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Clinical Med > postmidterm 2 > Flashcards

postmidterm 2 Flashcards

1
Q

what are reticulocytes?

A

early RBCs that still have nucleus

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2
Q

PT (prothrombin time) / INR (international normalized ratio) tests what and what pathway? what med would make you test this pathway?

A 
Tests extrinsic coagulation pathway (VII); (common pathway V, X, II)
**Time (seconds) for clot to form
Measures:
Production of coagulation proteins
-Liver function
-Vitamin K dependent 
monitor in warfarin or coumadin therapy
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3
Q

PTT (partial thromboplastin time) tests what and what pathway? what med would make you test this pathway?

A

Tests intrinsic pathway (XI, IX, VIII); (common pathway V, X, II)
Measures:
**Production of coagulation proteins
Antibody interference with coagulation (lupus “anticoagulant”)
**heparin therapy

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4
Q

give an example of how physical injury can cause accelerated blood cell destruction

A

mechanical heart valve can shear RBCs

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5
Q

Erythropoietin produced by kidney in response to:

A
  • Anemia (low red blood cell mass)
  • Hypoxemia (low oxygen delivery)
  • -High altitude
  • -Lung disease: smokers
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6
Q

T/F: mild anemia is usually asymptomatic

A

true

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7
Q

T/F: anemia can trigger angina

A

yes with underlying heart disease

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8
Q

4 main anemia categories:

A
  • iron deficiency: microcytic
  • vit B12 def: macrocytic
  • sickle-cell: normocytic
  • beta-thalassemia: microcytic
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9
Q

what are some systemic complications of anemia?

A
  • Stomatitis: inflamm of mouth, tongue atrophy
  • Dysphagia, esophageal web
  • Nail changes (koilonychia - flat, spoon-shaped)
  • Pica: dirt eating
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10
Q

what are some ocular complications of anemia?

A
  • Conjunctival pallor
    • Conjunctival/retinal flame hemorrhages
    • Blue sclerae
    • Retinal venous distension
    • Retinal edema, exudates
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11
Q

what are some lab findings in iron def anemia?

A

Microcytic, hypochromic anemia

  • Low serum iron level (< 50 ug/dl)
  • High serum iron-binding capacity (> 400 ug/dl)
  • Low serum ferritin (< 20 ng/ml)
  • Decreased iron stores on marrow biopsy
  • *reticulocytes should be elevated to compensate
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12
Q

pernicious anemia:

A

destroyed gastric parietal cells

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13
Q

what role does vit B12 play in RBC formation?

A

critical in conversion of homocysteine to methionine for RBC creation

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14
Q

how is vit B12 absorbed?

A

B12 binds to intrinsic Factor (IF: secreted by gastric parietal cells) in the stomach

IF + B12 complex is absorbed in the distal ileum

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15
Q

what are some possible causes of vit B12 def?

A 
veganism
alcoholism
Pernicious anemia (autoimmune destruction of parietal cells)
Gastrectomy
Inability to absorb IF + B12
Ileal resction, ileitis, celiac disease
Digestive enzymes absent
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16
Q

what are some neurologic side effects of vit B12 def

A
  • Numbness, other sensory abnormalities
    • Weakness, ataxia
    • Depression, memory loss, dementia
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17
Q

what are some ocular side effects of pern anemia def

A
  • Retinal, choroidal hemorrhages
  • Optic neuropathy
  • Ophthalmoplegia (rare)
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18
Q

lab findings for pern anemia def?

A
  • Macrocytic, megaloblastic anemia
    • Pancytopenia
      • Low serum B12 level
      • Elevated methylmalonoic acid and homocysteine
      • (Abnormal Schilling test)
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19
Q

what else should you check for with pernicious anemia?

A

autoimmune or gastric carcinoma

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20
Q

what is erythroid aplasia? what are some causes?

