
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Papillary carcinoma
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type of RCC
10-15% of RCC frequently multifocal associated with trisomies 7,16,17, loss of Y. |
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Chromophobe renal carcinoma
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Type of RCC
Grow from intercalated cells of collecting ducts Malignant form of oncocytoma Great prognosis |
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Patterns of familial vs sporadic RCC
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Sporadic - usually one tumor
Familial - usually several |
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Wilm's tumor
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Most common primary renal tumor in children
4th most common pediatric malignancy in US |
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WAGR syndrome
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Wilms tumor (33% chance)
Anidiria Genital Abnormalities Mental retardation Caused by germline deletions of 11p13 |
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Denys-Dash syndrome
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90% risk of Wilms tumor
gonadal dysgenesis |
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Urothelial carcinoma of renal pelvis and ureter
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Presents early, noticeable hematuria
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Polycystic kidney disease
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5-10% of all chronic renal failure
bilateral Multiple expanding cysts |
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Medullary sponge disease
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multiple cystic dilation of the collecting duct
seen on radiology complications: tones, hematuria, infection |
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Molluscum contagiosum
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adult STI
poxvirus of skin and mucous membranes |
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Trichomonas infection
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Protozoan
vaginal seen on pap wet prep discharge, dysuria, dyspareunia |
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Gardnerella infection
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BV, not sexually transmitted
organisms cover squamous cells |
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Lichen sclerosis
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vulvar disease
squamous hyperplasia smooth white plaques benign |
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Condyloma accuminatum
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Genital warts
spiky proliferation with koilocytic change, enlarged irregular nucleus with perinuclear halo HPV 6,11 |
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Vulvar intraepithelial neoplasia (VIN)
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Epidermal atypia with no BM envasion.
Associated with HPV 16 OR in older women, longstanding lichen sclerosis VIN I, II, III based on how deep. |
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Invasive SCC of the vulva
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when VIN breaks the BM
basaloid/warty if HPV is present differentiated if HPV isn't present (older women) |
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Extramammary Paget Disease
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Intraepithelial Adenocarcinoma in situof the vulva - probably arises from glandular cells in vulvar skin.
Shotgun pattern |
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Vaginal adenocarcinoma
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rare - mainly clear cell
Associated with DES in mothers during pregnancy |
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Vaginal dysplasia
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VaIN I, II, III - depends on how deep, doesn't break BM
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Embryonal rhabdomyosarcoma
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Can present in young girls' vaginas as a bunch of grapes.
Racket cells. |
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Cervical anatomy/microanatomy
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Ectocervix - mature squamous epithelium
Endocervix - mucous producing glandular epithelium Transformation zone - endocervical gland epithelium undergoes squamous metaplasia, changes with age, these cells are especially susceptible to HPV |
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Endocervical polyps
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benign
may produce spotting, post coital bleeding |
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HPV virus interferes with human genes...
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Rb and p53 tumor suppressor genes. Extends the life of infected cells.
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Pap smear results
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normal, low grade SIL, high grade SIL (squamous intraepithelial lesion)
because it's not a biopsy - no CIN grading |
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Invasive carcinoma of the cervix
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80% SCC
15% adenocarcinoma 5% adenosquamous or neuroendocrine All caused by HPV |
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Infections of the endometrium
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rare
associated with D&C, post partum, IUD, TB Plasma cells must be seen |
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Endometrial polyps
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Benign, not premalignant
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Adenomyosis
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Endometrial tissue present within the myometrium.
very painful |
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Endometrial hyperplasia
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Prolonged unopposed estrogen can cause this.
Can lead to atypia, adenocarcinoma. May have PTEN deletion |
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Endometrial carcinoma
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almost always adenocarcinoma
2 types Type I - 55-65, Fat, HTN, DM, unopposed estrogen (from obesity). PTEN deletion, endometrioid Type II - older thin, no unopposed estrogen. Can be serous, clear cell, malignant mixed mullerian. |
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MMMT - malignant mixed mullerian tumor
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type II endometrial carcinoma
poorly differentiated, sarcomatous. Arises in endometrial atrophy. p53 mutation poor prognosis |
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Leiomyoma
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fibroids, very common, benign
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Leiomyosarcoma
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malignant, arises de novo (not from leiomyoma)
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STUMP
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smooth muscle tumors of uncertain malignant potential - not sure if it's a leiomyoma or leiomyosarcoma
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Endometrial stromal sarcoma
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spindle shaped cells between glands become malignant.
