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BOARDS! > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

TTP (thrombotic thrombocytopenic purpura) pathophys

A
  • due to impaired function of ADAMTS13 (vWf-cleaving protease)
    • vWf multimers are PRO-thrombotic and cause:
      • diffuse microvascular thrombosis
      • microangiopathic anemia
      • thrombocytopenia
  • acquired (auto-Ab) or hereditary
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2
Q

relationship between HbF and HbA

A
  • HbF (alpha 2-gamma 2):
    • high oxygen affinity
    • made in final 7 mo
  • –switches to–
  • HbA (alpha 2-beta 2):
    • during first 6 months of lide, switch to this
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3
Q

What drives angiogenesis?

A
  • vascular endothelial GF (VEGF)
    • stimulation angiogenesis in: nml, chronically inflammed, healing, or neoplastic tissue
  • Fibroblast GF (FGF)
    • FGF-2 involved in endothelial cell proliferation, migration and differentiation
    • –and–
    • embryonic development, hematopoiesis, wound repair
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4
Q

Lead Poisoning

A. peripheral blood smear

B. high risk groups

A

A. periph smear:

  • coarse erythrocyte basophilic stipling
  • microcytic hypochromic anemia

B. high risk groups:

  • young kids ingesting paint chips (old, rundown buildings)
  • industrial workers inhaling particulate lead
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5
Q

Aplastic Anemia

A
  • low Hgb
  • thrombocytopenia
  • no hematopoietic cells in bone marrow
  • compensatory: increase in circulating EPO
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6
Q

Iron Overload (Hemosiderosis)

A
  • common, serious complication of chronic hemolytic anemia AND frequent blood transfusions
  • *hemosiderin accumulation
  • chelation therapy reduces parenchymal iron deposition
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7
Q

What is a patient with chronic hemolytic anemia predisposed to?

A
  • folic acid deficiency
  • macrocytic changes due to an increase in erythrocyte turnover
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8
Q

What is the relationship between Vitamin K and clotting?

A
  • Vit K is needed for carboxylation and functionality of conjugation factors 2,7,9,10
  • newborns without prophylactic supplementation are at risk for bleeding complications
  • patients with CF are at risk for Vit K deficiency due to poor absorption of fat-soluble vitamins
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9
Q

Burkitt Lymphoma

A
  • aggressive rapid growth
  • strry sky microscopic appearance
  • Path: translocation of c-myc oncogene on long arm of chromosome 8 with IgHC region on chromosome 14
    • produces a nuclear phosphoprotein (c-myc) that functions as a transcription activator
  • “african mccormick with a sharp jaw line wears a burkha under the starry night sky”
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10
Q

Follicular lymphoma

A
  • tumor cells express pan B-cell antigens: CD19, 20, 21, 10 (…a)
  • t(14:18); bCl2-IgH
    • overexpression of bcl2 protein products inhibits apopotosis of tumor cells and facilitates neoplastic growth
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11
Q

Spleen’s Job (2)

A
    1. BLOOD FILTER-can remove circulating pathogens
    1. major site of OPSONIZING Ab synthesisi
  • asplenic pts prone to infections cause by ncapsulating organisms:
    • S. pneumo
    • H. flu
    • N. mening
  • spleen=most commonly injured organ with blunt abdo trauma
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12
Q

T-cell ALL

A
  • CP: mediastinal mass that…
    • can compress great vessels=SVC syndrome
    • can compress eophagus=dysphagia
    • can compress trachea=dyspnea and stridor
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13
Q

Folate deficiency

A
  • inhibits the formation of dTMP
    • causes limited DNA synthesis
    • promotes megaloblastosis and erythroid precursor cell apoptosis
  • thymidine supplementation can moderately INC dTMP levels, so it can reduce erythroid precursor cell apoptosis
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14
Q

A. Aplastic anemia

B. In a sickle cell pt what is the most common VIRAL cause of an APLASTIC CRISIS?

A

A. AA causes pancytopenia; BM is replaced by fat cells and marrow stroma

**absence of splenomegaly on PE

BM biopsy useful in making diagnosis; marked hypocellularity

B. an infection of erythroid progenitor cells with parvovirus B19 (non envelpped, single-stranded, DNA virus) is the most common viral causes/infection

others: autoimmune, drugs (CARBAMAZEPINE, CHLORAMPHENICOL), exposure to radiation or toxins

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15
Q

Vitamin K

A
  • needed for CARBOXYLATION and functionality of coagulation factors 2,7,9,10
  • newborns without prophylactic supplementation are at risk for bleeding complications
  • pts with cystic ibrosis are at risk for Vit K deficiency due to poor absorption of fat-soluble vitamins
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16
Q

A pt with chronic hemolytic anemia is predisposed to: (2)

A
  • folic acid deficiency
  • macrocytic changes due to increase in erythrocyte turnover
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17
Q

HgbC due to missense mutation

A
  • glutamate is subsituted by lysine (if it were valine, would get HbS) in beta-chain
    • causes a decrease in negative charge of Hgb
  • speed of Hgb during gel electrophoresis:
    • HgbA>HgbS>HgbC
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18
Q

Hereditary breast cancer

A
  • most commonly associated with mutations in BRCA1 and 2 (tumor suppressor genes involved in DNA repair, mutations increase risk of developping breast and ovarian cancer)
  • CP: peau d’orange=pitting edema in subcutaneous breast tissue and skin thickening around exaggerated hair follicles
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19
Q

Intravascular hemolytic anemia

A
  • INCREASED: LDH and bilirubin
  • DECREASED: serum haptoglobin
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20
Q

Hemolytic disease of the Newborn (erythroblastosis fetalis)

A
  • cause: maternal sensitization to Rh antigens during a prior pregnancy with and Rh(D+) fetus
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21
Q

Pure red cell aplasia

A
  • rare form of marrow failure
  • sever hypoplasia of marrow erythroid elements in the setting of normal granulopoiesis and thrombopoiesis
  • associated with:
    • thymoma
    • lymphocytic leukemias
    • parvovirus B19 infection
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22
Q

