High Yield Facts Flashcards
What cells produce surfactant
Type 2 pneumocytes
How does pulmonary HTN present on cardiac exam
Loud P2. LUSB
What kind of emphysema is seen in smokers?
Centriacinar which effects upper lobes
“Smoke rises”
What cell reacts to silica in silicosis?
Macrophages
Leads to inflammation followed by fibroblasts and collagen deposition
High prevalence of TB and bronchogenic carcinoma
Immune response involved in sarcoidosis
Accumulation of TH1 CD4+ helper T cells
Also involves IL2 (stimulates TH1 proliferation) and IFN gamma (macrophage activation)
Classic sarcoidosis findings
Hilar lymphadenopathy on CXR Cough + SOB African American female Often asymptomatic May have high ACE levels and hypercalcemia
Electrolyte disturbance in sarcoidosis
Hypercalcemia
Elevated 1 alpha hydroxylase activity in alveolar macrophages leads to increased active vitamin D
what cells are involved in regeneration of the lung following lobar pneumonia?
Type 2 pneumocytes
pneumonia + hyponatremia
most likely legionella
immune response in TB
Cell mediated –> TH1
CD4 T cell activation, INF gamma release–> macrophage activation and cytotoxic C cells
Primary TB findings on CXR
Hilar lymphadenopathy (like sarcoidosis)
Ghon complex
Seen in primary TB
Ghon foci + lymph nodes –> subpleural granuloma seen in mid to lower lung. Called a ranke complex once calcified
CXR in secondary TB
Cavitation in upper lobes
due to caseous and liquefactive necrosis
Delayed separation of the umbilical cord
LAD1 (leukocyte adhesion deficiency type 1)
First step of hemostasis and mediators involved
transient vasoconstriction of the vessel mediated by reflex neural stimulation and endothelin release
Where does von willebrand factor come from
Weibel-Palade bodies of endothelial cells
Alpha granules of platelets
Tromboxane A2 is a synthesized by what?
Platelet cyclooxygenase
Cause of TTP
Acquired autoantibody against ADAMTS13 - enzyme responible for vWF multimer degradation. results in impaired platelet adhession–>microthrombi
Major cause of HUS
E coli O157:H7
What happens to PT/PTT in HUS and TTP?
NORMAL -coagulation cascade not effected
Effect of Aspirin on cyclooxygenase
irreversibly inactivates it
How to distinguish Hemophilia A and coagulation factor inhibitor
Mixing study - patient plasma + normal donor plasma
Hemophilia A - PTT will correct
Inhibitor: PTT will remain elevated
Most common inherited coagulation disorder
Von willebrand Disease
Von willebrand disease test
Abnormal ristocetin test - induces platelet aggregation by causing vWF to bind platelet GPIb. Lack of vWF = no agglutination
Von willebrand treatment and mechanism
desmopression (ADH analog): increases vWF release from weibel-Palade bodies in endothelial cells
Coagulation factors requiring vitamin K
2, 7, 9, 10
rattlesnake bite
venom activates coagulation cascade –> DIC
Best screening test for DIC
D-dimer
product of lysing fibrin crosslinks (real final step after clotting -cause healing). DIC = massive amounts of microthrombi so you have increased fibrinolysis and thus increased D-dimer
How do you differentiate disorders of fibrinolysis from DIC?
DIC will have elevated D-dimer and low platelets
DoF: d-dimer normal because cleaving serum fibrinogen rather than fibrin in clots. also normal platelet count
Effective of elevated homocysteine and how it occurs
Vit B12 deficiency - cant take methyl from THF and transfer it onto homocysteine, which normally results in cystathionine. Thus homocysteine accumulates
High levels damages endothelium and leads to thrombosis
Genetic cause: Cystathionine beta synthase deficiency
Major drug to be concerned about giving in protein C and S deficiency
Warfarin Skin necrosis risk is increased
Warfarin blocks vit K effects
Protein C and S are effected first followed by 2, 7, 9, 10
Since already deficient in C and S, drops to severely low levels if given warfarin so very low ratio compared to other factors. thrombosis ensues
run heparin at same time when initially given
What makes amniotic fluid thrombotic?
LOADED with tissue thromboplastin
Treatment for neutropenic patients receiving chemo?
GM-CSF or G-CSF - boosts granulocyte production
Most sensitive cell to radiation?
Lymphocytes
Describe “Left Shift” seen in leukocytosis
release of pools of neutrophils including immature neutrophils (left shift) from bone marrow. Immature forms lack the Fc receptors (CD16). important because Fc allows interaction with Ig
SO: DECREASED CD16
mechanism of Eosinophilia in hodgkins lymphoma
increased IL5
Basophilia is associated with what disease?