A

many causes, but RBCs not made properly
causes:
**Parvovirus B19 (Fifth disease / erythema infectiosum)
Infectious
Hepatitis viruses
HIV
-Iatrogenic (caused by meds)-usually reversible

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21
Q

what is Parvovirus B19 (Fifth disease / erythema infectiosum)?

A
  • Slapped cheek appearance with reticular peripheral rash in children
  • Arthralgias in adults-not actually arthritis
  • can lose baby
  • Aplastic crisis in sickle cell disease?
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22
Q

what causes sickle cell?

A

Mutation in hemoglobin beta chain (Glu6 -> Val6)

-Combination with normal a-chains produces Hemoglobin S

23
Q

what are some systemic assoc with anemia?

A
  • Splenic infarction
  • Recurrent bacterial infections (lung, bone, etc.)
  • Cerebrovascular events
  • Growth retardation
  • Liver, renal disease
  • Osteonecrosis
  • Recurrent aplastic marrow crises
24
Q

what are some ocular assoc with anemia?

A
  • Scleral icterus
  • Comma-shaped conjunctival veins
  • Retinal vascular occlusions, edema, atrophy
  • Neovascularization, retinal detachment
  • Hemorrhagic glaucoma, rubeosis iridis
  • Retinal, vitreous hemorrhages
  • Angioid streaks
  • “Sunburst” chorioretinal scars
25
Q

what is sickle cell “disease”

A

Milder disease
Higher blood viscosity
Retinopathy may be more severe (than SS)

26
Q

what is thalassemia?

A
  • Unbalanced production of a- and b-chains

- Accelerated destruction of erythrocytes within marrow

27
Q

what is Relative polycythemia?

A

Volume depletion (e.g. dehydration)

28
Q

what are 2 drug induced causes of polycythemia?

A 
EPO doping (sports)
androgen overuse
29
Q

what are some systemic effects of polycythemia?

A

Chronic tissue hypoxia:

  • Chronic lung diseases -Smoking / chronic CO exposure
  • Arteriovenous shunts -Abnormal Hgb (high O2 affinity)
  • High altitudes
30
Q

what is Polycythemia Vera?

A

A clonal proliferation of early hematopoietic stem cells generally seen in older patients (60-80 yo)

  • Inappropriate overproduction of RBCs, WBCs & platelets
  • Increased blood viscosity
  • Despite increased platelets, function often ineffective (bleeding)
31
Q

what clinical side effects do you see with Polycythemia Vera?

A

Facial plethora=red face Headache, dizziness, malaise
Pruritis (especially feet) Cerebrovascular events
Thrombophlebitis=clots in veins
Epistaxis, easy bruising
Hepatosplenomegaly Extramedullary hematopoiesis

32
Q

what are some ocular features of polycythemia vera

A
  • Conjunctival, retinal venous engorgement
  • Congested (“dusky red”) fundus
  • Retinal arterial, venous occlusions
  • Retinal hemorrhage, neovascularization
  • Ischemic optic neuropathy
  • Papilledema
33
Q

what’s one major cause of luekopenia?

A

drug-induced (just know there are many)

  • Antibiotics
  • NSAID’s
  • Anti-thyroid drugs
  • Antihypertensives
  • Thiazide diuretics
  • Anticonvulsants
  • Alkylating agents
34
Q

what are some causes of leukemia?

A
  • Mutations of cellular oncogenes – genetic (Down’s etc.), somatic, viral (HTLV), radiation, chemotherapy
  • Progressive infiltration/replacement of marrow, disruption of normal hematopoiesis -> bleeding, infection, anemia
35
Q

what are the systemic side effects of leukemia?

A
  • Anemia: Fatigue, headache, anorexia, weight loss
  • Abnormal bleeding (epistaxis, bleeding gums, ecchymosis)
  • Infection (often bacterial)
  • Veno-occlusive events, bone pain
  • Infiltration of liver, spleen, lymph nodes, skin (rash)
36
Q

what are the ocular side effects of leukemia?

