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Exam 3 Flashcards

1
Q

Acute Kidney Injury

(Cause and Clinical manifestations)

A

Causes:

  • Reduce perfusion (Injury)
  • Some kidney diseases can cause AKI

Clinical Manifestations/Symptoms:

  • Oliguria - Greatly reduced urine flow
  • Anuria - No urine flow
  • Azotemia - Accumulation of nitrogenous wastes (Greatly reduced GFR)
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2
Q

Chronic Kidney Disease

(Cause, Oral manifestations, Cellular Changes/appearance, Clinical Manifestations/symptoms)

A

Cause:

  • All kidney diseases can lead to CKI if left untreated long-term
  • Multiple insults

Cellular changes/Appearance

  • Scarring/Obliteration of glomeruli
  • Intestinal fibrosis
  • Tubular atrophy

Clinical Manifestation Symptoms

  • Greatly reduced GFR
  • Hypertension, Proteinuria, Azotemia, Uremia -> End-stage renal disease (Treatment = transplant or dialysis)

Oral manifestations:

  • Patients have poor oral hygiene
  • Pallor of oral mucosa -> anemia from reduce Erythropoietin
  • Hemorrhage, petechiae, or ecchymoses -> from platelet dysfunction and anticoagulant use
  • Dry mouth -> from restricted fluid intake
  • Uremic Fetor (ammonia breath) and metallic taste -> increase urea in saliva and ammonia
  • Erosions on lingual surface of teeth -> Frequent vomiting
  • Infections -> Candidiasis (immunosuppression and dialysis)
  • Bone Lesions - demineralization -> Fractures, tooth mobility (Secondary to osteodystrophy - lack Vit D, cannot secrete phosphate -> Hypocalcemia, hyperphosphatemia, hyperparathyroidism)
  • Gingival hyperplasia (secondary from meds)
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3
Q

What are the two types of glomerular diseases discussed in class?

  • Briefly explain each
A

1. (Primary) Nephrotic Syndrome = Activation of COMPLEMENT damages podocytes and basement membrane (Massive Proteinuria -> hypoalbuminemia -> generalized edema​

2. (Secondary) Nephritic Syndrome = INFLAMMATION AND GROSS HEMATURIA

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4
Q

What are the syndromes produced by Nephrotic Syndrome and Nephritic syndrome?

A

Nephrotic Syndrome

  • Minimal change disease
  • Focal segmental glomerulosclerosis (FSGS)
  • Membrane nephropathy
  • Membranoproliferative glomerulonephritis

Nephritic Syndrome

  • Acute post-infectious glomerulonephritis
  • IgA nephropathy
  • Systemic lupus erythematosus (SLE)
  • Goodpasture’s syndrome
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5
Q

Explain the Filtration membrane changes with Nephrotic syndrome

How does this impact blood albumin levels?

A

Nephrotic Syndrome (Primary)

  • Subepithelial immune complex deposit between podocytes and on the glomerular basement membrane
  • Activates complement
  • Damages podocytes and basement membrane
  • Effacement of foot processes (Flattening of podocytes)
  • Food processes/podocytes detach
  • Degradation of basement membrane
  • MASSIVE PROTEINURIA > 3.5 g/day

Hypoalbuminemia -> Low plasma oncotic (pulling) pressure -> Decreases the driving force for fluid movement from interstitial space back to capillaries -> Generalized edema

  • Along with kidney disease -> Na+ & H2O Retention -> Edema

In addition, Nephrotic syndrome is associated with Hyperlipidemia and lipiduria

  • Hypoalbuminea -> Triggers the liver to increase albumin and lipoprotein production -> Hyperlipidemia (High LDL and VLDL)
  • Damage to the filtration membrane -> Allows lipds to be filtered -> Lipiduria (lipids in the urine)
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6
Q

In summary: What are the clinical manifestations of nephrotic syndrome?

