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Pathology Sp 16 > Exam 2: Diseases 2 > Flashcards

Exam 2: Diseases 2 Flashcards

1
Q

What is anemia?

What does anemia cause?

A

anemia: Dec red cell mass (RBC and hemoglobin)

anemia causes SOB, weakness, fatigue, pallor

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2
Q

What is intravascular hemolysis?

what is extravascular hemolysis?

A

Intravascular: destruction of RBCs within circulation
extravascular: destruction of RBCs within reticuloendothelial system: tissue macrophages of spleen and liver

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3
Q

What does extravascular hemolysis lead to

A

DEC haptoglobin, Hyperbilirubinemia and reticulocytosis

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4
Q

Hereditary spherocytosis is what kind of hemolysis defect? what is hereditary spherocytosis and what helps relieve the anemia caused by it?

A

Hereditary spherocytosis is a INTRINSIC membrane defect. an abnormality of spectrin leading to less deformable RBCs that can squeeze thru splenic sinusoids so they are sequestered and destroyed in the spleen. a splenectomy helps relieve the problems but RBCs remain abnormal shaped

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5
Q

what is a intrinsic defect that is autosomal codominant inheritance? what does it protect from when in a heterozygous state

A

Sickle Cell anemia

heterozygous state protective against malaria

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6
Q

what are two leading causes of ischemia related death for sickle cell anemia pts

A

Acute chest syndrome and stroke

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7
Q

what is a point mutation gene deletion, that is a defect in the synthesis of alpha or beta global chains leading to dec global production and ineffective EPO in bone marrow?

A

Thalassemia

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8
Q

Describe the anemia associated with Thalassemia.

what are the target cells of thalassemia? what people is Thalassemia common in?

A

Thalassemia - microcytic, hypochromic anemia that has target cells of basophilic stippling
Common is Mediterranean, African and Southeast Asian decent

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9
Q

what two diseases are protective against malaria

A

sickle cell: heterozygous state

Thalassemia

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10
Q

what does Thalassemia lead to that may show up in the mouth

A

skeletal deformities

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11
Q

What is a X linked inheritance that causes RBCs susceptible to oxidant injury, where oxidized Hb denatures and attaches to RBC membrane

A

Glucose 6 Phosphate Dehydrogenase Deficiency

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12
Q

What is a clinical hallmark of Glucose 6 Phosphate Dehydrogenase deficiency?
Intravascular or Extravascular hemolysis

A

G6P Dehydrogenase deficiency = BITE cells

Extravascular hemolysis in spleen

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13
Q

What is an Extrinsic defect autoimmune: occurs in uteri, that is blood group incompatibility

A

Hemolytic disease of newborn

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14
Q

What is the hallmark of autoimmune hemolytic anemia

A

Spherocytes

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15
Q

What indicates hemolysis due to mechanical trauma

A

Schistocytes (RBC fragments)

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16
Q

What is the most common basis of anemia worldwide

A

Iron Deficiency

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17
Q

What are the lab results of iron deficiency anemia

A

Microcytic (Low MCV RBCs), hypochromic, DEC serum ferritin, DEC serum iron
Absent reticulocyte response
INC serum Fe binding capacity

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18
Q

what is caused by autoABs to parietal cells and IF, what is this associated w

A

Pernicious anemia

Associated w loss of gastric parietal cells, achlorhydria and deficient IF

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19
Q

what is a disease where bone marrow is replaced by tumor or fibrosis and you see teardrops RBCs as well as DEC in platelets

A

Myelophthisic Anemia

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20
Q

What is an INC in RBC mass

A

Polycythemia

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21
Q

what does relative polycythemia cause

A

dehydration and diarrhea

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22
Q

what does absolute polycythemia cause
Primary?
Secondary?

A

Primary: neoplastic proliferation of RBCs
SecondaryL INC EPO production caused by cyanotic heart disease pulmonary disease, living at high altitudes EPO producing tumors

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23
Q

what is taken up by bones and developing teeth- competing with Ca and interfering w remodeling process produces ? lines on x ray?

A

Lead

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24
Q

what does Lead do in the mouth

A

Pb= gingival hyperpigmentation = lead line of soft tissue

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25
Q

what kind of anemia develops bc of Lead?

What is a hallmark sign of lead poisoning?

