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HIV drugs from the outside in

Maraviroc: CCR5 receptor inhibitor
Enfuvirtide: fusion inhibition by blocking gp41
Efavirenz, nevirapine: NNRTI (do not require intracellular phosphorylation for activation)
Zidovudine, emtricitabine: NRTIs (must be converted to monophosphate form by cellular thymidine kinase before conversion to active triphosphate forms)
Raltegravir: integrase inhibition
Ritanovir, saquinavir: protease inhibition


How do WBCs get from the intravascular space to the site of infection?

Margination: vascular leakage causes leukocyte margination toward vascular walls

Rolling: loose binding of sialylated carbohydrate groups on the endothelium (Sialyl Lewis X & PSGL-1) to L-selectin (PMNs) or E/P-selectin (endothelial cells).

Activation: slow rolling allows PMNs to sample chemokines being secreted from inflamed tissue, resulting in a conformational change in their expressed integrins

Tight adhesion and crawling: PMNs firmly attach to ICAM-1 or CD18 beta-2 integrins (Mac-1 and LFA-1) on endothelial cells
***LAD type 1 = absence of CD18 -> decreased synthesis of Mac-1 and LFA-1 skin infections without pus formation and delayed umbilical cord separation.
***LAD type 2 = less severe
***LAD type 3 = similar to type 1, but associated bleeding due to poor synthesis of beta-3 integrins on platelets

Transmigration: after crawling to the periphery of the endothelial cells, PMNs attach to PECAM-1 and squeeze out of the vasculature


Types of hemoglobin that make up the RBCs in a normal person

97% HbA = alpha2beta2
2.5% = HbA2 = alpha2delta2 *elevated in thalassemia


Region of the lymph node largely populated by T-cells and dendritic cells

Parafollicular cortex (poorly developed in DiGeorge syndrome)


What is the difference between the primary and secondary follicles in the lymph node.

Primary: dense packing of dormant B-cells
Secondary: proliferating B-cells and follicular dendritic cells


Lymph nodes changes in patients with X-linked (Bruton's) agammaglobulinemia

Poorly formed primary follicles and germinal centers due to poor B-cell differentiation


What makes up the medulla of the lymph node?

Medullary cords: B cells, plasma cells and macrophages
Medullary sinuses: reticular cells and macrophages


Cell surface receptor that binds parvovirus and allows cellular entry

Erythrocyte P antigen


Origin of cells in carcinoid tumors

Enterochromaffin cells


Normal platelets and poor aggregation after addition of normal plasma and ristocetin vs. good aggregation after ristocetin and plasma.

Ristocetin increases expression of Gp1b on platelets. In vWF deficiency, there is little vWF to bind Gp1b and there is minimal improvement despite increased expression of Gp1b on platelets.

Bernard-Soulier syndrome is due to absence of Gp1b on platelets. Although platelets will not aggregate with ristocetin, addition of normal plasma will induce aggregation.

Glanzmann thrombasthenia is due to defective GpIIb-IIIa that prevents platelet-platelet adherence. Ristocetin test will be normal in these patients.


Aminocaproic acid vs. protamine sulfate

Aminocaproic acid - reverses tPA conversion of plasminogen to plasmin
Protamine sulfate - reverses heparin by binding to and inactivating heparin


Enzymes that take heme in the periphery to conjugated bilirubin in the bile

Heme oxygenase breaks down heme to biliverdin -> biliverdin reductase reduces biliverdin to bilirubin and it is transported to the liver bound to albumin -> glucuronyl transferase conjugates bilirubin to glucuronic acid, making soluble and excretable in bile


Sickle cell anemia mutation

AR point mutation in the 6th codon of the beta-globin gene causing Glu -> Val. This results in formation of HbS, which polymerizes with other Hgb at low O2 tension.

This can be diagnosed by Hgb electrophoresis, with the HbS moving more slowly than the other Hgb due to the mutation.