A

Massive proteinuria > 3.5 g/day

Hypoalbuminemia

Generalized edema

Hyperlipidemia and lipiduria

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7
Q

Explain the changes to the filtration membrane with Nephritic syndrome

A
  • Subendothelial immune complex deposition
    • Glomeruli are ‘clogged with cells’
    • Decreased GFR
  • Recruits leukocytes
  • Inflammation
  • Severe damage to the filtration membrane

Clinical Manifestations:

  • Protein and RBC’s can get through the membrane and into the urine
    • Gross hematuria
  • Hypertension (Fluid retention), Azotemia (BUN and Creatinine increased), Oliguria (Urine decreased below 100 ml/day), Proteinuria (Protein loss <3.5 g/day)
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8
Q

Name the diseases affecting tubules and interstitium

A
  • Tubulointerstitial nephritis (TIN)
    • Acute Pyelonephritis
    • Chronic Pyelonephritis
    • Drug-induced Nephritis
  • Acute Tubular Injury/Necrosis (ATI or ATN)
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9
Q

Explain what Pyelonephritis is vs. Cystitis

A
  • Pyelonephritis = Involves the kidneys (Upper urinary tract)
  • Cystitis = Involves the lower urinary tract or bladder
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10
Q

Acute Pyelonephritis

(Bacterial Infections)

A
  • ASCENDING INFECTION = Bacteria reflux/travel “up” the ureter to infect kidney. Intrarenal reflux.
    • Predisposing conditions =
      • Female (Short urethra close to rectum),
      • Catheters,
      • BPH (obstruction=stasis of urine),
      • Vesicoureteral reflux (Valve = incompetent between ureter and bladder -> kids)
      • Bacteria enter the bladder and/or colonize urethra (E.coli)
  • DESCENDING INFECTION = bacteria in the blood infect the kidney by traveling “down” the aorta and renal arteries
    • Predisposing conditions = Septicemia/bacteremia, infective endocarditis
  • SIGNS/SYMPTOMS OF BOTH =
    • Yellow, raised abcesses in intestinal tissue
    • Chills/fever/malaise (Infection)
    • Flank/back pain, dysuria (painful urination), pyuria (Bacteria/WBCs in urine)
    • Costovertebral angle tenderness
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11
Q

Chronic Pyelonephritis

A
  • Chronic Obstruction or congenital vesicoureteral (born w/valve not working) reflux ( PLUS recurrent infections)

Clinical Manifestations:

  • Cortical scars and blunted calyx
  • Loss of renal parenchyma -> hypertension -> Decreased GFR -> Secondary glomerulosclerosis and CKD -> ESRD
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12
Q

Drug-Induced Interstitial Nephritis

A
  • Antibiotics and NSAIDs (Act as a hapten) -> bind to tubular cells -> IgE and cell-mediated type 1 hypersensitivity ->interstitial inflammation

Clinical Manifestations:

  • Fever, rash (25%), Eosinophilia, Hematuria, Leukocyturia.
  • No/MINIMAL PROTEINURIA
  • Can progress to AKI if drug is not stopped
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13
Q

What are some of the main symptoms of acute kidney injury?

A

Low urine output and high serum creatinine

(Decreased GFR -> Oliguria (Urine output < 400 ml/day) and Azotemia

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14
Q

Acute Tubular Injury (ATI) or Acute Tubular necrosis (ATN)

A
  • Caused by:
    • ISCHEMIA (Leads to hypotension and shock) or
    • NEPHROTOXINS (Heavy metals, ethylene glycol/antifreeze, drugs, radiograph contrast agents)

Clinical Manifestation: MUDDY BROWN CASTS IN URINE (proteins and others in urine) and oliguria and azotemia (same as AKI)

Biopsy Appearance: Ragged epithelium and necrosis of tubular

  • Tubules can regenerate and complete recovery is possible
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15
Q

What are the diseases involving blood vessels discussed in class?