A

Lead= microcytic and Hypochromic anemia

Lead poisoning = wrist drop and footdrop

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26
Q

what is the CDC threshold level for concern for Lead?

when is chelation therapy started?

A

5 micrograms or more

chelation therapy= 45 or greater micrograms

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27
Q

what does lead do to the Gi tract? kidnys

A

Lead causes colicky pain, severe not localized in GI tract

Lead causes damage to tubules, fibrosis, renal failure in kidney

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28
Q

use of ecstasy is associated with what?

A

E (ecstasy)= bruxism

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29
Q

what is common when 20% or more of body is burned

A

Massive fluid shifts= hypovolemia
infections: Pseudomonas and Candida
electrolyte and nutrition lost

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30
Q

Hypothermia causes what

A

bradycardia, atrial fibrillation and loss of consciousness
at cellular level= crystalization of water
vasoconstriction, edema, long term causes atrophy and fibrosis

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31
Q

what does acute radiation syndrome include describe each phases time frame and symptoms

A

hematopoietic (2-10 sv, Dec WBC hair loss, infections, sepsis, bleeding and death in 2-6 weeks
GI: 10-20 sV = vomitting, bloody diarrhea, shock, sepsis, death in 5-14 days
Cerebral: 50 sV, listlessness, drowsiness, seizures, coma, death in 1-4 hours

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32
Q

2 disorders of Protein energy malnutrition describe each

A

Marasmus= deficiency in calorie intake, use proteins fro energy depletes somatic protein compartment, extremities appear emaciated, head is large
Kwashiorkor: deficient in proteins, found in Africa and SE asia, depletes visceral protein compartment, weight is between 60-80% of normal but misleading bc of edema

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33
Q

2 functional protein compartments

when weight falls to below 60 %of normal child has what?

A

somatic= skeletal m, marasmus
visceral: liver= kwashiorkor
weight below 60% of normal= marasmus

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34
Q

what disease causes skin changes of alternating zones of hyper and hypo pigmentation w desquamation and causes an enlarged fatty liver

A

Kwashiorkor

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35
Q

what causes elevated BUN and creatinine levels due to DEC GFR

A

azotemia

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36
Q

what is azotemia plus other symptoms like gastroenteritis, peripheral neuropathy, dermatitis, acidosis, pericarditis, hyperkalemia

A

uremia

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37
Q

what is a major clinical renal syndrome that causes proteinuria (mild/ moderate), hematuria, hypertension

A

acute nephritic syndrome

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38
Q

what causes severe proteinuria (over 3.5 grams per day), low serum albumin, anasarca, high serum lipid, lipiduria

A

Nephrotic syndrome

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39
Q

What are two congenital cystic renal diseases

A 
autosomal dominant (adult) polycystic kidney disease 
autosomal recessive (childhood) polycystic kidney disease
40
Q

what causes autosomal dominant (adult) polycystic disease

A

mutation in PKD 1 gene in chromosome 16, that causes a defective protein called polycystic 1

41
Q

what does autosomal dominant (adult) polycystic kidney disease cause in a pt? incidence of disorder

A

causes UT hemorrhage, pain, gradual onset of renal failure in affected adult
affects 1: 500to 1000 persons

42
Q

What is the significant pathology result of Autosomal Dominant Polycystic kidney disease?

A

Saccular (berry) aneurysms affecting circle of Willis

43
Q

What is the gross pathology of Autosomal dominant Adult polycystic kidney disease?
Clinical symptoms of it?

A

Pathology: large kidneys w numerous cysts at all levels of nephron
Clinical signs: flank pain around 4th decade, hematuria, hypertension and UTI, renal failure

44
Q

what is the sudden onset of azotemia with oliguria/ anuria called?

A

acute renal failure

45
Q

What gene mutation causes Autosomal Recessive Childhood polycystic kidney disease?
affected protein?
Incidence?

A

Childhood Polycystic disease = recessive = mutation of PKHD1 gene!!
Affected protein = fibrocystin
occurs 1:20,000 live births

46
Q

describe what happens with autosomal recessive (childhood) polycystic kidney disease. What is the time frame for this

A

Numerous uniform sized cysts arise from collecting tubules causing fibrosis and renal failure shortly after birth to several years of age

47
Q

What are the 3 mechanisms of Glomerular disease

A
  1. Immune complex deposits in GBM or mesangium
  2. anti GBM AB
  3. epithelial and endothelial cell injury
48
Q

What is a glomerular disease thats most obvious clinical sign is severe edema, also causes heavy proteinuria, hypoalbuminemia, hyperlipidemia, and lipiduria

A

Nephrotic syndrome: most obvious clinical sign is severe edema!