Undifferentiated/Anaplastic Tumors

A
  • do NOT resemble tissue of origin
  • composition:
    • pleomorphic cells with large hyperchromatic nuclei that grow in disorganized fashion
    • may have numerous abnormla mitoses and giant tumor cells
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23
Q

Tumor Lysis Syndrome

A
  • can develop during chemo from cancers with rapid cell turnover (poorly differentiated lymphomas and leukemias)
    • substantial tumor burden
    • high sensitivity to chemo
  • CP:
    • hyperphosphatemia
    • hypocalcemia
    • hyperkalemia
    • hyperuricemia
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24
Q

RCC and blood d/o

A
  • RCC can cause anemia of chronic dz and iron deficiency anemia d/t chronic hematuria
  • some renal cell tumors can produce erythropoietin and cause polycythemia
  • rare in younger pts
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25
Q

common paraneoplastic syndromes

A
  • CP, frequently assoc neoplasms, etiology
  • Cushing syndrome
    • small cell lung cancer, pancreatic CA
    • ectopic production of adenocorticotropic hormone/corticotropin-releasing hormone
  • SIADH (syndrom of inapprop antidiuretic hormone secretion)
    • small cell lung ca
    • ectopic vasopressin production
  • subacute cerebellar degeneration
    • small cell lung ca
    • breat, ovarian, and uterina ca
    • anti-Yo anti-P/Q and anti-Hu Ab
  • Lambert-Eaton myasthenic syndrome
    • small cell lung ca
    • voltage gate calcium channel ab
  • Myasthenia gravis
    • thymoma
    • acetylcholine receptor Ab
  • Hypercalcemia
    • squamous cell lung ca
    • ectopic production of parathyroid hormone-related protein
  • dermatomyositis/polymyositis
    • variable
    • autoimmune
  • erythrocytosis
    • renal cell ca
    • ectopic erythropoietin production
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26
Q

Paraneoplastic cerebellar degeneration

A
  • CP:
    • progressively worsening dizziness
    • limb and truncal ataxia
    • dysarthria
    • visual disturbances
  • etio: immune resp against tumor cells that cross reacts with Purkinje neuron Ag leadint to cute onset rapid degen of the cerebellum
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27
Q

Restless leg syndrome

A
  • CP:
    • uncomfortabe urge to move legs with:
      • unpleasant sensations in the legs
      • onset with inactivity or at night
      • relief with movemet (stretching, walking)
  • Etio:
    • idiopathic
    • iron deficiency
    • uremia
    • diabetes (especially with neuropathy)
    • MS, PD
    • drugs (antidepressants, metoclopramide)
  • Tx:
    • avoidance of aggravating factors (alcohol, sleep deprivation)
    • supportive measures:
      • leg massage, exercise, heating pads
    • dopamine agonists (Pramipexole)
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28
Q

Xeroderma pigmentosum

A
  • AR due to decreased ability to repair DNA following damage by UV light
  • skin is nml at birth
  • CP:
    • erythema
    • scaling
    • subsequent hyperpigmentation and lentigo formation on light-exposed areas (especially face)
    • later:
      • skin of affected area shows atrophy, telengiectasias, intermingling areas of hypo and hyper-pigmenations
  • skin malignancies (SCC, BCC, malignant melanoma) develop as early as 5-6 yo
  • Etio: genes that code for various DNA repair enzymes are abnml
    • leads to defects in excision of abnml nucleotides or defects in replacement of nucleotides following excision
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29
Q

dz associated with impaired DNA repair

A
  • xeroderma pigmentosum
  • Fanconi anemia (AR, hypersensitivity to DNA cross-linking agents)
  • Bloom syndrome (AR, hypersensitivity to UV damage and chemotherapeutic agents)
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30
Q

Great saphenous vein

A
  • located superficially inthe leg, longest vein in the body
  • accessed by surgeons in the medial leg (most commonly) or less commonly, near its pt of termination in the femoral triangle of the upper thigh
  • femoral triangle:
    • inguinal ligament superior
    • sartorius muscle lateral
    • adductor longus muscle medially
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31
Q

Femoral Triangle

A

consists of (lateral to medial; NAVL):

  • femoral nerve
  • femoral artery
  • emoral vein
  • deep inguinal nods/lymphatic vessels
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32
Q

Hereditary angioedema

A
  • inherited AD condition
    • low C1 esterase inhibitor activity leads to increases in bradykinin activity
  • causes episodes of painless, non-pitting, well-circumscribed edema
  • face, neck, lips, tongue most commonly affected
  • can also be acquired-associated with ACEi tx
  • DONT use ACEi with these pts!!
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33
Q

Failures of Embryologic processes

A
  • proliferation=unilat aplasia of the fibula
  • apoptosis=a.i. dz due to persistence of autorxv B/T cells
  • obliteration=branchial cleft cyst
  • migration=Hirschsprung dz-failure of migration of neural crest cells that form the colonic ganglion cells
  • fusion=hypospadias (failure of urethral folds to fuse)
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34
Q

TGA (transposition of the great arteries)

A
  • diagnostic: aorta lying anterior to and to the right of the pulm artery
  • TGA results from failure of fetal aorticopulmonary septum to spiral normally during septation of the truncus arteriosus
  • life-threatening cyanosis at birth
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35
Q

Anaphylactic shock

A
  • charac: vasodilatation, increased vascular permeabilit, bronchoconstriction
  • epinephrine counteracts these physiological mechanism, so is drug of choice for tx
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36
Q

Actinic keratosis (AK)

A
  • develops on chronically sun-exposed areas of the skin in predisposed indivs
  • lesions consist of erythematous papules with a central scale and a rough “sandpaper-like” texture
  • considered pre malignant lesions and have the potential to progress to squamous cell carcinoma
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37
Q

Bacterial meningitis

A
  • classic triad: fever, stiff neck, altered mentation
  • eval: prompt blood cultures, empiric AB, lumbar puncture and CSF analysis to confirm the diagnosis, id the offending organism, and determine AB susceptibility
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38
Q

