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exam3 guide Flashcards

1
Q

Childhood Polycystic Kidney Disease Etiology

A

Autosomal recessive

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2
Q

Childhood Polycystic Kidney Disease Characteristics

A

Enlarged bilateral kidneys that resemble sponges, non-fx at birth

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3
Q

Childhood Polycystic Kidney Disease Clinical Presentation

A

Quickly leads to renal failure shortly after birth

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4
Q

Childhood Polycystic Kidney Disease histo

A
  • Numerous small cysts in cortex and medulla all the way to calecis
  • Cyst appears to arise from epithelium of collecting duct
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5
Q

Adult Polycystic kidney Disease Etiology

A

Autosomal dominant affects 1 in 600 people

Manifests in 3rd or 4th decade with s/s of renal failure.

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6
Q

Adult Polycystic kidney Disease Characteristics

A

Multiple, expanding serous or purulent-filled cysts of both kidneys that destroy intervening parenchyma. Pressure from expansion can => hemorrhage, infx, HTN.
Kidneys can get up to size of liver, 4000 gms
Cysts derived from obstructed tubules but reason for obstruction is unknown

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7
Q

Adult Polycystic kidney Disease Clinical Presentation

A

Early sign: dull, aching pain in abd. or back (d/t pressure from expanding cysts). ESRD by age 50, tx with kidney transplant

  • Peritonitis, hemorrhage, infection
  • HTN – 75% of patients
  • Hematuria – d/t ruptured intracystic hemorrhage
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8
Q

Adult Polycystic kidney Disease histo

A
  • Enlarged kidneys composed solely of mass of cysts of varying sizes, with little intervening parenchyma
  • No demarcation of pelvis, calices

-Cyst appear to arise from any part of nephron and have atrophic lining

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9
Q

Adult Polycystic kidney Disease a/w

A
  • Saccular berry aneurysms – 10-30% of patients who have increased risk of rupture, esp. combined with HTN.
  • Also assoc w/ liver cysts
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10
Q

• Horseshoe kidney

A

Occurs 1 in 600 persons. fusion of kidney at midline. Usually no problem unless defect favors obstruction to renal flow. More susceptible to UTI due to flow of ureters.

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11
Q

• Renal cystic dysplasia –

A
  • MC of renal develop disorders. Abnormal differention of renal structures during embryonic period + cystic formation.
  • Usually unilaterally and histologically tube-like structures enclosed by mesenchyme, foci of cartilage, immature glomeruli and tubules. No association with malignancy. Kidney doesn’t function.
  • Can also cause Potter’s syndrome
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12
Q

Acute UTI Cause

A
  • Gram negative rods. E Coli.

- Antibx can be used, but infx usually subsides if patient is immunocompetent

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13
Q

Acute UTI Description

A

Acute pyelonephritis = foci of pus and focal abscesses. In severe cases, may permeate entire kidney and fill renal pelvis.

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14
Q

Acute UTI Clinical Presentation

A

Acute pyelonephritis: sudden, sharp pain in costovertebral angle along with chills, fever, malaise. Urinalysis: pyuria and bacteriuria, along with leukocytosis

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15
Q

Acute UTI Grossly (pyelo)

A

Acute pyelonephritis:
Round, yellow, raised abscesses present on renal surface surrounded by areas of congestion.
Lots of neutrophils, white pus pockets

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16
Q

Acute UTI grossly (cystitis)

A

Acute cystitis: hemorrhagic wall, lots of neutrophils

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17
Q

Acute UTI comp

A

Renal Papillary necrosis

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18
Q

Chronic UTI Cause

A

Chronic pyelonephritis: can evolve from acute pyelonephritis, esp. if recurrent. Also radiation, prior surgery, autoimmune

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19
Q

Chronic UTI Description

A

Chronic pyelonephritis: Recurrent infections superimposed on obstructive lesions => recurrent bouts of interstitial inflammation and scarring. Kidneys become small and irregularly scarred.