A
  • Nephrosclerosis
    • Most likely caused by chronic or essential hypertension
    • Sclerosis (‘hardening’) of small renal arteries and arterioles
    • AKA:
      • Arterionephrosclerosis
      • Hypertensive nephrosclerosis
      • Benign nephrosclerosis
  • Malignant hypertension
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16
Q

Nephrosclerosis

A
  • Involves blood vessels

Caused by:

  • Chronic hypertension
  • sclerosis of renal arteries/arterioles
  • Age
  • Diabetics (underlying kidney disease)
  • High Blood pressure patients
  • More common in African Americans
  • HYALINE ATHEROSCLEROSIS (morphologic changes in small arterioles => “artery hardening” narrowing of the lumen)
    • -> Progress to CKD and ESRD

Clinical manifestations:

  • Some decrease GFR and proteinuria
  • GLOMERULAR ISCHEMIA and scarring
  • GRANULAR APPEARANCE of the kidney
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17
Q

Malignant hypertension

A

BP > 200/120 -> Progressed to acute kidney injury and renal failure (normal/healthy blood pressure = 120/80)

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18
Q

Cystic diseases of the kidney

Simple kidney cysts

A
  • Generally innocuous.
  • Multiple or single.
  • Generally in the cortex.
  • No clinical significance
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19
Q

Cystic diseases of the kidney

Polycystic Kidney Disease (PKD)

A
  • AUTOSOMAL RECESSIVE
    • Childhood PKD
    • Rare (do not survive for long)
    • Mutation in PKHD1 GENE -> Fibrocystin
    • Cells convert from absorptive to secretory phenotype
    • Small cysts and remain in contact with urinary system
  • AUTOSOMAL DOMINANT
    • Adult PKD
    • mutation in PKD1/PKD2 Genes -> Polycystin 1 or 2
    • Tubular proliferation and secretory phenotype
    • Large cysts, lose their connection to functioning nephron
      • Results in secretion of fluids into the cysts and hyperplasia of cyst epithelium
    • ADPKD = no cysts @ birth, progresses slow, symptoms @ 40, high mortality -> Flank pain, Intermittent gross hematuria, hypertension (ESRD @ 50 yrs)

Both found in primary cilia and alter the Chemo and mechanosensors function in tubular epithelial cells

20
Q

Urinary Outflow Obstruction

what are some of the complications

A
  • Due to calculi or stones, enlarged prostate (BPH)
    • Note Urolithiasis = kidney stones

Types and Causes:

  • Calcium Oxalate/Calcium phosphate = most common (80%)
    • Associated with Idiopathic hypercalciuria (50%)
  • Uric Acid/Cystine stones (9%) = least common
    • Occurs with ACIDIC URINE
  • Magnesium, ammonium, Phosphate/Struvite stones (10%)
    • ALKALINE URINE (pH > 7.2) AND AMMONIA
      • Kidney infection with urease containing bacteria -> Urea is converted to ammonia -> causes alkaline urine
        • Combination of high ammonia and alkaline urine -> precipitation of Mg, NH4, and PO4 -> Struvite stone
      • May be asymptomatic but -> recurrent kidney infections will eventually destroy the kidney

COMPLICATIONS OF KIDNEY STONES

  • Many stones = asymptomatic and not produce significant renal damage
  • When stone passes down the ureter -> Renal or urethral colic (intense pain) and Gross Hematuria (damage the ureter w/spikes)
  • Obstruction of urine flow can also be caused -> Bacterial infections (stasis of urine) -> Hydronephrosis
21
Q

Hydronephrosis

A

Swelling of the kidney due to urinary obstruction

  • Caused by:
    • kidney stone obstruction that dilates the renal pelvis and calyces -> intense pressure on kidney -> loss/atrophy of renal tissue
    • Tumors
    • Enlarged prostate (BPH, cancer, prostatitis )
    • Ureteritis
22
Q

What are the types of kidney neoplasms?