Kozak consensus sequence

A
  • occurs on eukaryotic mRNA
  • defined by the following sequence:
    • (gcc)gccRccAUGG
    • R=adenine or guanine
  • sequence helps initiate translation at the methionine start codon (AUG)
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39
Q

Seborrheic keratosis (SK)

A
  • benign epidermal tumor, presents as tan or brown, round lesion with well-demarcated border and “stuck-on” appearance
  • epi: middle-aged/elderly
  • rapid onset of numerous SK=undiagnosed internal malignancy (Leser-Trelat sign)
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40
Q

Acanthosis nigricans

A
  • CP: hyperpigmented, velvety plaques found on axilla or neck (flexural areas)
  • assoc with insulin-resistant states: DM, obesity, acromegaly and visceral malignancy, or an endocrinopathy
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41
Q

Lichen planus

A
  • 5 P’s: polygonal, planar, pruritic, purplish plaques on wrists, hands, trunk, legs
  • fine white lines: Wickham striae may be rpesent on plaque surface
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42
Q

patent foramen ovale (PFO)

A
  • usually remains functionally closed b/c LA pressure>RA pressure
  • most pts: asymptomatic
  • BUT! conditions that raise RA pressure above LA pressure (Valsalva) can produce a transient R-to-L shunt across the PFO…may result in paradoxical embolization (stroke in the setting of venous thromboembolism)
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43
Q

Rb protein

A
  • regulator of the G1–>S phase transition
  • present in one of two forms:
    • active-hypO-phosphorylated
    • inactive-HYPER-phosphorylated
      • cells are allowed to transition unchecked via proliferation signals which activate CDK4 (=hyperphos)
  • resting cells in the G0 phase contain active (hypophosphorylated) Rb protein
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44
Q

[cutaneous] Angiosarcoma (Stewart-Treves syndrome)

A
  • RF: chronic lymphedema (axillary LN dissection is a RF for CL involving ipsi arm)
  • histo: infiltration of the dermis with slit-like abnml vascular spaces
  • prognosis: poor b/c tumor is usually widespread by time of diag
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45
Q

viral meningitis

A
  • elevated protein
  • nml glucose
  • lymphocytic predominance
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46
Q

bacterial meningitis

A
  • low glucose
  • high protein
  • neutrophilic predominance of CSF
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47
Q

Leprosy (Hansen dz)

A
  • deforming infection of skin and nerves
  • caused by Mycobacterium leprae
  • transmission: inhygienic conditions, respiratory route, prolonged skin-to-skin contact
    • also armadillo contact
  • range of clinical manifestations depends on strength of cell-mediated immune response
  • TT (tuberculoid leprosy)=least severe form often self-limited; limited intact CMI (Th1)
    • CP: mild skin plaques, hypopigmentation, hair follicle loss, focally decreased sensation
  • LL (lepromatous leprosy)=most severe form, occurs in pts with a weak CMI (Th2)
    • CP: skin thickening, plaque-like hypopigmentation (often with hair loss), leonine facies, paresis, regional anesthesia, testicular destruction, blindness
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48
Q

Melanoma

A
  • most common metastatic tumors to the brain: lung ca, renal ca, melanoma
  • malignancy of melanocytes
  • embryologically derived from neural crest cells
  • ABCDE
    • Asymmetry
    • border irregularities-uneven edges, pigment fading
    • Color variegation-brown, tan, red, blk
    • diameter > or =6mm
    • evolving: lesion changing in size, shape, color, or new lesion
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49
Q

Mitochondrial encephalomyopathy

A
  • neuromuscular lesions, ragged skeletal mu fibers, lactic acidosis
  • mitochondrial d/o follow maternal inheritance pattern
  • mit responsible for ATP production via oxidative phosphorylation, so defect=lactic acidosis, affect tissue with highest metab rates (neural tissue, muscular tissue)
  • heteroplasmy=having different mitochondrial genomes within a single cell
    • variable clinical expression in affected family members
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50
Q

Giant cell arteritis (GCA)

A
  • pt with HA, visual and muscular s/s. enlarged temporal artery, elevated erythrocyte sedimentation rate
  • Prog: cell-mediated immunity
    • production of cytokines, in particular IL-6 closely correlates to severity of s/s
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51
Q

what is an important difference between unfractionated heparin and LMWH?

A
  • they can both bind to anti-thrombin to INC its activity against Factor 10a
  • only unfractionated can bind both anti-thrombin and thrombin to allow anti-thrombin to inactivate thrombin
    *
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52
Q

paroxysmal nocturnal hemoglobinuria (PNH)

A
  • d/t gene defect (acquired mut in PIGA gene)
    • causes absence of GPI anchor (needed to attach CD55/DAF and CD59/MAC inhibitory protein)
    • CD55 and CD59 help inactivate complement and prevent MAC from forming on nml cells
  • leads to uncontrolled complement-mediated hemolysis
  • classic triad:
    • hemolytic anemia (hemoglobinuria)
    • pancytopenia
    • thrombosis (at atypical sites) <ie></ie>
  • chronic hemolysis can cause iron deposition in the kidney (hemosiderosis)
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53
Q

high-affinity hemoglobinopathies

A
  • high-O2-affinity hemoglobins have a DEC P50 that is represented by a leftward shift of the oxygen dissociation curve
  • reduced ability to release oxygen within the peripheral tissues (selfish bastard dont want to let the O2 go!), leading to:
    • renal hypoxia
    • INC erythropoietin synthesis
    • compensatory erythrocytosis
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54
Q

caseating granulomas of TB

A
  • almost always contain large epitheliod macrophages
    • pale pink ranular cytoplasm
    • surface CD14 at periphery
    • surround a central region of necrotic debris
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55
Q

