Renal cell carcinoma often invades renal vein 2. Hepatocellular carcinoma often invades hepatic vein 3. Follicular carcinoma of the thyroid 4. Choriocarcinoma C. Seeding of body cavities is characteristic of ovarian carcinoma, which often involves the peritoneum 'omental caking', Fig, 3. We 11 diff eren i i ated, f oil ic ula r ade noma of thyroid. Benign t u m o r s tend to be slow g r o w i n g , well circumscribed, distinct, and mobile. Malignant t u m o r s are usually rapid growing, poorly circumscribed, infiltrative, and fixed to s u r r o u n d i n g tissues and local structures.
Biopsy or excision is generally required before a t u m o r can be classified as benign or m a l i g n a n t with certainty. Some benign t u m o r s can grow in a malignant-like fashion, and some malignant t u m o r s can grow in a benign-like fashion. Benign t u m o r s are usually well differentiated Fig.
Characteristics include 1. Organized growth 2. Uniform nuclei 3. Low nuclear to cytoplasmic ratio 4. M i n i m a l mitotic activity 5. Lack of invasion of basement m e m b r a n e or local tissue 6.
No metastatic potential B. Malignant t u m o r s are classically poorly differentiated anaplastic. Disorganized growth loss of polarity 2. Nuclear p l e o m o r p h i s m and hyperchromasia 3. High nuclear to cytoplasmic ratio 4. High mitotic activity with atypical mitosis 5. Invasion through basement m e m b r a n e or into local tissue C. Metastatic potential is the h a l l m a r k of malignancy—benign t u m o r s never metastasize. Proteins released by t u m o r into s e r u m e.
Useful for screening, monitoring response to treatment, and m o n i t o r i n g recurrence C. Elevated levels require tissue biopsy for diagnosis of carcinoma e. Microscopic assessment of differentiation i. Well differentiated low grade —resembles normal parent tissue 2. Poorly d i ffere n t iat ed high g rad e —does no t resem ble pa rent t i s su e B. I m p o r t a n t for d e t e r m i n i n g prognosis; well-differentiated cancers have better prognosis t h a n poorly-differentiated cancers.
Assessment of size a n d spread of a cancer B. Key prognostic factor; more i m p o r t a n t t h a n grade C. Determined after final surgical resection of the t u m o r D. Utilizes T N M staging system 1. N—spread to regional lymph nodes; second most important prognostic factor 3.
Integrity of the blood vessel is necessary to carry blood to tissues. Damage to the wall is repaired by hemostasis, which involves formation of a thrombus clot at the site of vessel injury.
Hemostasis occurs in two stages: primary and secondary. Secondary hemostasis stabilizes the platelet plug and is mediated by the coagulation cascade. Step 1—Transient vasoconstriction of damaged vessel 1. Mediated by reflex neural stimulation and endothelin release from endothelial cells B.
Step 2—Platelet adhesion to the surface of disrupted vessel 1. Von Willebrand factor vWF binds exposed subendothelial collagen, 2. Platelets bind vWF using the GPlb receptor. Step 3—Platelet degranulation l.
Adhesion induces shape change in platelets and degranulation with release of multiple mediators. Step 4—Platelet aggregation 1. Platelet plug is weak; coagulation cascade secondary hemostasis stabilizes it.
Usually due to abnormalities in platelets; divided into quantitative or qualitative disorders B. Clinical features include mucosal and skin bleeding. Symptoms of mucosal bleeding include epistaxis most common overall symptom , hemoptysis, Gf bleeding, hematuria, and menorrhagia. Intracranial bleeding occurs with severe thrombocytopenia.
Symptoms of skin bleeding include petechiae m m. Useful laboratory studies include 1. Bleeding t i m e — n o r m a l 2 - 7 minutes; prolonged with quantitative and qualitative platelet disorders 3. Blood smear—used to assess n u m b e r and size of platelets 4. Bone marrow biopsy—used to assess megakaryocytes, which produce platelets III. Most c o m m o n cause of thrombocytopenia in children and adults B, Autoantibodies are produced by plasma cells in the spleen.