A
  • Pediatric
    • Wilms tumor
  • Adult
    • Benign = Papillary adenoma
    • Malignant = Renal cell carcinoma (RCC)
23
Q

Wilms Tumor

A
  • PEDIATRIC
  • Nephroblastoma (blast = immature)
  • Mutation in WT1 gene coding for transcription factor needed for renal development
    • Resembles the developing fetal nephrogenic zone of the kidney
  • Appearance: Tan/Gray colored kidney
  • Treatment: Removal (Nephrectomy + chemo) = 95% survival
24
Q

Papillary Adenoma

A
  • BENIGN ADULT TUMOR
  • Tumor SIZE differentiates papillary adenoma from carcinoma
    • <= 0.5 cm = adenoma
      • Note: > 0.5 cm = renal cell carcinoma
  • no clinical significance (40% of adults are diagnosed)
25
Q

Renal Cell Carcinoma (RCC)

A
  • MALIGNANT ADULT TUMOR
  • Tumors => 0.5 cm.
  • Highly vascular tumors
    • Derived from the renal tubular or collecting duct epithelium
  • Triad of symptoms
    • Flank pain
    • Painless hematuria
    • Palpable mass
  • Most of the time tumors are detected incidentally
26
Q

What is Anemia and Polycythemia?

A
  • Anemia = too few RBC/hemoglobin -> Decreased oxygen carrying capacity (lack of O2)
  • Polycythemia = too many RBC/hemoglobin -> Thrombosis
27
Q

What are the two ways to assess the oxygen carrying capacity of the blood?

A
  1. Amount of hemoglobin in blood
    1. Males: 13.8 - 17 g/dL
    2. Females: 12 - 15 g/dL
  2. Hematocrit
    1. The fraction or % of blood that is packed with red blood cells ( = RBC/total cells)
      1. Note: WBC and platelets form buffy coat
28
Q

What is Hematopoiesis?

A

The production of new blood cells

  • Normally occurs in red bone marrow
    • Marrow contains stem cells = hemocytoblasts
      • Certain growth factors will stimulate the proliferation and differentiation of hemocytoblasts to either form RBC, WBC or platelets
  • Erythropoietin = growth factor involved in the proliferation and differentiation of erythrocytes (RBC) = Erythropoesis
    • under certain extreme conditions this can occur in the liver and spleen
    • Stem cell -> maturing cell (in bone marrow) -> lose nucleus -> Reticulocyte (goes to blood) -> lose RNA -> Erythrocyte (Takes 24 hours to lose its RNA and turn to RBC in blood)
      • RBC remain in circulation for 110 - 120 days before being removed via hemolysis in the spleen
        • Macrophage in spleen or liver phagocytose the damaged RBC
          • Globin -> Amino acid
          • Heme ->
            • Iron recycled
            • Converted into bilirubin (yellow pig)
29
Q

What are the main causes of anemia?

A
  1. Anemia of blood loss
    1. Acute or chronic bleeding
  2. Anemias of diminished erythropoiesis
    1. Decreased red cell proliferation (cannot make enough RBCs)
  3. Hemolytic anemia (Hallmark = Erythroid hyperplasia and Reticulocytosis)
    1. Increased red cell destruction
      1. Two main mechanisms for Hemolysis:
        1. Red cell membrane is damaged and the cell bursts in the blood vessel - intravascular hemolysis (mechanical forces, toxins)
        2. Red cells are defective - undergo extravascular hemolysis by macrophages mainly in the spleen (liver = backup) = outside blood vessels
          1. If spleen contains many more RBC and macrophages because they are deformed (ex. sickle cell anemia) and cannot get out = SPLENOMEGALY
          2. Extravascular hemolysis also causes increased bilirubin in blood (hyperbilirubinemia) and it deposits in the tissue (Jaundice) and liver -> high level in bile -> Gallstones
30
Q

What are the three types of Hemolytic anemias discussed in class?