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20
Q

Chronic UTI Grossly

A

Chronic pyelonephritis: Hallmark = scarring involving pelvis or calyces, or both, => papillary blunting and calyceal deformities

  • May involve one or both kidneys.
  • Kidneys are small and irregularly scarred.
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21
Q

Chronic UTI Histology

A

Microscopically: interstitial fibrosis of mononuclear cell infiltration
-Dilation and contration of tubular lining epitelium with atrophy of cells. Dilated tubules contain pink, glassy coloid casts that look like thyroid tissue (thyroidization). Proliferative arteriosclerosis

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22
Q

Chronic UTI comp

A

Can be important cause of CRF, esp. if obstruction is underlying cause

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23
Q

General features of stones

A

● Most stones found in renal pelvis or urinary bladder

● Stones may resemble crystals, or be small, round, or irregular masses

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24
Q

• Typical symptoms of stones

A

● Hematuria, urinary colic (spasmotic pain caused by contraction of obstructed ureter). Painful, lower back pain radiating towards groin

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25
Tx stones
-prompt treatment important, obstruction increases risk of infection, stone formation, and permanent renal atrophy ● Smaller stones may be voided. Large stones require surgery or mechanical extraction after stones have been broken down by lithotripsy
26
mc Stone
Composition: calcium oxalate (US) or phosphate (England) | Accounts for 75% of all stones
27
Calcium (MC)
Associated with hyperexcretion of calcium in patients who have abnormal calcium metabolism (hyperparathyroidism, diffuse bone disease, other hypercalcemic states)
28
Struvite Aka triple ammonia or ammonia stones or staghorn calculi
- Typically complication of UTI, which lead to formation of ammonia from urea in the urine. - Infections with urea-splitting bacteria (e.g. proteus) converts urea to ammonia. - Form some of the largest stones, can fill entire pelvis assoc. with infx
29
Uric Acid
50% of patients have gout. Others have diseases involving rapid cell turnover, like leukemia Stones are usually radiolucent (not easily detected)
30
RENAL CELL CARINCOMA Epidemiology
- Median age: 55 years; - Men>women - Risk factors unknown, link to cigarette smoking
31
RENAL CELL CARINCOMA Grossly
Nodules or masses sharply demarcated from renal parenchyma Arise from either upper or lower poles Cross section: yellow, bosselated, encapsulated tumors that can extend through renal capsules into perirenal fat, adrenal, renal vein
32
RENAL CELL CARINCOMA HIstology
Cuboidal cells reminiscent of renal tubules. Clear or granular cytoplasm filled with glycogen and lipids (adenocarcinoma)
33
RENAL CELL CARINCOMA Clinical
MC presentation is hematuria. Classic triad: dull flank pain, palpable abd. mass, hematuria. Some may have non-specific symptoms like weight loss, long-standing fever, HTN. May have distant mets to lungs and bones
34
RENAL CELL CARINCOMA dx and tx
-50% diagnosed accidentally on CT scan - Surgically 5 year survival 35%
35
TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS Epidemiology
Papillary neoplasms of renal pelvis, resemble carcinomas of urinary bladder Low to high grade lesions
36
TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS Clinical
Hematuria or urinary obstruction early in course
37
TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS tx:
Surgical removal = good results for grade 1 or 2 lesions. 5 year survival 70%
38
WILMS TUMOR Epidemiology
#1 pediatric malignancy (1 in 10,000) Present at time of birth, manifests between 2nd and 4th years of life Highly malignant
39
WILMS TUMOR Grossly
Solitary or multinodular abd. mass that replaces kidney – usu palpable
40
WILMS TUMOR histo
composed of blastic or immature cells
41
WILMS TUMOR tx
Good prognosis with surgery and chemo – 85% cures
42
urinary bladder carcinoma Epidemiology
MC urinary tract neoplasms 52,000 new cases each year, with 10,000 deaths. 2x as common as renal cell carcinoma but same number of deaths Peak incidence in men 60-80 years old
43
urinary bladder carcinoma Etiology
● Transitional cell carcinomas (90%) | -other types as well but not common
44
urinary bladder carcinoma Risk Factors