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Types of ovarian tumors:
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surface epithelium - young women
germ cell - very young women sex cord stroma - all ages |
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Types of surface epithelial ovarian tumors:
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Serous - Most common, mostly benign. Psammoma bodies. Smooth and glistening surface - benign. Often bilateral
Mucinous - Most are benign/borderline. Tall columnar epithelium, sticky fluid inside. Endometrioid - associated with endometrial adenocarcinoma, malignant. Brenner - transitional type epithelium, almost all benign |
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Germ cell tumors:
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Most are benign, most are mature cystic teratomas
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Types of germ cell tumors:
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dysgerminoma - no maturation, female version of seminoma
Embryonal carcinoma - somewhat matured. Yolk sac tumor - looks like glomerulus, increased alpha fetoprotein. Choriocrcinoma - placental tissue or trophoblast, usually in combination with other germ cell tumor. Aggressive, hCG. |
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Sex cord tumors - female
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from stroma, and theca or granulosa cells.
usually unilateral Cal-Exner bodies, nuclear groove Patients present with abnormal hormone production. Sertoli/leydig cell tumor - masculinization |
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Meigs syndrome
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ovarian fibroma, unilateral, ascites
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placenta acreta
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decidua doesn't develop
placenta implants in myometrium can hemorrhage, perforate |
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TORCH organisms
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hematogenous causes of placental infection
Toxoplasmosis Other syphilis, TB, listeria Rubella CMV Herpes |
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Preeclampsia
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widespread maternal endothelial dysfunction: hypertension, edema, proteinuria
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HELLP syndrome
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Hemolysis, Elevated Liver enzymes, Low Platelets
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Gestational trophoblastic disease
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Neoplasms characterized by proliferation of placental villi or placental trophoblast or both.
Includes hydatidiform moles, choriocarcinoma, placental site trophoblastic tumor PSTT |
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Complete hydatidiform mole
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46 chromosomes - but all male DNA. Placental villi form. High high high hCG. No fetal material
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Partial hydatidiform mole
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69 chromosomes - dispermic fertilization of a normal ovum. Fetal parts can be identified. No cytologic atypia.
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Gestational choriocarcinoma
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nto the same as germ cell choriocarcinoma! can develop after normal pregnancy. 50% develop after complete hydatidiform mole.
Atypical trophoblast with NO placental villi |
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Placental site trophoblastic tumor
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rare tumor of intermediate trophoblast
Presents as a uterine tumor. Occurs after pregnancy |
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Chronic mastitis
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Lots of names
Associated with smoking Dilated ducts fill with keratin - foreign body rxn. Presents as a mass |
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Fibrocystic change
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so common - not a pathology
Too much estrogen, common in young women 20-40. Apocrine metaplasia. Cysts and fibrosis and adenosis (too many ducts and acini) Presents as lumpy breasts. |
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Proliferative breast disease
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slight increased risk of malignancy
Epithelial hyperplasia Sclerosing adenosis Papillomatosis Complex sclerosing lesion/radial scar |
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Epithelial hyperplasia
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ductal hyperplasia, atypical ductal hyperplasia, and lobular hyperplasia (acinar)
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Intralobular stromal tumors of the breast
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Fibroadenoma - benign palpable mass in young women. May get larger during menstrual cycle. May take it out or leave it in.
Phyllodes tumor - stroma outgrows epithelium, looks like a leaf. |
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Interlobular stromal tumors of the breast
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same stromal tissues you would see anywhere else - leiomyoma, lipoma, angiosarcoma
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Benign Epithelial tumors of the breast
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Tubular adenoma
Papilloma |
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Malignant epithelial tumors (carcinoma) of the breast associated with what risk factors:
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BRCA1, BRCA2, Her2Neu overexpression
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Categories of breast carcinoma
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Ductal - 90%
Lobular |
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Ductal carcinoma in situ
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Low grade - almost identical to atypical ductal hyperplasia. Cell appearance is the same, amount of them is different.
High grade - ugly cells, sometimes comedone necrosis |
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Infiltrating ductal carcinoma
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many types:
Medullary Mucinous/colloid Tubular Paget's disease Basal like carcinoma triple negative carcinoma - bad |
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Medullary carcinoma
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An infiltrating ductal carcinoma
Medullary carcinoma - well circumscribed, ugly cells, younger women, better prognosis |
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Mucinous/colloid carcinoma
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An infiltrating ductal carcinoma
Mucinous/colloid carcinoma - lots of mucin, better prognosis |
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Tubular carcinoma
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well differentiated ductal carcinoma
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Paget's disease of the breast
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presents as a rash. Little malignant cells penetrate the epidermis
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Basal like carcinoma, triple negative carcinoma
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No estrogen, progesterone, her2neu receptors. very aggressive, doesn't respond well to therapy.