A
  1. Hereditary Spherocytosis (RBC’s are spherical)
  2. Sickle cell anemia
  3. Thalassemia
31
Q

Hereditary Spherocytosis

A
  • Hemolytic anemia
  • Signs:
    • General anemia = tired, lethargic, pale skin
    • Specifically Hemolytic anemia = gallstones, jaundice, splenomegaly, elevated reticulocyte count in blood (lots of RBC production to make up for the damaged RBCs), Anemia (Subclinical to severe)
  • GENETIC -> AUTOSOMAL DOMINANT TRAIT
  • SHERICALLY SHAPED and small RBCs
    • Mutation in any of these proteins: Band 3, Ankyrin, Spectrin
      • ->Weakens link between cytoskeleton and bilayer-> Unsupported areas of lipid bilayer -> lose more membrane than cytosol -> decrease in surface to volume ration -> spherical shape
  • Hereditary spherocytosis of a hemolytic anemia occurs MAINLY IN THE SPLEEN (EXTRAVASCULAR) because it is a deformation
  • How can you diagnose someone with this?
    • Peripheral blood smear and look for spherocytes!
      • Normal Smear = Normochromic (color), Normocytic (size)

Treatment: Splenectomy (Pro: Reduce RBC destruction to correct anemia; Con: risk of infection)

32
Q

Sickle cell anemia

A
  • Hemolytic anemia
  • Mutation in beta-globin chain of Hb
    • Sickle-shaped RBCs
  • AUTOSOMAL RECESSIVE TRAIT
    • Sickle cell anemia = if baby born with sickle cell anemia, both parents needed to have sickle cell trait
      • both mutated alleles (No HbA, mostly HbS)
    • Sickle cell trait = asymptomatic recessive
      • One normal and one mutated allele = asymptomatic
  • O2 removed -> HbS polymerizes -> reversible sicking
  • Multiple cycles of sickling -> extensive membrane damage -> increased membrane fragility and decreased membrane deformability -> lead to hemolysis and phagocytosis by macrophages in the spleen and liver -> MUCH SHORTER RBC lifespan (20 days)
  • HbF prevents symptoms from appearing until 5-6 mo old in babies w/disease (where HbF -> HbA)
  • Signs/symptoms: Pallor and fatigue, Jaundice, gallstones, increased reticulocytes, elevated erythropoietin (Typical of hemolytic anemia)
  • VASO-OCCLUSIVE CRISIS (spontaneous - blocked vasculature due to clotting, common in legs/extremities) - vascular congestion, thrombosis, infarction, bone pain
    • Commonly caused by Precipitating stimulus or spontaneously, infection, inflammation, dehydration -> sickling and sticking of sickled cells to endothelium -> micro-vascular occlusions -> tissue or organ ischemia, infarction and sudden, severe pain
    • More often this occurs in the bones = bone pain . Blood flow tends to be slower and sluggish and hemoglobin undergoes progressive deoxygenation and increased sickling -> results in significant bone pain, and over time, degenerative changes in bone
  • AUTOSPLENECTORMY in children -> more susceptible to infection
    • What happens with these children: First develop splenomegaly -> Autosplenectomy (numerous splenic infarctions secondary to vaso-occlusion) -> Small remnant spleen (turns to scar tissue)
      • Functionally asplenic -> increased risk of infection

What are the outcome or prognosis for a person with sickle cell anemia?

  • Many chronic complications
  • better than it use to be with more supportive care
  • Functionally asplenic -> risk of infections
  • Use of antibiotics to prevent (children under 5) or treat infections has improved outcomes
33
Q

alpha or beta - Thalassemia

A
  • Hemolytic anemia
  • Reduced synthesis of beta-globin chain -> inadequate HbA formation -> RBCs have less Hb or Hb aggregation and precipitation -> membrane damage ->
    • Extravascular hemolysis (Small)
    • Apoptosis of RBC precursors in marrow -> ineffective erythropoiesis (larger pathway)

RBC Appearance:

  • Small (microcytic) and
  • pale cells (hypochromic)
  • Variation in size and shape
  • TARGET-CELL APPEARANCE (puddling)

How does the body respond?