A
  • Conjunctival, retinal hemorrhages
  • Retinal vascular occlusions
  • Orbital, conjunctival, retinal infiltration
  • Orbital chloroma (AML)??
37
Q

what are some ocular side effects of lymphoma?

A
  • Lid, conjunctival infiltrates
  • Orbital, lacrimal gland infiltration
  • Proptosis, diplopia. optic nerve compression
38
Q

Hodgkins vs non-hodgkins lymphoma?

A

Hodgkin’s lymphoma diagnosed with Reed-Sternberg cell on pathology

39
Q

Waldenstrom’s macroglobulinemia:

A

excess IgM secretion -Hyperviscosity syndrome (IgM)

40
Q

what are some systemic side effects of multiple myeloma?

A
  • Fatigue, weight loss, back pain, headache
  • Anemia
  • Abnormal bleeding, recurrent infection
  • Hypercalcemia, bone erosion
  • Renal failure
41
Q

what are some ocular side effects of multiple myeloma?

A
  • Crystalline deposits in cornea, conjunctiva
  • Band keratopathy, pars plana cysts
  • Orbital infiltration, papilledema, ophthalmoplegia
  • Retinal engorgement, edema, exudates, hemorrhages
  • Retinal vascular occlusions
42
Q

how does aspirin vs NSAIDs affect platelet function?

A

Aspirin (irreversible inhibition), NSAIDS (reversible)

43
Q

when do you see thrombocytopenia vs thrombocytosis?

A

Thrombocytopenia=low platelet

  • Idiopathic Thrombocytopenic Purpura (ITP)=kids
  • Thrombotic Thrombocytopenic Purpura (TTP)

Thrombocytosis=high platelet

  • Infection, inflammation
  • Trauma, blood loss (reactive)
  • Post-splenectomy (spleen stores platelets)*
44
Q

what are some ocular side effects of thrombocytopenia?

A
  • Conjunctival petechiae
  • Orbital, retinal hemorrhages
  • Ophthalmoplegia (orbital or CNS hemorrhage)
  • Stroke syndromes (CNS hemorrhages)
  • Ischemic optic neuropathy (systemic hypotension)
45
Q

what is von willebrand’s disease?

A

Inherited bleeding disorder
-VW factor functions in:
Platelet plug formation
Platelet adhesion to site of vascular injury
*so basically these people can’t form platelet plug, although platelet count is normal

46
Q

what is hemochromatosis?

A

hereditary disorder with excessive absorption of dietary iron /abnormal accumulation of iron in tissues

47
Q

what are some clinical features of hemochromatosis?

A
  • Skin pigmentation
  • Arthritis
  • Hepatomegaly *splenomegaly
  • Cardiomyopathy -Diabetes, other endocrinopathy
  • Conjunctival, lid-margin hyperpigmentation
48
Q

T/F: genetics is not involved in hemochromatosis

A

false, it is involved; common in caucasians and north american ancestry

49
Q

what should you rule out in the context of DM with liver disease?

A

hemochromatosis

50
Q

Excesses of procoagulant proteins is assoc with what factor?

A

Factor V Leiden

51
Q

Deficiencies of natural anticoagulant proteins is assoc with what proteins?

A

protein S and C

52
Q

Protein C does what?

what are these patients at risk for?

A

Inactivates Factors Va and VIIIa, which are trying to clot

  • protein C is a vitamin K dependent protein
  • at risk for thrombosis, especially:
  • Deep vein thrombosis (DVT) in 65%
  • Pulmonary embolism (PE) in 40%
53
Q

what is the function of Factor V leiden? what happens when it is mutated?

A

Factor V binds to platelets, serves as receptor for Xa
Inactivated by activated Protein C
-in mutation, protein C can’t bind and deactivate it, creates hypercoagulable state
***Most common genetic thrombophilias
BCP risk is additive, also at risk for spontaneous abortion

Clinical Med (10 decks)

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