Unknown. Cigarette smoking – most important factor (proportioned to total number smoked) - Also linked to industrial carcinogens: Azo dyes and chemicals used in rubber industry, textile printing - In Egypt, Schistosoma haemotabium infx can lead to cancer of urinary bladder
45
urinary bladder carcinoma Grossly
Tumors are either papillary or flat; invasive or non-invasive by histologic examination Progression leads to extension of tumor into muscle layers of bladder and adjacent pelvic organs Mets in pelvic lymph nodes, later stages tumor may met to distant sites
46
urinary bladder carcinoma Clinical
Hematuria, dysuria, lower abd. pain
47
urinary bladder carcinoma dx
Cystoscopy and histologic biopsy
48
urinary bladder carcinoma tx
Surgical resection and chemo Prognosis based on histological grade and type, clinical staging. Stage A Grade I tumor = 98% 5-year survival. Stage D (distant mets) have 15% 5-year survival
49
Nephrotic S/SxS
``` ● Heavy proteinuria (3-3.5 g/pro/day) ● Hypoalbuminemia ● Edema ● Hyperlipidemia ● Lipiduria ```
50
Nephrotic Pathology
Permeability defect in glomerular capillaries allows protein to be lost from plasma into urine => hypoproteinemia => edema => decreased plasma volume =. RAS activation => worsening edema Decreased plasma proteins => increased production of proteins by liver (inc. liproproteins)
51
Nephrotic Etiology
● Minimal Change Disease (nils Disease) responsible for 70% of Nephrotic Syndrome in children, only 20% of adults ● Systemic diseases that involve kidney (DM, amyloidosis, SLE) responsible for 20-30% in adults, rarely in children. #1 cause in adults membranous glomerulonephritis ● Also associated with infx, malignancies, drugs (heroin)
52
Nephrotic and nephritic dx
Renal biopsy is only definitive diagnosis
53
Nephritic S/SxS
``` Hematuria variable degrees of proteinuria, decreased GFR Elevated BUN/SCr Oliguria Fluid retention HTN Mild edema RBC casts in urine ```
54
Nephritic Pathology
Mild proteinuria and hematuria d/t injury of glomerular capillaries Manifestations can develop rapidly, progress rapidly, and persist for years (continuous or intermittent) and progress slowly to CRF
55
Nephritic Etiology
Diseases that cause this syndrome characterized by inflammatory changes in glomeruli with leukocytes and necrosis. ● #1 cause: Acute post-infectious glomerulonephritis
56
CL = capillary lumen
- DM = tufts in glomerulus (glomerulosclerosis or Kimmelstiel-Wilson Disease) - Nephrotic syndrome = permeability defect - Nephritic syndrome = injury of glomerular capillaries - Chronic glomerulonephritis = thick walled arteries with narrowed lumina
57
FP = food processes
Minimal Change Disease = fusion of epithelial foot processes
58
acute post strept GMN Epidemiology
Typically affects children 6-10, but can affect adults (can be pretty bad in adults) Uncommon d/t antibiotics, but in undeveloped areas
59
acute post strept GMN Pathology
- Immune-mediated inflammatory glomerulopathy that occurs 1-2 weeks after strep throat OR strep skin infection with GABHS. - Inflammatory mediators attract neutrophils and monocytes, stimulate proliferation of mesangial and endothelial cells => marked hypercellularity of glomerulus (big honkin’ glomeruli) - Deposition of antigen and antibody (immune complex) in glomerular basement membrane. Immune complex trapped in GBM, activate complement and inflammatory cells (esp. neutrophils) into glomeruli.
60
acute post strept GMN S/S
90% of people will have low complement d/t consumption in glomeruli
61
acute post strept GMN HIstology On EM
On EM subepithelial dense deposits shaped like humps on epithelial side of basement membrane
62
acute post strept GMN On IF
On IF microscopy, granular deposits (lumpy bumpy) seen are both IgG and complement along basement membrane
63
acute post strept GMN tx
95% of children recover, only 1-2% progress to rapidly progressive GMN
64
membranous GMN Etiology
Immune-mediated glomerulopathy | Cause unknown in 85% of cases
65
membranous GMN Clinical
No inflammatory cells in glomeruli and urine devoid of RBCs (like in APS-GMN) Causes nephrotic syndrome (unlike APS-GMN)
66
membranous GMN Histologically
Light microscopy: glomeruli have thickened BM but are normocellular EM: thickening of BM attributed to deposition of dense immune complexes IF: granularity of deposits of IgG
67
membranous GMN Prognosis