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Infiltrating lobular carcinomas
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have signet cells, indian filing (single file line of cells), tends to be multicentric and bilteral
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Inflammatory cell carcinoma of the breast
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Lots of inflammation - bad prognosis
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Metastasis of breast carcinomas
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first to axillary lymph nodes, then bone lung liver adrenal brain.
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Top causes of cirrhosis
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Alcohol (60-70%)
Viral hepatitis (10%) Biliary disease (5-10%) cryptogenic cirrhosis (10-15%) Primary hemochromatosis (5%) |
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presentation of cholestasis
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jaundice
pruritis skin xanthomas elevated alk phos intestinal malabsorption of fat |
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Criggler Najjar syndrome type I
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Complete absence of UGT1A1
inability to conjugate bilirubin Death in infancy |
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Criggler Najjar syndrome type II
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Reduced UGT1A1
Mild disease, non fatal, risk of CNS damage |
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Gilbert syndrome
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reduced UGT1A1
Innocuous, mild fluctuating unconjugated hyperbilirubinemia. 6% of the population has this |
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Dubin-Johnson syndrome
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autosomal recessive, loss of MRP2 which is responsible for transport of b. glucuronides into bile
Innocuous disease - pigmented liver. conjugated hyperbilirubinemia |
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Rotor sydrome
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autosomal recessive, decreased uptake/storage or excretion of bilirubin, innocuous, normal lives, occasional jaundice due to conjugated hyperbilirubinemia
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Chronic hepatitis due to HBV cells look like:
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ground glass cytoplasm
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Chronic hepatitis due to HCV microscopically looks like:
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lymphoid aggregates and diffuse steatosis
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treatment for chronic viral hepatitis
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pegylated IFN and ribavirin
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What is fulminant hepatitis?
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hepatic insufficiency that progresses from onset of symptoms to hepatic encephalopathy within 2-3 wks.
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Pathogenesis of alcoholic liver disease
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Steatosis -> cyp 450 -> ROS -> Lipid peroxidation.
Malnutrition and vitamin deficiencies. Inflammatory cytokines lead stellate cells to become myofibroblasts = cirrhosis |
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Causes of death in alcoholic liver disease
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hepatic coma
GI bleed Infection hepatorenal syndrome HCC |
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NAFLD and NASH
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Most common cause of chronic liver disease in US. 10-20% will develop cirrhosis.
Lifestyle modification to treat. NAFLD - steatosis without inflammation and fibrosis NASH - NAFLD progessing with inflammation and fibrosis |
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Hereditary hemochromatosis
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Autosomal recessive disorder that causes excess intestinal absorption/accumulation of body iron.
C282Y mutation has .45% frequency of homozygous Symptoms rare before 40. Bronze skin,cirrhosis. 200x risk of HCC. |
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Wilson disease
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Autosomal recessive accumulation of copper.
Sudden onset of hemolysis, dementia, chronic liver disease, kayser fleisher rings. |
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Alpha 1 antitrypsin deficiency
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Autosomal recessive - lack antitrypsin which turns off proteases.
Abnormal protein retained in ER, creating apoptosis or mitochondrial dysfunction -> hepatocyte damage. Cirrhosis, emphysema common. Liver transplant to treat. |
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alpha 1 antitrypsin deficiency morphology
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Globular inclusions are acidophilic by H&E and PAS.
Fatty change Mallory hyaline |
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Wilson's disease morphology
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Macrovesicular steatosis
vacuolated nuclei Mallory bodies Cirrosis or massive liver necrosis |
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Hemochromatosis morphology
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deposition of hemosiderin
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Secondary biliary cirrhosis
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Obstruction in the extrahepatic biliary tree.
Increased alk phos, bile acids, cholesterol. |
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Primary biliary cirrhosis
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Intrahepatic bile duct inflammation, non suppurative.
Associated with autoimmunity. Antimitochondrial ab present Symptoms: pruritis, jaundice, xanthelasma, dark urine, light stoold, HSM Liver transplant to treat |
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Primary sclerosing cholangitis
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obliterative fibrosis of intra and extrahepatic bile ducts, causing structures and dilation of affected ducts.
2:1 male asymptomatic, increased alk phos Increased risk for cholangiocarcinoma Walter Payton! |
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Spiral valves of Heister
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mucosal constrictions at the neck of the gallbladder that extend to the cystic duct.