Pol mutation

A
  • responsible for acquired resistance to HIV reverse transcriptase inhibitors and HIV protease inhibitors
  • ENV gene mutations enable escape from host neutralizing Ab
  • (high mutability of HIV1 allows for evasion of host humoral and cellular immune responses and the development of resistance to anti-retroviral drugs)
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56
Q

superficial inguinal nodes

A
  • all skin from the umbilicus down including the anus (below the dentate.pectinate line) drains to the superficial inguinal LN…except for:
    • testes
    • glans penis (drains into deep inguinal LN)
    • (cutaneous) posterior calf (drains into depp inguinal LN)
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57
Q

lymph from the testes

A
  • fro the testes to the abdominal para-aortic (retroperitoneal) LN (paralleling blood supply from the testicular arteries which arise directly from the abdominal aorta
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58
Q

ISONIAZID and sideroblastic anemia

A
  • ISONIAZID inhibits pyridoxine phosphokinase (converts B6 to active form) =pyridoxine (Vit B6) deficiency
  • Pyridoxine (B6) active form is the cofactor for <delta>amino-levulinate synthase [catalyzes the rate-limiting step of heme synthesis]
    </delta><ul>
    <li>inhibition of this step can result in sideroblastic anemia--microcytic hypochromic anemia</li>
    </ul></delta>
  • this is why B6 is prescribed with ISONIAZID!
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59
Q

How is sideroblastic anemia diagnosed

A
  • BM examination with Prussian blue stain
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60
Q

Warfarin-induced skin necrosis

A
  • in pts with protein C or S (natural ANTI-coagulants) deficiency who are started on WARFARIN
  • after the initiation of WARFARIN a rapid drop in factor 7 and protein C levels
  • if there is already protein C deficiency, transien procoag/ANTIcoag imbalance is exaggerated=relative hypercoag state with thrombotic occlusion of the microvasculature and skin necrosis
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61
Q

acute intermittent porphyria

A
  • AD condition
  • PP: porphobilinogen deaminase deficiency
  • S/S: most pts remain asymptomatic
    • minority:
      • acute attacks with:
      • abdominal pain + vomiting
      • peripheral neuropathy
      • neuro-psych symptoms
      • reddish-brown urine
  • tx: IV glucose or heme preparations (hemin)
    • down regulate ALA synthase (rate-limiting enzyme in hepatic pathway of heme synthesis) activity
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62
Q

hereditary spherocytosis: epidemiology and CP

A
  • epi:
    • AD inheritance (approx 75%)
    • N. euro descent
  • CP:
    • hemolytic anemia
    • jaundice
    • splenomegaly
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63
Q

hereditary spherocytosis: lab findings

A
  • INC mean corpuscular Hgb concentration
  • spherocytes on peripheral smear
  • NEG Coombs test
  • INC osmotic fragility on acidified glycerol lysis test
    • d/t DEC SA:volume ratio
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64
Q

hereditary spherocytosis: tx and complications

A
  • tx: splenectomy
  • complications:
    • pigmented gallstones
    • aplastic crises f/m parvovirus B19 infection
65
Q

hereditary spherocytosis: pathophys

A
  • red cell cytoskeleton abnormalities
  • mc: plasma-membrane scaffolding proteins: spectrin and ankyrin
  • without the scaffolding, spherocytes are less deformable than nml RBCs and are prone to sequestration and subsequent accelerated destruction in the spleen
66
Q

ALA synthase

A
  • UPregulated by CYP450 inducers:
    • most anti-epileptics
    • griseofulvin
    • rifampin
  • DOWNregulated by heme and glucose
67
Q

hereditary spherocytosis: complications

A
  • pigmented gallstones
  • aplastic crises from parvovirus B19 infection
68
Q

Factor V Leiden

A
  • 1-9% Caucasians worldwide are heterozygote carriers
    • modified to resist activated Protein C
  • resulting HYPER-coaguable state predisposes to DVT=source of MOST PE
    • also: cerbebral vein thrombosis and recurrent preagnancy loss
  • mc c/o inherited thrombophiia
69
Q

What are the two main uses for DDAVP/vasopressin therapy

A
  • mild hemophilia A and type 1 von Wilebrand dz
    • INC circulating factor 7 (vWF non covalently attached, increases its stability) and endothelial secretion of vWF to stop bleeding
  • central diabetes insipidus and nocturnal enuresis
    • binds to V2R in renal tubular cells
    • leads to:
      • INC aquaporin chanels
      • INC water reabsorption
      • DEC urine output
70
Q

Metalloproteinases and Invasion

A
  • zinc-containing enzymes that degrade the ECM and basement membrane
  • composed mostly of: laminin and collagens 4 and 7
  • tissue remodeling and embryogenesis
  • also: tumor invasion through the BM and connective tissue
71
Q

Metalloproteinases and BM penetration

A
  • tumor cells DETACH from surrounding cells (process determined by DECreased expression of adehesion molecules-E-cadherins)
  • tumor cells ADHERE to the BM, facilitated by INC expression of laminin and otehr adhesion molecules
  • tumor cells INVADE the BM via enhanced secretion of proteolytic enzymes (metalloproteinases, cathepsin D protease)
72
Q

cytochrome c

A
  • mitochondrial enzyme
  • activates caspases
  • indirecty brings about cell death through intrinsic pathway apoptosis
73
Q

What are the two phases of apoptosis

A
  • initiation phase (two diff pathways)
    • protein-hydrolyzing caspases activated
  • execution phase
    • caspases bring about cell death by cleaving cellular proteins and activating DNAses
74
Q

What are the two diff pathways of the initiation phase of apoptosis

A
  • intrinsic (mitochondrial)
  • extrinsic (death receptor)
75
Q

Intrinsic (mitochondrial) pathway of stage 1-initiation of apoptosis

A
  • mit more permeable and pro-apoptotic substances are released into the cytoplasm in resp to stress or the cessation of survival signals
  • ANTI-apoptotic proteins (Bcl-2 and Bcl-x) that are in mit membranes and cytoplasm are replaced with PRO-apoptotic proteins (Bak, Bax, Bim)
  • PRO-apop allow INC permeability of mit=release of caspase-activating substances: cytochrome c
76
Q

extrinsic pathway of stage 1-initiation of apoptosis

A
  • engagement of death receptors on the cell surface: TNFR1 and Fas (CD95)
  • after cross linkage of Fas with its ligand mulecules of Fas come together and form binding site for a death-domain containing adaptor protein called FADD
  • FADD binds an inctive form of a caspase…cascade
77
Q

