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Patho 3 Shea > exam3 guide > Flashcards

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
Q

Tx stones

A

-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

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26
Q

mc Stone

A

Composition: calcium oxalate (US) or phosphate (England)

Accounts for 75% of all stones

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27
Q

Calcium (MC)

A

Associated with hyperexcretion of calcium in patients who have abnormal calcium metabolism (hyperparathyroidism, diffuse bone disease, other hypercalcemic states)

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28
Q

Struvite Aka triple ammonia or ammonia stones or staghorn calculi

A
  • 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
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29
Q

Uric Acid

A

50% of patients have gout. Others have diseases involving rapid cell turnover, like leukemia
Stones are usually radiolucent (not easily detected)

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30
Q

RENAL CELL CARINCOMA Epidemiology

A
  • Median age: 55 years;
  • Men>women
  • Risk factors unknown, link to cigarette smoking
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31
Q

RENAL CELL CARINCOMA Grossly

A

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

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32
Q

RENAL CELL CARINCOMA HIstology

A

Cuboidal cells reminiscent of renal tubules. Clear or granular cytoplasm filled with glycogen and lipids (adenocarcinoma)

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33
Q

RENAL CELL CARINCOMA Clinical

A

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

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34
Q

RENAL CELL CARINCOMA dx and tx

A

-50% diagnosed accidentally on CT scan
- Surgically
5 year survival 35%

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35
Q

TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS Epidemiology

A

Papillary neoplasms of renal pelvis, resemble carcinomas of urinary bladder
Low to high grade lesions

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36
Q

TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS Clinical

A

Hematuria or urinary obstruction early in course

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37
Q

TRANSITIONAL CELL CARCINOMA OF RENAL PELVIS tx:

A

Surgical removal = good results for grade 1 or 2 lesions. 5 year survival 70%

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38
Q

WILMS TUMOR Epidemiology

A

1 pediatric malignancy (1 in 10,000)

Present at time of birth, manifests between 2nd and 4th years of life
Highly malignant

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39
Q

WILMS TUMOR Grossly

A

Solitary or multinodular abd. mass that replaces kidney – usu palpable

40
Q

WILMS TUMOR histo

A

composed of blastic or immature cells

41
Q

WILMS TUMOR tx

A

Good prognosis with surgery and chemo – 85% cures

42
Q

urinary bladder carcinoma Epidemiology

A

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
Q

urinary bladder carcinoma Etiology

A

● Transitional cell carcinomas (90%)

-other types as well but not common

44
Q

urinary bladder carcinoma Risk Factors

A

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
Q

urinary bladder carcinoma Grossly

A

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
Q

urinary bladder carcinoma Clinical

A

Hematuria, dysuria, lower abd. pain

47
Q

urinary bladder carcinoma dx

A

Cystoscopy and histologic biopsy

48
Q

urinary bladder carcinoma tx

A

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
Q

Nephrotic S/SxS

A 
●	Heavy proteinuria (3-3.5 g/pro/day)
●	Hypoalbuminemia
●	Edema
●	Hyperlipidemia
●	Lipiduria
50
Q

Nephrotic Pathology

A

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
Q

Nephrotic Etiology

A

● 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
Q

Nephrotic and nephritic dx

A

Renal biopsy is only definitive diagnosis

53
Q

Nephritic S/SxS

A 
Hematuria
variable degrees of proteinuria, decreased GFR
Elevated BUN/SCr
Oliguria
Fluid retention
HTN
Mild edema
RBC casts in urine
54
Q

Nephritic Pathology

A

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
Q

Nephritic Etiology

A

Diseases that cause this syndrome characterized by inflammatory changes in glomeruli with leukocytes and necrosis.
● #1 cause: Acute post-infectious glomerulonephritis

56
Q

CL = capillary lumen

A
  • 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
Q

FP = food processes

A

Minimal Change Disease = fusion of epithelial foot processes

58
Q

acute post strept GMN Epidemiology

A

Typically affects children 6-10, but can affect adults (can be pretty bad in adults)
Uncommon d/t antibiotics, but in undeveloped areas

59
Q

acute post strept GMN Pathology

A
  • 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
Q

acute post strept GMN S/S

A

90% of people will have low complement d/t consumption in glomeruli

61
Q

acute post strept GMN HIstology On EM

A

On EM subepithelial dense deposits shaped like humps on epithelial side of basement membrane