Brain centers that trigger vomiting

Area postrema in the 4th ventricle has M1, H1, D2, 5-HT3 and neurokinin-1 chemoreceptors

Nucleus tracts solitaires in the medulla receives neuronal input from GI tract (CN IX, X), area postrema, vestibular system (CN VIII) and CNS


Best drugs for treatment of chemotherapy-induced vomiting

5-HT3 antagonists: ondansetron, granisetron
D2 antagonists: metaclopramide, prochlorperazine
NK1 antagonists: aripepitant, fosaprepitant


A patient has a lymph node biopsy that shows packed follicles that obscure the normal lymph node architecture, with abundant centrocytes (small cleaved cells) and a t(14;18) translocation. What is causing his condition?

Overactivation of the anti-apoptotic gene Bcl-2 occurs as a result of this translocation and causes follicular lymphoma, which is consistent with his biopsy



BCR-ABL translocation resulting in constitutively active tyrosine kinase activity and CML


A patient with a lymph node biopsy presents with diffuse medium sized lymphocytes with interspersed macrophages, a high proliferation index represented by a Ki-67 fraction around 95% and a t(8;14) translocation.

Over activation of the transcription regulator c-MYC resulting in Burkitt lymphoma


Causes of left and right shifts on the Hbg binding curve

-Decreased H+
-Decreased 2,3-BPG
-Decreased temperature

-Increased H+
-Increased 2,3-BPG
-Increased temperature



Result of Glu -> Lys substitution on Hgb. Cells do not sickle because Lys is negatively charged. This hgb moves even slower than HbS on Hgb electrophoresis


A patient presents with DIC. Peripheral blood smear shows immature myeloid cells with needle-shaped intracytoplasmic inclusions that stain positive for peroxidase. What caused this patients condition? Treatment?

Acute promyelocytic anemia (M3 AML) is due to t(15;17) that causes fusion of the retinoic acid receptor to the PML gene. Consequently, these patients are highly responsive to treatment with all trans retinoic acid.


Why is DRE a good test for prostatic adenocarcinoma

The neoplastic growth typically occurs in the peripheral zone of the prostate


Process leading to cellular apoptosis

-Intrinsic damage from toxins, radiation, heat -> expression of phosphatidyl serine and/or thrombospondin on plasma membrane
-Extrinsic TNF and Fas ligand binding to TNF receptor 1 or Fas receptor (CD95), respectively
-Mitochondrial mediated pathway

-Intrinsic: Bas, Bam and Bim replace anti-apoptotic molecules Bcl-2 and Bcl-x in the mitochondrial membrane, release of cytochrome c and caspase activation
-Extrinsic: binding death receptor brings caspases in close proximity

-Cysteine on caspases cleave aspartic acid residues and digest cellular proteins


Pure red cell aplasia

Inhibition of red cell precursors by IgG antibodies or cytotoxic T-lymphocytes resulting in reduced erythropoietic products and normal granulopoiesis and thrombopoiesis. Causes include thymomas, lymphocytic leukemias and parvovirus B19 infection.


Most common childhood brain tumors and how to differentiate between them

1) Pilocytic astrocytoma: benign, cystic cerebellar or hemispherical mass with solid tumor protruding from cyst wall. Biopsy shows Rosenthal fibers.

2) Medulloblastoma: malignant, mass in cerebellar vermis, biopsy shows sheets of small round blue cells

3) Ependymomas: ventricular masses presenting with hydrocephalus, biopsy shows rosettes


Mutation seen in patients with polycythemia vera

Constitutive activation of cytoplasmic JAK-2 tyrosine kinase


Where is factor VIII produced

Endothelial cells


Lymph node drainage for all cutaneous areas beneath the umbilicus, exceptions?

Pretty much all cutaneous areas below the umbilicus drain to the superficial inguinal nodes. Exceptions include the testes (para-aortic LNs), glans and posterior calves (both drain to deep inguinal nodes).


Common cause of adult T-cell lymphoma



Why does the spleen enlarge in patients with hereditary spherocytosis

The RBCs cannot pass through the cords of Billroth and are sequestered in the spleen