TTP clinical features

A
  • new onset neuro symptoms
  • hemolytic anemia with schistocytes
    • INC LDH
    • DEC haptoglobin
  • thrombocytopenia
    • INC bleeding time
    • nml PT/PTT
  • acute kidney injury
78
Q

HbS

A
  • d/t pt mut (valine at 6th position of beta chain for glutamic acid)
    • abnl beta chain-polymerize when deoxy or dehydrated
  • aggregates in the deoxygenated state!!
  • plymers form fibrou strands that reduce RBC membrane flexibility and promote sickling
  • under what conditions does sickling occur?
    • conditions assoc w/ anoxia: low pH and HIGH 2,3-BPG
    • inflexible erythrocytes predispose to microvascular occlusion and micro-infarcts
79
Q

What is the classic triad of Wiskott-Aldrich syndrome?

A
  • triad:
    • eczema
    • thrombocytopenia
    • combined B-lymphocyte and T-lymphocyte deficiency
  • dz onset is early in life
  • CP: repeated infections, espec by encapsulated organisms
80
Q

Calcium Chelation

A
  • pts who receive the equivalent of more than one body blood volume (5-6L) of whole blood transfusions –or– packed RBC over a pd of 24 hrs may develop: elevated plasma levels of CITRATE
    • ​CITRATE is a substance added to stored blood
    • CITRATE chelates calcium and magnesium and may reduce their plasma levels=paresthesias
81
Q

What is one of the mc causes of folate deficiency anemia

A
  • ALCOHOLISM d/t:
    • poor dietary intake
    • impaired folate absorption, utilization, and enterohepatic recycling
    • anemia within a few WEEKS
82
Q

pathophys of folate deificiency

A
  • reduced form of folic acid: tetrahydrofolic acid is necess for synthesis of AA, thymidine, and purine
  • impaired nucleotide syn=defective DNA production in blood cell precursors=abnml cell division and megaloblastic hyperplasia of the BM
  • peripheral blood smear: pancytopenia, hypersegmented neutrophils containing nuclei with >5 lobes
  • RBC abnormalities: ovalocytosis and macrocytosis: MCV>100 nanom^3
83
Q

paraneoplastic cachexia

A
  • cachexia:
    • anorexia
    • malaise
    • anemia
    • weight loss
    • generalized wasting d/t underlying systemic dz
  • mediated by TNF-alpha (“cachectin”)
    • along with IL-6 and IL-1beta
  • how?
    • suppresses appetite and INC BMR
84
Q

myeloma and amyloidosis

A
  • AL myloid forms d/t accumulation of monoclonal Ig LC
  • apple green on Congo red
  • contrib to renal failure in MM
  • (also deposited in heart, tongue, nervous system)
85
Q

malig EBV associations

A
  • Hodgkins and NHL (Burkitt)
  • nasopharyngeal carcinoma
86
Q

Hydroxyurea MOA

A
  • Hydroxyurea INC fetal Hg (Hb F) synthesis
  • reserved for pts with frequent pain crises
    *
87
Q

MTX and Folinic acid (LEUCOVORIN)

A
  • leucovorin can reverse the toxicity of MTX in non-cancerous cells in the GI mucosa and BM if administered at the approp time
  • Leuco=reduced form of folic acid that does NOT require the action of DHFR
  • when used in combo with 5-FU, Leucovorin potentiates the cytotoxic action of 5-FU (by binding thymidylate synthetase)
    • frequently used in CRC therapy regimens
88
Q

Beta thalassemia

A
  • DEC beta globin chain synthesis=hypochromic, microcytic anemia (MCV<80)
  • reduced beta glbin synthesis:
    • membrane damage
    • death of red cell precursors in BM (ineffective erythropoiesis)
    • lysis of circulating erythrocytes (extravascular hemolysis)
89
Q

Plummer-Vinson syndrome

A
  • characterized by:
    • dysphagia (esophageal web formation)
    • iron deficiency anemia
      • koilonychia (spoon-shaped nails)
      • shiny red tongue
      • most symptoms resolve with iron supplementation
90
Q

what are cells commonly seen in beta-thalassemia

A
  • small red cells with INC area of ctl pallor
  • alsooo:
    • anisopoikilocytosis (variation in size and shape)
    • target cells
    • teardrop cells
    • nucleated red cell precursors
    • basophilic stippling
91
Q

Hemophilia lab findings

A
  • PTT prolongation
  • nml bleeding time and nml PT
  • 8A and 9B (malibu and bitch neighbor)
92
Q

Hemophilia A and B clinical features

A
  • delayed/prolonged bleeding after mild trauma or procedure:
    • hemathrosis. hemophilic arthropathy
    • intramuscular hematomas
    • GI or GU tract bleeding
93
Q

von Willenbrand disease

A
  • mc inherited bleeding d/o
  • AD pattern of inheritance and variable penetrance
  • absence of vWfactor=
    • impaired platelet function (prolonged bleeding time)
    • coagulation pathway abnormalities (d/t DEC factor 8 activity)–prolonged PTT)
94
Q

How do you spot Plasmodium infection on a peripheral blood smear

A
  • Giemsa staining
  • RBC have multiple small rings (trophozoites) and banana-shaped gametocytes
95
Q

Aspirin and NSAIDS reversible or nah

A
  • Aspirin is a NSAID that IRREVERSIBLY inhibits COX1 and 2 via ACETYLATION
  • other NSAIDS (diclofenac, ibuprofen, indomethacin) REVERSIBLY inhibit
96
Q

telomerase

A
  • RNA-dependent DNA polymerase that synthesizes telomeric DNA sequences that can replace lost chromosomal ends of the telomers
  • cancer cells typically contain INC telomerase activity to allow for continued proliferation
97
Q