62
Q

acute post strept GMN On IF

A

On IF microscopy, granular deposits (lumpy bumpy) seen are both IgG and complement along basement membrane

63
Q

acute post strept GMN tx

A

95% of children recover, only 1-2% progress to rapidly progressive GMN

64
Q

membranous GMN Etiology

A

Immune-mediated glomerulopathy

Cause unknown in 85% of cases

65
Q

membranous GMN Clinical

A

No inflammatory cells in glomeruli and urine devoid of RBCs (like in APS-GMN)
Causes nephrotic syndrome (unlike APS-GMN)

66
Q

membranous GMN Histologically

A

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
Q

membranous GMN Prognosis

A 
Prognosis better in children
After 20 years:
25% have spontaneous remission
50% have persistent proteinuria with stable renal fx
25% have ESRD
68
Q

membranous GMN Tx

A

Corticosteroids for those with progressive renal failure

69
Q

Goodpasture’s Syndrome

A
  • 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
Q

Lumpy bumpy IF

A

Acute Post-Streptococcal GMN

71
Q

Linear IF

A

Goodpasture’s Syndrome

72
Q

Prolactinoma (MC) General

A

(typically) Microadenomas composed of prolactin-secreting cells

73
Q

Prolactinoma (MC) S/S

A
  • 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
Q

Prolactinoma (MC) Tx

A

Function can be inhibited with bromocriptine (inhibits prolactin secretion)
Transnasal surgery to sella tursica for larger tumors

75
Q

Somatotrophic Adenoma general

A

Macroadenoma composed of growth hormone (75% visible with naked eye or CT scan).

76
Q

Somatotrophic Adenoma s/s

A

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
Q

Somatotrophic Adenoma Tx

A

Surgical removal

78
Q

Corticotrophic Adenoma general

A

Typically microadenoma. Composed of ACTH-secreting cells.

79
Q

Corticotrophic Adenoma s/s

A

Typical s/s of Cushings disease, fatigue, weakness, mental instability

80
Q

Corticotrophic Adenoma tx

A

Removal of tumor

81
Q

Craniopharyngiomas

A
  • Benign tumor that arises from pituitary
  • Easily removed
  • Does not produce hormones, but can get big enough to cause hypofunction of pituitary
82
Q

Graves Disease

Hyperthyroidism Etiology

A

Autoimmune disease

Occurs 10x more often in women than men.

83
Q

Graves Disease
Hyperthyroidism
Patho

A

Antibodies bind to surface of thyroid follicular cells, cause stimulus similar to TSH.
Causes hypersecretion of T3 and T4

84
Q

Graves Disease

Hyperthyroidism Charc

A

Enlarged thyroid, composed of hyperplastic follicles lined with hyperactive, tall, cuboidal cells
Thyroid contains lymphoid follicles (signs of autoimmune disease)

85
Q

Graves Disease

Hyperthyroidism dx

A

Microscopic material

High T3 and T4 / Low TSH

86
Q

Graves Disease
Hyperthyroidism
tx

A

Antithyroid drugs; if ineffective, subtotal thyroidectomy

87
Q

Hashimoto’s Thyroiditis

Hypothyroidism Etiology

A

Autoimmune – IgG antibodies cuase destruction of gland

More common in women, typically 45-65

88
Q

Hashimoto’s Thyroiditis

Hypothyroidism Patho

A

Graduaal failure d/t immune destruction of gland

Increased risk for B-cell lymphomas

89
Q

Hashimoto’s Thyroiditis

Hypothyroidism Charc

A

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
Q

Hashimoto’s Thyroiditis

Hypothyroidism dx

A

Low T3 and T4 / High TSH

91
Q

Hashimoto’s Thyroiditis

Hypothyroidism tx

A

Synthetic thyroid hormones. Good results. Must take for rest of lives

92
Q

Know the four types of thyroid tumors in general

A
  • 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
Q

Thyroid Adenoma Etiology

A

MC benign tumor

Composed of thyroid follicles

94
Q

Thyroid Adenoma Presentation

A

Small, well-encapsulated with fibrous tissue.

95
Q

Thyroid Adenoma Dx/Tx

A

Biopsy

Not premalignant, no tx if small nodules

96
Q

Know general features of diabetes insipidis

A
  • 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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