49
Q

nephrotic syndrome is caused by an INC in glomerular capillary permeability to plasma proteins, what 4 things cause nephrotic syndrome

A

minimal change disease, focal segmental glomerusclerosis, membranous nephropathy, and Nodular glomerularsclerosis (aka diabetes)

50
Q

What is the most common cause of nephrotic syndrome in children, 2/3 of all cases?
what is the tx for this?

A

Minimal change disease treated by corticosteroids

51
Q

Minimal Change disease has what pathology for the LM? IF? EM?

A

LM: normal appearing glomeruli
IF: no immune complex deposits
EM: foot process effacement

52
Q

what is a common cause of adult nephrotic syndrome that has poor response to corticosteroid tx? what may this disease be?

A

Focal segmental Glomerulosclerosis may be primary or secondary to other glomerular diseases w some cases being familial

53
Q

Pathology of focal segmental glomerulosclerosis for LM? IF? and EM

A

LM: focal and segmental sclerosis w obliteration of capillary loops
IF and EM: no immune complex deposits in primary forms

54
Q

What cause of nephrotic syndrome may be primary or secondary to infection, malignancy, SLE, or drugs and has a poor response to corticosteroid tx? who is this disorder most common in

A

Membranous Nephropathy

most common in adults, may affect children

55
Q

what is the pathology of membranous nephropathy of LM? IF? EM?

A

LM: normal
IF: immune complex deposits
EM: deposits in sub epithelial side of GBM

56
Q

What is second to MI as cause of death from diabetes?

A

renal failure

57
Q

What are the clinical changes seen with diabetes?

A

hyaline arteriosclerosis
atherosclerosis
nephrosclerosis

58
Q

What is characterized by acute onset of hematuria, oliguria and azotemia and hypertension

A

nephritic syndrome

59
Q

what is the result of proliferation of cells within glomeruli accompanied by inflammatory cells severely injuring capillaries walls in nephritic syndrome

A

nephritic syndrome results in blood passing into urine as well as reduced GFR

60
Q

what are the two causes of nephritic syndrome

A

acute post infectious glomerulonephritis by Poststreptococcal
and IgA nephropathy

61
Q

what is most common in children and usually follows streptococcal pharyngitis? (1-4 weeks)

A

acute post infectious glomerulonephritis

62
Q

what affects children and young adults resulting in hematuria 1-2 days post URT infection?

A

IgA nephropathy

63
Q

when renal disease is associated with IgA nephropathy what happens? whats a hallmark of this disorder?

A

Hallmark: Henoch Schonlein Purpura

IgA nephropathy results in purpuric skin rash, GI pain, arthritis

64
Q

What is a clinical syndrome, not a specific form of glomerulonephritis that is a progressive loss of renal functions that results in death from renal failure in weeks to months untreated

A

Rapidly Progressive Glomerulonephritis

65
Q

What is a characteristic finding of Rapidly progressive glomerulonephritis

A

Crescentic glomerulonephritis due to proliferation of epithelial cells with infiltration of histiocytes

66
Q

What happens when untreated glomerular disease leads to loss of glomeruli and tubules with fibrosis leading to the original renal disease not being able to be identified

A

chronic end stage renal disease

67
Q

how can chronic end stage renal disease be detected? what is necessary for pt survival?

A

proteinuria, hypertension or azotemia at a routine exam

renal dialysis and kidney transplant are necessary for pt survival

68
Q

what is the suppurative inflammation of kidney and renal pelvis caused by a bacterial infection called? what does it involve

A

acute pyelonephritis involves tubules, interstitial, and renal pelvis

69
Q

how does a acute pyelonephritis infection spread? what cell is most prominent in the tubules of this disease

A

acute pyelonephritis infection spreads from bladder (Most commonly UTI) to the kidney through the blood
neutrophils infiltrate the tubules (neutrophil casts)

70
Q

what are the predisposing conditions to acute pyelonephritis?

A

UT obstruction, instrumentation, ureteral reflux, pregnancy, female gender, immunosupression, diabetes

71
Q

what drugs may cause drug induced interstitial nephritis

A

ABs, NSAIDS, diuretics

72
Q

What is the clinical aspect of drug induced interstitial nephritis? what cell is common from this disorder? what is missing from this disorder?