Raltegravir

A
  • integrase inhibitor
  • disrupts the ability of dbl-stranded HIV DNA to integrate into the host cells chromosomes=prevent host cellular machinery from transcribing viral mRNA
98
Q

what is the area postrema/chemorceptor trigger zone (CTZ)

A
  • in the fourth ventricle
  • area postrema has a CTZ
  • it can respond to many NT, drugs, toxins
  • sends info to nucleus tractus solitarius (NTS) in the medula
99
Q

what are inputs for the NTS

A
  • area postrema
  • GI tract (via vagus)
  • vestibular system
  • CNS (meninges, hypothalamus)
100
Q

where do neurons from the NTS project

A

other medullary nuclei and coordinate the vomiting process

101
Q

what are the 5 main receptors that regulate the vomiting reflex

A
  1. M1 muscarinic
  2. D2 dopaminergic
  3. H1 histaminic
  4. 5-HT3 serotonergic
  5. neurokinin 1 (NK1) receptors
102
Q

in pts with sickle cell anemia and other chronic hemolytic d/o what is the mc c/o an anaplastic crisis?

A

infection of erythroid progenitor cells with parvovirus B19 (a non-enveloped ssDNA virus)

103
Q

motion sickness, hyper-emsis gravidarum (Promethazine)

A
  • antimuscarnics (anticholinergics): scopolamine
  • antihistamines:
    • Diphenhydramine
    • Meclizine
    • Promethazine
104
Q

dx for chemotherapy-induced emesis

A
  • DA-R ANT-agonists:
    • Prochlorperazine
    • Metoclopramide
  • Seretonin (5-HT3)-R ANT-agonists
    • Ondansetron
    • Granisetron
  • Neurokinin 1-R ANT-agonist
    • Aprepitant
    • Fosaprepitant
105
Q

What is the mc c/o primary (hereditary) hemochromatosis?

A
  • HFE protein mutations
    • inactivation of the HFE protein results in DEC hepcidin synthesis by heptocytes anddd INC DMT1 expression by enterocytes (**hepatocytes detect falsely low iron levels)
    • ^^^leads to–>iron overload
  • pts at INC risk for:
    • liver cirrhosis
    • hepatocellular carcinoma
106
Q

nml HFE function

A
  • interacts with transferrin receptor to INC endocytosis of the iron-transferrin complex
  • once inside cell, transferin degraded, released iron added to labile iron pool
    • controls expression of proteins involved in iron absorption and storage
107
Q

when do pts develop the classic triad of HFE protein mutations

A
  • when body iron levels exceed 20g:
    • micronodular cirrhosis
    • diabetes mellitus
    • skin pigmentation (bronze diabetes)
  • at INC risk for: hepatocellular carcinoma, CHF, testicular atrophy/hypogonadism
108
Q

what is the tx for cyanide poisoning?

A
  • NITRITIES
    • oxidizing agents
    • induce methemoglobinemia
    • methemoglobin contains ferric (Fe3+) instead of ferroUS (Fe2+)
    • CN binds to ferric more avidly than to mitochondrial cytochrome c oxidase enzyme, thus diminishing cyanide’s toxic effect
109
Q

s/s cyanide poisoning

A
  • reddish skin discoloration
  • tachypnea
  • HA
  • tachycardia
  • NV
  • confusion
  • weakness
  • can progress to seizures and CV collapse
  • d/t inability of tissue to extract arterial oxgen:
    • severe LA + narrowing of venous-arterial PO2 gradient
110
Q

What is methemoglobin

A
  • hemoglobin with ferric iron (Fe3+)
  • incapable of carrying oxygen, BUT has high affinity for cyanide
  • binds and sequesters CN in th blood=inhibit it from banging a/r with cytochrome oxidase=limits its toxic effects
111
Q

what are three antidotes for cyanide poisoning

A
  1. **inhaled amyl nitrite
  2. hydroxycobalamin (Vit B12 precursor)
  3. sodium thiosulfate
112
Q

What are anaplastic cells?

A
  • neoplastic cells that demonstrate a complete lack of differentiation
113
Q

What are the (FIVE) main features of anaplastic tumors?

A
  1. loss of cellpolarity with complete disruption of nml tissue architecture
    1. cells coalesce into sheets/islands in a disorganized/infiltrative way
  2. significant variation in:
    1. shape/size of cells (cellular pleomorphism)
    2. nuclei (nuclear pleomorphism)
  3. disproportionately large nuclei (high N:C ratio) that are often deep-staining (HYPER-chromatic) with abundant, coarsely-clumped chromatin and large nucleoli
  4. numerous, often abnml mitotic figures
  5. giant, multinucleated tumor cells
114
Q

define metaplasia and give an example

A
  • metaplasia=process of switching from one differentiated cell type to another
  • often occurs in response to irritants (tobacco smoke, gastric acid)
  • ex: bronchial epithelial cells undergoing phenotypuc switch from columnar epithelium to squamous epithelium
115
Q

AML peripheral blood smear

A
  • very large nucleated cells with scant cytoplasm…BLAST CELLS
    • in the cells: linear, purple-red inclusions=AUER RODS
116
Q

AML CP

A
  • complications of PAN-cytopenia
    • fatigue from anemia
    • bruising/bleeding from thrombocytopenia
    • infections from possible functional neutropenia despite leukocytosis
  • median white blood ct: 15k mm^3 (nml: 4k-10k)
117
Q

WBC differential from highest to lowest:

A
  • neutrophils like M.E. better
  • neutrophils: 55-60
  • lymphocytes: 25-35
  • monocytes: 5
  • eosinophils: 2
  • basophils: <1
118
Q

What are five important neutrophil chemotactic agents?