  • Splenomegaly, hepatomegaly (big liver), Skeletal abnormalities (Frontal Bossing)
    • because of the ineffective erythropoiesis, the reticulocyte count may not be as high as you may expect (cannot make RBC’s)
    • But because of the huge stimulus for erythropoiesis, the blood may also contain normoblasts
    • Child will have GROWTH RETARDATION AND CACHEXIA
      • due to ineffective erythropoietic precursors consuming lots of nutrients

Treatment:

  • Bone marrow transplant
  • Blood transfusion throughout life (required for survival)
    • major problem with blood transfusion = iron overload due to cannot clear iron fast enough
      • Iron overload prevented by Iron chelators (long term survival)

BETA-THALASSEMIA MAJOR VS. MINOR??

  • Minor:
    • Mild microcytic hypochromic anemia
    • target cells
    • asymptomatic
34
Q

What are anemias of diminished erythropoiesis?

A
  • Inadequate nutrients
    • Iron
    • Folic acid
    • Vitamin B12
  • Bone marrow failure (aplastic anemia)
  • Systemic inflammation (anemia of chronic disease)
  • Bone marrow infiltration by tumor or inflammatory cells (myelophthisic anemia)
35
Q

Iron deficiency anemia

A
  • Diminished erythropoiesis.
  • Elevated erythropoietin (kidneys aren’t working)
  • Low reticulocyte count (cannot make RBC’s)
  • Iron is required to produce Hemoglobin (cannot transport O2)

Signs/symptoms:

  • General anemia: fatigue, listlessness, pale (hypochromic), weakness, small cells (microcytic)
  • Iron deficiency anemia: THIN AND SPOONING FINGERNAILS
    • CRAVING FOR CLAY/DIRT
    • LOW IRON STORES
      • = main way to differentiate beta thalassemia minor from iron deficiency anemia

Main causes:

  • Chronic blood loss (GI tract, uterus)
  • Pregnancy (increased requirement)
  • dietary insufficiency (Not is US)
    • Generalized intestinal malabsorption (gastrectomy or celiac disease)
    • Iron absorption changes based on iron stores:
      • Low iron stores -> liver makes less hepcidin (inhibit iron absorption)-> increased iron absorption
      • High iron stores -> liver makes more hepcidin -> decreased iron absorption
36
Q

What is the difference between Aplastic anemia and Myelophthisic anemia?

A
  • Aplastic Anemia (bone marrow destroyed)
    • Toxins, radiation, chemotherapy, drugs
      • -> Destroy bone marrow
        • -> Anemia (low RBC count), leukopenia (Low WBC count), thrombocytopenia (low platelet count)
  • Myelophthisis anemia (Destroy precursor cells…)
    • Metastatic cancer inflammatory cells
      • -> infiltrate bone marrow
        • -> Destroy normal hematopoietic cells
          • -> Anemia, leukopenia, thrombocytopenia
37
Q

Megaloblastic anemia

A
  • Vitamin B12 or Folic acid deficiency
    • Diminished erythropoiesis
    • Elevated erythropoietin, low reticulocyte count
  • Erythroid progenitor -> lacking either folate or B12 -> Insufficient DNA synthesis and cell division and unimpaired RNA and protein (Hemoglobin) synthesis -> Macro-ovalocytes or LARGE SPHERICAL PALE RBCS (megaloblastic anemia)
    • Cell appearance: large, no zone of central pallor (spherical)

Clinical signs/symptoms:

  • Inflammation and atrophy of lingual papillae
  • How can you tell the difference between folic acid deficiency and Vit B12 deficiency?
    • Measure blood folate and vit B12 levels, determine if any neurological problem -> Vit B12 deficiency can cause nerve demyelination in spinal cord
      • B12 deficiency can cause CNS problems -> numbness, tingling, unsteady gait
        • While megaloblastic anemia is reversible, the neurological problems can be irreversible