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Rokitanski-Aschoff sinuses
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outpouchings of the GB mucosa into the muscularis, usually associated with inflammation and gallstones.
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Acute calculous cholecystitis ACC
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Most common reason for acute gallbladder surgery.
RUQ pain, mild fever, anorexia, tachycardia, n/v, jaundice |
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Complication of gallstones
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empyema, perforation, cholangitis, ostructive cholestasis, gallstone ileus, carcinoma
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Focal nodular hyperplasia of the liver
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spontaneous mass lesion, usually in young females. Typically there is a central gray white stellate scar, with normal intervening hepatocytes.
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Nodular regenerative hyperplasia of the liver
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Associated with portal htn, solid organ transplantation, vasculitis.
Affects entire liver with spherical nodules without fibrosis. |
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Cavernous hemangiomas
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most common benign neoplasm of the liver. red-blue soft nodules, less than 2cm, directly beneath capsule.
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Liver cell adenoma, hepatic adenoma
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Benign neoplasm from hepatocytes. Young women on OC, regress after stopping pill. Can rupture during pregnancy (lots of estrogen).
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Liver cell adenoma morphology
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Pale yellow bile stained nodules, can be very large, well demarcated but not often encapsulated. Sheets and cords of cells that look normal. Lots of glycogen - pale staining. Portal tracts absent, prominent arterial and venous supply charaacteristic.
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Hepatoblastoma
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young childhood tumor. Fatal within weeks without tx. can grow all sorts of tissues - ducts, acini, osteoid, cartilage, striated muscle.
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angiosarcoma of the liver
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resemble angiosarcomas elsewhere.
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4 main etiologic factors of HCC
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Chronic viral infection (HBV, HCV)
Chronic alcoholism NASH Food contaminants (aflatoxins) |
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Achalasia
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failure of esophagus to relax to pass food, or failure of peristalsis
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Zenker diverticulum
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most common esophageal diverculum. Above UES, mass in the neck, dysphagia, regurgitation, aspiration and pneumonia.
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Mallory Weiss syndrome
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Longitudinal tear in esophagus at GE jxn secondary to severe vomiting, usually in alcoholics.
caused by failure to relax lower sphincter before vomiting |
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Reflux esophagitis
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extremely common in US up to 40%
decreased LES tone |
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Morphology of reflux esophagitis
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erythema and erosions early
thickened gray white epithelium chronicaly, sometimes ulcers. Inflammatory cells in sqamous epithelium. Basal zone hyperplasia extent of change not well correlated to symptoms! |
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Eosinophilic esophagitis
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allergic esophagitis, associated with atopic disease, food allergies.
Vomiting, pain, dyspepsia. Eliminate food allergens, corticosteroids. |
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Barrett esophagus
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occurrence of specialized columnar epithelium lining a segment of the distal esophagus above the LES.
1. endoscopic evidence of columnar epithelium 2. histologic evidence of intestinal metaplasi - presence of goblet cells. Premalignant condition |
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esophageal adenocarcinoma
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about half of all esophagus cancers in the US
As many as 10% of BE patients will get adenocarcinoma. Insidious onset - gradual dysphagia. |
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Esophageal squamous cell carcinoma
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More common outside the US.
Alcohol, smoking, hot liquids risk factors. Insidious onset - gradual dysphagia. |
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Cushings ulcer
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gastric ulcer from increased intracranial pressure
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Curlings ulcer
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gastric ulcer from severe burn or trauma
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Zollinger Ellison syndrome
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Hypersecretion of gastrin due to gastrinoma, leading to hyperacidicity, PUD, gastric gland hyperplasia
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Menetrier disease
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hyperplasia of mucus cells, no increase in acid secretion
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Hypertrophy- hypersecretory gastropathy
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parietal and chief cell hyperplasia with acid hypersecretion. A pure form of parietal hyperplasia my occur with long term use of PPIs
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Gastric carcinoma
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Incidence declining in US.
95% of all gastric malignant tumors. Increased risk with h pylori, nitrates, low ses, smoking. |
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Gastric lymphoma
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associated with h pylori,
lots of translocations Usually CD5, CD10, CD23 neg |
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Gastrointestinal stromal tumors
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most commonly in stomach. Arise from interstitial cells of cajal.
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carcinoid
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similar to carcinoma but notas aggressive. arise from endocrine cells, in GI tract that release hormones.