A
  1. C5a
  2. IL-8
  3. LTB4
  4. kallikrein
  5. platelet-activating factor
119
Q

HEME is a PORPHYRIN

A
  • synthesized in the liver for use in the cytochrome p450 enzyme system AND in the BM for Hgb
  • deficiency in any of the enzyme respondible for porphyrin synthesis can result in porphyria
  • CP result from accumulation of porphyrin precursors in blood, tissues, urine
  • AIP attakcs are d/t accumulation of ALA and PBG
120
Q

what causes an accumulation of ALA

A
  • ALA synthase induction, typically precipitated by:
    • certain medications:
      • Phenobarbital
      • Griseofulvin
      • Phenytoin
    • alcohol use
    • smoking
    • progesterone (eg puberty)
    • low-calorie diet
121
Q

(FOUR) necessary components of PCR

A
  1. primers that are complementary to regions fo DNA flanking the segment of interest
  2. thermostable DNA polymerase
  3. deoxynucleotide triphosphates
  4. source DNA template strand
122
Q

three steps of DNApolymerase in PCR

A
  1. denature
  2. anneal
  3. elongation
123
Q

which signal-transduction pathway is activated when growth factor binds to its receptors?

A
  • PI3k/Akt/mTOR
      1. GF binds receptor tyrosine kinase
    • auto-phosphorylation of specific tyrosine residues within the receptor
    • phosphotyrosine residues activate PI3k which phosphoryltes PIP2 (located in plasma membrane) to PIP3
      • activation of Akt (protein kinase B)
    • Akt activates mTOR
    • mTOR translocates to the nucleus and induces genes involved in:
      • cell survival
      • ANTI-apoptosis
      • angiogenesis
    • mTOR activation is inhibited by PTEN (tumor suppressor protein that removes the phosphate group from PIP3)
124
Q

inositol phospholipid pathway

A
  • uses Gq proteins that stimulate hydrolysis of membrane-bound phospholipids via phospholipase C
  • pathway INC cytoplasmic Ca2+ levels through IP3-mediated Ca2+ efflux from the ER
125
Q

what is the clinical presentation of hemolytic anemia

A
  • anemia
  • elevated LDH (lactate dehydrogenase)
  • indirect HYPER-bilirubinemia
126
Q

What is the difference between hereditary scperocytosis and autoimmune hemolytic anemia?

A
  • similar findings:
    • indirect HYPER-bilirubinemia
    • elevated LDH
    • spherocytes on peripheral blood smea
  • difference with AIHA:
    • NOT heritable
    • positive direct antiglobulin (Coombs) test
    • propensity to develop a.i dz (eg SLE)
127
Q

What are triggers of G6PD deficiency

A
  • drugs:
    • sulfonaide
    • antimalarials
  • fava beans
  • infectious:
    • viral hepatitis
    • pneumonia
    • typhoid
128
Q

pentose phosphate pathway (HMP shunt)

A
  • generates:
    • NADPH-for use in reductive rxns
    • ribose-5-phosphate, precursor for synthesis of nucleotides
  • two types ofr rxns: oxidative (IRREVERSIBLE) and nonoxidtive (reversible!!)
  • NON-oxi:
    • rib5P excess=glycolytic intermediates used for ATP generation
    • rib5P low: pathway REVERSES, uses transketolase and transaldolase to convert glycolytic intermediates to rib5P!!
129
Q

What is a major difference between direct factor 10a inhibitors and direct thrombin (2a) inhibitors

A
  • 10a INC:
    • NO EFFECT on thrombin time
    • PT
    • activated PTT
  • 2a (thrombin) INC:
    • thrombin time
130
Q

isotype switching

A
  • occurs in germinal centers of LN
  • requires interaction of the CD40-R on B-cells with the CD40 ligand (CD154) expressed by activated T-cells
  • IgG=main serum Ig of the secondary resp
131
Q

negative selection

A
  • deletio of T-cell clones that strongly bind to self-MHC antigens
  • occurs in the fetal thymus and contributes to teh development of tolerance to one’s own antigens
132
Q

When are mature B-cells exposed to antigens?

A
  • when they leave the BM and migrate to lymphoid organs and peripheral tissues
  • once activated, there are two pathways:
    • short lived plasma cells that release Ag-specific IgM through a T-cell independent process
    • most of them: migrate to lymphoid follicles in LN cortex, form GC (site of B-cell proliferation d/r immune response)
133
Q

what are thalassemias

A
  • disorders presenting with reduced -or- absent globin chain production
  • almost all thalassemia cases result in hypO-crhomia and microcytosis (low MCV)
134
Q

chronic alcoholics and megaloblastic macrocytic anemias

A
  • nutritional deficiency of vit B12 or folate
  • impaired synthesis of purine and pyrimidine bases
    • aka diminished thymidine synthesis
135
Q

where does heme synthesis occur

A
  • partly in the mitochondria (first and final three steps) and cytoplasm
  • heme in synthesized principally in:
    • erythrocyte precursor cells (in BM)
    • hepatocytes (use heme in microsomal cytochrome P450 system)
136
Q

bony metastasis

A
  • two characterizations:
    • osteolytic (lucent)-d/t osteoCLAST stimulation=aggressive ca
    • osetoblastic (sclerotic)-d/t osteoBLAST=more indolent course
  • bony pain in older man with osetoBLASTic lesions on imaging=highly suspicious for prostate ca
  • renal cell ca bone mets are commonly osteoLYTIC
  • myreloma cells suppress osteoblasts would cause osteoLYTIC lesions
137
Q

(FIVE) osteoLYTIC bone mets

(THREE) osteoBLASTIC

(TWO) mixed

A
  1. multiple myeloma
  2. non-small cell lung ca
  3. NHL
  4. RCC
  5. melanoma
  6. prostate ca
  7. small cell lung ca
  8. hodgkin
  9. GI
  10. breast
138
Q

proto-oncogenes (1-hit GAIN of function)

A
  • RAS (GTP-binding protein)
    • cholangiocarcinoma
    • pancreatic adenocarcinoma
  • MYC (TF)
    • burkitt lymphoma
  • ERBB1 (EGFR)
    • lung adenocarcinoma
  • ERBB2 (HER2)
    • breast cancer
  • ABL
    • CML
  • BRAF
    • hairy cell leukemia
    • melanoma
139
Q

tumor suppressor genes (2-hit LOSS of function)