A

rapid onset (2-40 days) of fever, eosinophilia, renal dysfunction w hematuria, but little to no proteinuria

73
Q

how do you treat drug induced interstitial nephritis? what is the prognosis and recovery time?

A

withdrawal of offending drug and with corticosteroids

prognosis is good w recovery in 6-8 weeks

74
Q

what disorder has interstitial mononuclear cell infiltration and edema w many eosinophils, w non necrotizing granulomas

A

drug induced interstitial nephritis

75
Q

what is a condition where renal function declines rapidly w evidence of tubular epithelial damage/ necrosis causing DEC GFR, oliguria, and electrolyte abnormalities

A

Acute Tubular necrosis

76
Q

what are the causes of acute tubular necrosis?

Path findings of acute tubular necrosis?

A

acute tubular necrosis is caused by severe trauma, ischemia, septicemia, toxins
path findings: dilation of tubules. edema. necrosis of tubular epithelium

77
Q

Treatment of acute tubular necrosis?

Prognosis?

A

Tx of acute tubular necrosis is supportive care and dialysis

prognosis: in absence of preexisting conditions good

78
Q

what is the thickening and sclerosis of renal arteries associated with benign hypertension called?

A

Arterionephrosclerosis

79
Q

what is the genetics of Arterionephrosclerosis

A

Apolilipoprotein L1 gene,

Affects african americans same linkages as in FSGS

80
Q

what is the pathology of Arterionephrosclerosis

A

small kidneys granular surface, hyaline arteriosclerosis. fibroelastic hyperplasia, tubular atrophy, global sclerosis of glomeruli

81
Q

What may Arterionephrosclerosis also be seen with? this can lead to what symptoms?

A

Arterionephrosclerosis can be seen w Malignant hypertension also!
causes INC cranial pressure (headache, nausea, visual impairment), proteinuria, ischemia leading to acute kidney injury

82
Q

What is the pathology of Arterionnephrosclerosis caused by malignant hypertension

A

Hyperplastic arteriolosclerosis

83
Q

whats an acquired defect in metalloproteinases that degrades vWD or an inherited ADAMTS 13 deficit?

A

thrombotic thrombocytopenia purpura (TTP)

84
Q

what is caused by an endothelial cell injury from Shiga Toxin E coli, and is a major cause of acute kidney injury in children?

A

Hemolytic Uremic Syndrome (HUS)

85
Q

What are TTP and HUS both related to?

A

TTP and HUS both lead to activation, aggregation, and consumption of platelets

86
Q

Whats the pathology of TTP and HUS?
specific site for TTP?
specific site for HUS?

A

TTP/ HUS = widespread microthrombi in capillaries w RBC damage (schistocytes)
TTP: primarily in kidney
HUS: more widespread organ including CNS involvement

87
Q

what clinical signs can urolithiasis (kidney stones) cause?

kinds of kidney stones?

A

maybe asymptomatic, obstruction, intense pain, infection, hematuria
Calcium, Magnesium ammonium phosphate (staph infection), or uric acid (gout)

88
Q

what is the dilation of renal pelvis/ calyces with parenchymal atrophy secondary to obstruction called

A

hydronephrosis

89
Q

risk factors for hydronephrosis

A

renal stones, congenital UT obstruction, enlarged prostate, neoplasms, neurogenic bladder, pregnancy

90
Q

what is a tumor that often invades renal vein commonly with pale clear cells.

A

Renal cell carcinoma Aka clear cell carcinoma

91
Q

Risk factors for renal cell carcinoma?

A

male, smoking, hypertension, obesity, acquired polycystic disease due to chronic dialysis

92
Q

clinical aspects of renal cell carcinoma

A

hematuria, mass, pain, fever, polycythemia (tumor producing EPO)

93
Q

TX of renal cell carcinoma?

prognosis based on what

A

surgery and radiation,

prognosis is stage dependent

94
Q

what is a common cancer in children that presents with an abdominal mass, pain, INC freq in some syndromes

A

Wilms Tumor

95
Q

What does Wilms Tumor present with pathologically?

TX? prognosis?

A

triphasic proliferation of cells, with epithelial, stromal and blasternal components
TX: surgery and chemo
Prognosis: very good

Pathology Sp 16 (7 decks)

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