Main causes of Folic acid deficiency:

  • Decreased dietary intake
  • Chronic alcoholism or liver disease (poor diet and decreased hepatic storage of folates)
  • Increased requirement (pregnancy)
  • Malabsorption syndrome (celiac disease and tropical sprue)
  • Drug induced

Main causes of Vit B12 deficiency:

  • Folate is destroyed by cooking, B12 IS NOT
  • Stores of folate will last only a few weeks; stores of B12 last for years
  • B12 deficiency is mainly caused by:
    • Loss of intrinsic factor =
      • PERNICIOUS ANEMIA (autoimmune disease to parietal cells or intrinsic factor), gastrectomy
    • Loss of acid and pepsin to release vitamin B12 from its bound form in food
      • Gastric atrophy or stomach acid reducing drugs
    • Loss of intrinsic factor - B12 absorption
      • inflammatory bowel disease, ileal resection
38
Q

What are the ways to classify neoplastic proliferations of white cells?

A

1. Based on origin of the tumor cells (Pluripotent stem cell)

  1. Myeloid stem cell -> Myeloid neoplasms (Some leukemias)
    1. Erythrocyte
    2. Platelet
    3. Granulocytes/monocyte
  2. Lymphoid stem cell -> Lymphoid neoplasms (some leukemias and non-hodgkin and hodgkin lymphoma)
    1. B cells
    2. T cells

2. Based on location

  1. Leukemia
    1. Starts in bone marrow (and blood) -> spread to lymph nodes
  2. Lymphoma
    1. Starts in lymph nodes -> spread to blood and bone marrow
39
Q

What are the types of leukemias based on?

A
  1. Cell lineage -> Myeloid or lymphoid
  2. Rate of development -> Acute or chronic
    1. How fast they develop certain symptoms

Big 4 types of leukemias discussed:

  1. Acute myeloid leukemia (AML)
  2. Chronic myeloid leukema (CML)
  3. Acute lymphoblastic leukemia (ALL)
  4. Chronic lymphocytic leukemia (CLL)
40
Q

Acute Myeloid Leukemia (AML)

A
  • From myeloid immature “blasts” ->Mutations that: stop differentiation, promote uncontrolled proliferation -> Acute leukemia

Features of Acute leukemias:

  • Large cells and very large nucleus
  • Nonfuncitonal cells
  • Rapidly dividing cells (present w/symptoms within weeks)
  • Rapidly fatal (< 6 months w/o treatment)

Clinical presentation: (replacement of bone marrow by blast cells)

  • Anemia (weakness, fatigue, pale skin)
  • Thrombocytopenia (Bleeding-petechiae-and hypocoagulation)
  • leukopenia/neutropenia (syseptible to infection, fever, ulcers)
  • Malaise, Fever/night sweats (hypermetabolic activity), bone pain and tenderness (marrow expansion, increased pressure in the medullary space)
  • ADULTS
41
Q

Acute lymphoblastic leukemia

A
  • From lymphoblasts immature “blasts” ->Mutations that: stop differentiation, promote uncontrolled proliferation -> Acute leukemia

CHILDREN

Features of Acute leukemias:

  • Large cells and very large nucleus
  • Nonfuncitonal cells
  • Rapidly dividing cells (present w/symptoms within weeks)
  • Rapidly fatal (< 6 months w/o treatment)

Clinical presentation: (replacement of bone marrow by blast cells)

  • Anemia (weakness, fatigue, pale skin)
  • Thrombocytopenia (Bleeding-petechiae-and hypocoagulation)
  • leukopenia/neutropenia (syseptible to infection, fever, ulcers)
  • Malaise, Fever/night sweats (hypermetabolic activity), bone pain and tenderness (marrow expansion, increased pressure in the medullary space)
  • Generalize lymphadenopathy Splenomegaly
    • ​​AKA: PRECURSOR B AND T CELL LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
42
Q