May be a part of MEN I and Zollinger Ellison syndromes |
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autoimmune enteropathy
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mutation of FOXP3, Ab to enterocytes, goblet, parietal, islet cells.
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Abetalipoproteinemia
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autosomal recessive rare mutation of MTP leads to abscence of apolipoprotein B.
Vacuolization of SI epithelial cells. RBC's look like burrs, burr cells. |
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noravirus
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Viral cause of diarrhea, common on cruise ships, schools, hospitals.
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Rotavirus
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cause of diarrhea in your children worldwide. severe osmotic diarrhea
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Adenovirus
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2nd most common cause of pediatric diarrhea. Atrophy of SI villi and crypt hyperplasia.
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Shigellosis
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blood diarrhea, fecal oral route, common in developing countries
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Salmonellosis
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water or bloody diarrhea
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Campylobacter species
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bloody or watery diarrhea, children, travelers
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Whipple disease
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malabsorption due to tropheryma whippelii. infects small intestine
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entamoeba histolytica
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flask shaped ulcers in colon. can cause abscess, abdominal pain, bloody diarrhea
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Crohn's disease
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frequently ileum, cecum,
associated with other autoimmune disease, non caseating granulomas, cobblestone appearance(serpentine linear ulcers with intervening normal tissue), edema, loss of normal mucosa texture. "skip" lesions |
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Ulcerative colitis
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a disease of young usually female
primarily affects rectum. Ony mucosa and submucosa. |
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Peutz-Jeghers syndrome
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rare autosomal dominant syndrome - mean age 11, multiple GI hamartomatous polyps and mucocutaneous hyperpigmentation. Increased risk of several malignancies.
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Cowden syndrome
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autosomal dominant hamartomatous polyp syndrome. Loss of PTEN.
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Tubular adenomas
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pedunculated, branching round/tubular glands on a stalk.
Larger the polyp, greater the chance of carcinoma |
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Villous adenoma
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sessile, broad based, numerous fingerliek projections of epithelium. more than 40% harbor carcinoma
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Familial adenomatos polyposis
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autosomal dominant - patients with 500-2500 polyps
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Gardner syndrome
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autosomal dominant, similar to FAP except there are multiple skin and bone lesions
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Hereditary nonpolyposis colorectal cancer
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autosomal dominant
lower numbers of polyps but occur earlier than general pop often in right colon |
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solitary rectal ulcer syndrome
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rectal bleeding, mucus discharge, inglammatory lesion of the anterior rectal wall
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hyperplastic polyp vs peutz-heghers polyp
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hyperplastic - serrated profile of epithelial layer
peutz jeghers - smooth muscle into the superficial portion of the pedunculated polyp. |
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APC
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promotes cell migration and adhesion
regulates cell proliferation inactivated in >80% of colorectal carcinomas |
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Enzymes elevated in pancreatitis
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amylase and lipase - they are the only ones secreted in active, not zymogen, form
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Acute pancreatitis is:
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the result of inappropriate release of enzymes from acinar cells, causing proteolysis, lipolysis, hemorrhage
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Hereditary acute pancreatitis
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autosomal dominant, cationic trypsinogen, recurrent attacks of severe pancreatitis
trypsin is resistant to inactivation |
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Most common cause of chronic pancreatitis
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alcohol abuse, long term
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Pathogenesis of chronic pancreatitis
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Ductal obstruction by concretions - alcohol can cause proteins to aggregate, they can calcify and obstruct.
Toxic-metabolic - toxins including alcohol, can exert a toxic effect on acinar cells. Oxidative stress - alcohol induced oxidative stress may generate free radicals in the acinar cells, attract mononuclear cells, fusion of lysosomes and zymogen granules, necrosis, inflammaiton, fibrosis. Necrosis - fibrosis Acute pancreatitis initiates a sequence of perilobular fibrosis, altered pancreatic secretions. Over time, loss of parenchyma |
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Pancreatic pseudocyst
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no true lining, necrotis debris surrounded by granulation tissue, inflammation, and fibrosis.
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Pancreatic adenocarcinoma
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usually in the head of the pancreas. Can obstruct bile duct. usually unresectable.
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glucagonoma
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causes mild DM
skin rash anemia most frequent in post/perimenopausal women |
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somatostatinoma
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delta cell dumor
associated with DM, cholelithiasis, steatorrhea, hypochlohydria. |
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VIPoma
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water diarrhea, hypokelemia, achlorhydria
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solid pseudopappillary tumor
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distinctive pancreatic tumor in young women
may present with abdominal pain, solid and cystic by imaging, cured by resection |