``` Prognosis better in children After 20 years: 25% have spontaneous remission 50% have persistent proteinuria with stable renal fx 25% have ESRD ```
68
membranous GMN Tx
Corticosteroids for those with progressive renal failure
69
Goodpasture’s Syndrome
* Autoimmune with formation of antibodies to body’s basement membrane components, collagen type 4 * Injury to lungs causes intraalveolar hemorrhage. Antibodies cause rupture of BM, causing macrophages to exit through holes of BM to accumulate in urinary space, forming crescents that compress capillary loops. Can lead to RPGN * Involves lungs and kidneys * Decreased blood flow through compressed capillary loops => glomerular filtration ceases => anuria * Most patients don’t recover, need dialysis or transplantation to survive
70
Lumpy bumpy IF
Acute Post-Streptococcal GMN
71
Linear IF
Goodpasture’s Syndrome
72
Prolactinoma (MC) General
(typically) Microadenomas composed of prolactin-secreting cells
73
Prolactinoma (MC) S/S
- Women of reproductive age: amenorrhea, galactorrhea, infertility (Inhibits pulsatile secretion of LH needed for normal ovulation) - Males: vague, may include. impotence or decreased libido
74
Prolactinoma (MC) Tx
Function can be inhibited with bromocriptine (inhibits prolactin secretion) Transnasal surgery to sella tursica for larger tumors
75
Somatotrophic Adenoma general
Macroadenoma composed of growth hormone (75% visible with naked eye or CT scan).
76
Somatotrophic Adenoma s/s
Prepubertal patients: stimulate longitudinal skeletal growth => gigantism Postpubertal: acromegaly => enlargement of acral parts of extremities, tongue, jaw (prognathism), nose. Internal organs also enlarged (heart, spleen, liver). Metabolic disturbance:, hyperglycemia hypercalcemia.
77
Somatotrophic Adenoma Tx
Surgical removal
78
Corticotrophic Adenoma general
Typically microadenoma. Composed of ACTH-secreting cells.
79
Corticotrophic Adenoma s/s
Typical s/s of Cushings disease, fatigue, weakness, mental instability
80
Corticotrophic Adenoma tx
Removal of tumor
81
Craniopharyngiomas
* Benign tumor that arises from pituitary * Easily removed * Does not produce hormones, but can get big enough to cause hypofunction of pituitary
82
Graves Disease | Hyperthyroidism Etiology
Autoimmune disease | Occurs 10x more often in women than men.
83
Graves Disease Hyperthyroidism Patho
Antibodies bind to surface of thyroid follicular cells, cause stimulus similar to TSH. Causes hypersecretion of T3 and T4
84
Graves Disease | Hyperthyroidism Charc
Enlarged thyroid, composed of hyperplastic follicles lined with hyperactive, tall, cuboidal cells Thyroid contains lymphoid follicles (signs of autoimmune disease)
85
Graves Disease | Hyperthyroidism dx
Microscopic material | High T3 and T4 / Low TSH
86
Graves Disease Hyperthyroidism tx
Antithyroid drugs; if ineffective, subtotal thyroidectomy
87
Hashimoto’s Thyroiditis | Hypothyroidism Etiology
Autoimmune – IgG antibodies cuase destruction of gland | More common in women, typically 45-65
88
Hashimoto’s Thyroiditis | Hypothyroidism Patho
Graduaal failure d/t immune destruction of gland | Increased risk for B-cell lymphomas
89
Hashimoto’s Thyroiditis | Hypothyroidism Charc
Painless, diffuse enlargement of thyroid extensive infiltration of follicles and stroma with mononuclear infiltration (lymphocytes and plasma cells), which destroy thyroid follicles and germinal centers. This may lead to healing and fibrosis and reduce size of thyroid
90
Hashimoto’s Thyroiditis | Hypothyroidism dx
Low T3 and T4 / High TSH
91
Hashimoto’s Thyroiditis | Hypothyroidism tx
Synthetic thyroid hormones. Good results. Must take for rest of lives
92
Know the four types of thyroid tumors in general
* Benign tumors are more common * Only 3-4 cases of thyroid cancer are diagnosed per 100,000 people, less than 1000 people die each year * No risk factors are known, more common in females
93
Thyroid Adenoma Etiology
MC benign tumor | Composed of thyroid follicles
94
Thyroid Adenoma Presentation
Small, well-encapsulated with fibrous tissue.
95
Thyroid Adenoma Dx/Tx
Biopsy | Not premalignant, no tx if small nodules
96
Know general features of diabetes insipidis
* Compression of pituitary stalk by tumor * Hypo release of ADH * Excess release of low osmolarity urine * Major symptoms: polyuria, noctura, polydipsia

Patho 3 Shea (19 decks)

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