Chronic Myeloid Leukemia (CML)

A
  • Chronic leukemia: More mature (but not full mature) -> mutations that stop differentiation and promote uncontrolled proliferation
  • Adults between 25-60

Features of chronic leukemias:

  • Cells appear normal (more differentiated) and retain some function, but not really functional
  • More slowly dividing
    • Can be asymptomatic for years

Clinical Presentation:

  • Asymptomatic or mild symptoms such as fatigue, malaise, weight loss, excessive sweating (not as bad as acute), bleeding episodes (platelet dysfunction)
  • Abdominal fullness (ENLARGED SPLEEN)
    • Advances through an accelerated phase and BLAST CRISIS (resembles acute leukemia)
  • PHILADELPHIA CHROMOSOME
    • bcr-abl fusion protein gene on chromosome 22
      • ​​produces a dysregulated tryrosine kinase involved in cell transformation
        • Drives the proliferation of granulocytic and megakaryocytic progenitors and release of immature cells in blood
43
Q

Chronic Lymphocytic Leukemia (CLL)

A
  • Chronic leukemia: More mature (but not full mature) -> mutations that stop differentiation and promote uncontrolled proliferation
  • ADULTS OVER 50
  • Cells appear normal and retain some function
  • More slowly dividing

Clinical presentation:

  • Asymptomatic
  • Mild systemic symptoms: Fatigue (anemia), Malaise, weight loss, anorexia, bleeding episodes (platelet dysfunction), Lymphadenopathy (enlarged lymph nodes) and splenomegaly (enlarged spleen)
    • Can transform to a higher grade neoplasm
      • Prolymphocytic transformation -> large cells in peripheral blood
      • RICHTER SYNDROME -> growing massive lymph node -> resembles diffuse large B cell lymphoma
44
Q

What are the two types of Lymphomas?

A
  • Hodgkin lymphoma (aka Hodgkin’s disease)
    • Neoplastic proliferation of an atypical lympoid cell - Reed-sternberg cell
  • Non-Hodgkin lymphoma
    • Neoplastic proliferation of B-cells, T-cells or rarely histiocytic cells (macrophages and dendritic cells)

Recall: Lymphomas:

  • Start in lymph node (typical)
    • -> Spread to spleen, liver and bone marrow (other organs in advanced disease)
45
Q

Explain Reed-sternberg cells

(Hodgkin lymphoma)

A

Reed-sternberc cells

(Hodgkin lymphoma)

  • -> Release many cytokines and chemokines
    • Inflammatory reaction and tissue fibrosis in the affected lymph node
    • Eosinophilia
    • Plasmacytosis (plasma cell development) and hypergammaglobinemia
    • Features of chronic inflammation (fever, anemia)
    • Leukocytosis (increased marrow production of leukocytes)
46
Q

Hodgkin Lymphoma

A
  • Neoplastic proliferation of atypical lymphoid cells/germinal center B cells
    • -> loss of B cells markers
      • -> REED-STERNBERG CELLS (OWL’S EYES)
        • = release cytokines/chemokies,
        • eosinophilia, plasmacytosis,
        • hypergammaglobinemia,
        • fever, anemia, leukocytosis, night sweats,
        • lymphadenopathy,
          • starts with enlargment of a single lymph node or group of lympn nodes
            • rubbery and firm nodes
  • Patient population:
    • ​​Bimodal age distribution:
      • ​​Peaks = 20 yrs old and 65 yrs old
47
Q

Non-Hodgkin Lymphoma

A
  • Neoplastic proliferation/malignant transformation of B and T cells
  • Varies tremendously depending on the type of lymphoma and area involvement:
    • Can be slow growing and waxing/waning over many years or
    • highly aggressive resulting in death within a few weeks
      • Rapidly growing mass
      • Systemic B symptoms (fever, night sweats, weight loss)

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