CML
What normally causes lymphocytic leukocytosis, and what is the exception to the rule
Viral infections - T lymphocytes undergo hyperplasia in response to virally infected cells
Bordetella pertussis infection is the exception - bacteria produces a lymphocytosis promoting factor whcih blocks circulating lymphocytes from leaving the blood to enter the lymph node
what region of lymph nodes and spleen is affect in infectious mononucleosis
Nodes:Paracortex because this is where the T cells are. IM causes T cell hyperplasia (because viral infection - CD8 response)
Spleen: PALS hyperplasia in white pulp–>splenomegaly
EBV and CMV cause IM
Classic presentation of Infectious mononucleosis but negative monospot test suggests what?
EBV is not the cause. Likely CMV
Major complication of infectious mononucleosis to worry about?
splenic rupture. patients are advised to avoid contact sports for the next year to prevent this
Leukemia and down syndrome
ALL seen after the age of 5
Acute megakaryobkastic leukemia seen after age of 5
Acute promyelocytic leukemia genetic cause and mechanism
t(15;17) - RAR (retinoic acid receptor) mutation prevents promyelocyte (blast) maturation
also risk for DIC because of tons of auer rods
APL treatment
ATRA - all trans retinoic acid - vit A derivative that binds altered receptor and causes blasts to mature
Acute monocytic leukemia key presentation
infiltrate the gums
Cause of splenomegaly in Hairy cell leukemia
RED PULP accumulates hairy cells (normally would expect it to be white pulp
Hairy cell leukemia treatment
2-CDA (cladribine). ADA inhibitro so adenosine accumulates to toxic levels in neoplastic B cells
Common cause of Adult T T cell Leukemia/Lymphoma - ATLL
HTLV-1 - seen in Japn and carribean
Classic presentation of Adult T T cell Leukemia/Lymphoma (ATLL)
lytic bone lesions and hypercalcemia and RASH
Rash points you toward ATLL and away from multiple myeloma (which also presents with lytic bone lesions and hypercalcemia)
Where is iron absorbed
Duodenum
Why does gastrectomy cause Iron deficiency?
Less acid. Means iron cant stay in Fe2+ form as easily and changes to Fe3+. this isnt as readily absorbed
How does iron deficency anemia initially appear on blood smear
As a normocytic anemia. Bone marrow notices less iron is available to make heme. So just makes less RBCs in roder to keep popping out normal cells. As things progress is when you end up with microcytic anemia.
Explain FEP test and Iron deficiency anemia
Free erythrocyte protoporphyrin will be high
Good test for this type of anemia because Iron + protophorohyrin is what makes heme. Since decreased iron for binding, more protoporphyrin is floating free
Also elevated in ACD - anemia of chronic disease
Plummer-Vinson Syndrome
iron deficiency anemia with esophageal web. Presents with anemia, dysphagia (web catches food), and beefy red tongue
Where is iron located in sideroblastic anemia?
Trapped in the mitochondria - due to lack of protoporphyrin but iron keeps getting transferred in despite having nothing to combine with
Most common cause of congenital sideroblastic anemia?
ALAS defect
Most common acquired causes of sideroblastic anemia?
Alcoholism - mitochondrial poison
Lead poisoning - inhibits ALAD and ferrochelatase
B6 deficiency - required ALAS cofactor - may be seen as side effect of isoniazid
What mechanism underlies beta thalassemias?
Gene mutations (point mutations in promoter or splice sites). Alpha thalassemias are DELETIONS
Characteristic appearance of xray (skull) in B thalassemia?
Crew cut appearance from erythroid hyperplasia (hematopoeisis expands to site where it normally isnt
Where is dietary folate absorbed
Jejunum
Hemosiderinuria in Intravascular hemolysis mechanism
Start with hemoglobinuria during hemolysis. Hgb taken up by renal tubular cells and broken down into Fe, which accumulates as hemosiderin. eventually sloughs off and leaves in urine. This happens a few days after hemolysis
Classic infant presentation in sickle cell disease
African American
6 months old
Dactylitis (swollen hands and feet due to vaso-occlusive infarcts in bones)
Major complication of concern in sickle cell trait
generally asymptomatic because <50% sickle cell do NOT sickle
Exception: renal medulla. Extreme hypoxia and hypertonicity in medulla causes sickling–> microinfarctions –> Microhemturia –> decrased ability to concentrate urine
Cause of paroxysmal nocturnal hemoglobinuria (PNH)
ACQUIRED defect in myeloid stem cells resulting in absent GPI (glycophosphatidylinositol). DAF and MIRL cant be expressed on RBC membranes and thus are susceptible to complement
Cancer concern for aptietns with paroxysmal nocturnal hemoglobinuria (PNH)
Progression to AML (10% of patients will get AML)
Why? this condition is due to a mutation in myeloid stem cells, not hard to get another mutation
What are causes of IgM mediated intravascular hemolysis
Infectious Mononucleosis
Mycoplasma pneumoniae
Mutation in polycythemia vera and classic unique symtpom
JAK2 kinase
Itching after bathing due to mast cell histamine release
Cause of ectopic EPO production
renal cell carcinoma