A
  • BRCA1/2 (DNA repair genes)
    • breast and ovarian ca
  • APC/beta-catenin (Wnt signaling pathway)
    • colon, gastric, and pancreatic ca
    • familial adenomatous polyposis (FAP)
  • TP53 (genomic stability)
    • **most cancers**
    • Li-Farumeni syndrome
  • RB (G1/S transition inhibitor)
    • retinoblastoma
    • osetosarcoma
  • WT1 (urogenital differentiation)
    • Wilms tumor
  • VHL (ubiquitin ligase component)
    • RCC
    • VHL syndrome
140
Q

tumor suppressor genes are involved in (FOUR) processes

A
  1. DNA repair
  2. cellular differentiation
  3. checkpoint control of the cell cycle
  4. transcription factor regulation
141
Q

HEPCIDIN-acute phase reactant

A
  • synthesized by LIVER
  • acts as central regulator of iron homeostasis
  • synthesis INC by:
    • high iron levels
    • inflamm conditions
  • levels lowered by:
    • hypoxia
    • INC erythropoiesis
  • influences body iron storage thru interaction with FERROPORTIN (TM protein, transfers intracellular iron to circulation)
  • **upon binding hepcidin, ferro is internalized and degraded=
    • DEC intestinal iron absorption
    • inhibits release of iron by macrophages
142
Q

8:14

A

Burkitt lymphoma (c-myc activation)

burke ATE 14 c nugs

143
Q

9:22 Philly

A

CML (BCR-ABL)

brooke and abel got 9 camels when they turned 22

144
Q

11:14

A

mantle cell lymphoma (cyclin D1 activation)

the clock on the mantle is lucky plus 3

145
Q

14:18

A

follicular lymphoma (BCL-2 activation)

dbl 7 and 9

146
Q

15:17

A

M3 type of AML

wizard AML started at 15, was an M3 by 17

147
Q

GBM macro and micro

A
  • mc primary brain neoplasm in adults
  • macro:
    • areas of necrosis and hemorrhage
    • poorly demarcated from surrounding tissue
  • micro:
    • pseudopalisading necrosis (foci of necrosis surrounded by tumor cells)
    • new vessel formation
    • small round cells, bizarre giant cells, large number of mitoses
148
Q

THREE common causes of acquired thrombocytopenia

A
  • INC platelet consumption
  • sequestration
  • and/or destruction
149
Q

ITP (immune thrombocytopenic purpura)

A
  • a.i. destruction of platelets by anti-platelet Ab
    • likely igG auto-Ab vs. platelet membrane glycoproteins GP2b/3a
  • peripheral blood smear: isolated thrombocytopenia
  • tx: systemic immunosuppression (corticosteroids)
  • sometimes assoc w/ HIV or Hep C
150
Q

OSA and secondary polycythemia

A
  • OSA is characterized by recurrent episodes of asphyxia during slep
  • peritubular cells in the renal cortex sense hypoxia and respond by releasing erythropoietin into the bloodstream
    • deficient erythropoietin production is the reason many pts with CKD develop anemia
  • erythropoietin stimulates erythrocyte production by binding to erythropoietin receptors on erythrocyte precursors in the BM=secondary polycythemia
151
Q

cyclophosphamide and ifosfamide SE

A
  • hemorrhagic cystitis
  • caused by urinary excretion of toxic metabolite acrolein
  • prevented by:
    • aggressive hydration
    • bladder irrigation
    • admin of MESNA-sulfhydryl compound that binds acrolein in the urine
152
Q

Iron deficiency secondary to menstrual blood loss-LABS

A
  • DEC BM iron stores (ferritin and heosiderin LOW)
  • DEC serum ferritin
    • INC serum total iron binding capacity (TIBC)–reflecting INC serum transferrin
  • DEC serum iron concentration
  • DEC blood Hgb
  • microcytic, hypO-chromic RBC
153
Q

ferritin and transferrin

A
  • ferritin:
    • cellular iron storage protein
    • marker of iron stores
    • serum ferritin is DEC in iron deficiency, ELEVATED in iron overload
    • acute phase reactant, may be elevated in pts with infections or inflamm dz
  • transferrin
    • transports iron through the plasma
    • iron deficiency=make more transferrin
154
Q

Whats so special about Type O moms

A

Ab are predom IgG–can cross placental and cause hemolysis in the fetus

155
Q

All the directions of all the blots

A
  • Northern: specific (m)RNA
  • Southern: specific DNA in an unknown sample
  • microarray-similer to south and north, involves hybridization of a large number of probes at once (genomic DNA or cDNA)
  • Southwest: DNA-binding proteins
  • Western: proteins
156
Q

what is the correlation between half-lives and a transient hypercoaguable state

A
  • occurs d/r first few days of warfarin therapy
  • in addition to inhibiting Vit K-dependent clotting factors, warfarin also DEC carboxylation of Protein C and S
    • C and S normally ANTI-coag through deactivation of factors 5 and 8
  • Prot C has a short half-life=anti coag activity quickly reduced when warfarin therapy starts
  • now have pro-coag form DEC protein C and pro-coag from persistent clotting factor 2,9,10
  • tx: overlapping co-admin of heparin (heparin bridge)
157
Q

DIC vs. TTP-HUS

A
  • DIC:
    • pts bleed
    • coagulation cascade activated
    • PT and PTT prolonged
    • low fibrinogen and INC FDP
  • TTP-HUS
    • usually do NOT bleed
    • only platelets are activated
    • nml PT and PTT
    • nml fibrinogen
158
Q

What does the number of reticulocytes in the peipheral blood indicate

A
  • indication of how effectively the BM is producing RBCs and thus responding to anemia
  • low or nml retic ct in setting of anemia=underproduction anemia

BOARDS! (14 decks)

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