C, Antibody-bound platelets are consumed by splenic macrophages, resulting in thrombocytopenia. D, Divided into acute and chronic forms 1, Acute form arises in children weeks after a viral infection or i m m u n i z a t i o n ; s e l f - limited, usually resolving within weeks of presentation 2. Chronic tbrm arises in adults, usually women of chitdbearing age. May cause short-lived t h r o m b o c y t o p e n i a in offspring since antiplatelet IgG can cross the placenta.
T megakaryocytes on bone m a r r o w biopsy F, Initial treatment is corticosteroids. Children respond well; adults may show early response, but often relapse. IV[G is used to raise the platelet count in symptomatic bleeding, but its effect is short-lived, 2.
Splenectomy eliminates the p r i m a r y source of antibody and the site of platelet destruction performed in refractory cases. Platelets are consumed in the formation of microthrombi.
RBCs are "sheared" as they cross microthrombi, resulting in hemolytic anemia with schistocytes Fig. Hemostasls and Related Disorders 33 1. Large, uncleaved multimers lead to abnormal platelet adhesion, resulting in m icrothrombi.
HUS is due to endothelial damage by drugs or infection. L Classically seen in children with E coli G;H7 dysentery, which results from exposure to undercooked beef 2. E coti verotoxin damages endothelial cells resulting in platelet microthrombi. Microangiopathic hemolytic anemia 3. Fever 4. Renal insufficiency more common in HUS —'Fhrombi involve vessels of the kidney.
Laboratory findings include 1. Thrombocytopenia with t bleeding time 2. Anemia with schistocytes 4. Treatment involves plasmapheresis and corticosteroids, particularly in TTP. Bernard-Soulier syndrome is due to a genetic GPfb deficiency; platelet adhesion is impaired.
Aspirin irreversibly inactivates cyclooxygenase; lack of TXA, impairs aggregation. Uremia disrupts platelet function; both adhesion and aggregation are impaired. Coagulation cascade generates thrombin, which converts fibrinogen in the platelet plug to fibrin.
Fibrin is then cross-linked, yielding a stable platelet-fibrin thrombus. Factors of the coagulation cascade are produced by the liver in an inactive state. Activation requires 1. Exposure to an activating substance i. Tissue thromboplastin activates factor VII extrinsic pathway. Subendothelial collagen activates factor XII intrinsic pathway. Phospholipid surface of platelets 3. Calcium derived from platelet dense granules II. Usually due to factor abnormalities B.
Clinical features include deep tissue bleeding into muscles and joints hemarthrosis and rebleeding after surgical procedures e. X-linked recessive predominantly affects males 2. C a n arise f r o m a new mutation de novo without any family history B. Presents with deep tissue, joint, and postsurgical bleeding 1. Clinical severity depends on the degree of deficiency. N o r m a l platelet c o u n t and bleeding time D.
Genetic factor IX deficiency 1. Acquired antibody against a coagulation factor resulting in impaired factor f u n c t i o n ; anfi-FVIII is most c o m m o n , t. Clinical and lab findings are similar to hemophilia A. P T T does not correct u p o n m i x i n g normal plasma with patient's plasma mixing study due to inhibitor; P T T does correct in hemophilia A. Genetic v W F deficiency 1. Most c o m m o n inherited coagulation disorder B. Multiple subtypes exist, causing quantftfttive a n d qualitative defects; t h e most c o m m o n type is autosomal d o m i n a n t with decreased v W F levels.
Presents with mild mucosal and skin bleeding; low v W F impairs platelet adhesion. T bleeding time 2. Disrupts function of multiple coagulation factors 1, Vitamin K is activated by epoxide reductase in the liver. Deficiency occurs in 1. N e w b o r n s — d u e to lack of GI colonization by bacteria that normally synthesize vitamin K. Hemostasls and Related Disorders 33 2. Long-term antibiotic therapy—disrupts v i t a m i n K-producing bacteria in the GI tract 3.
Malabsorption—leads to deficiency of fat-soluble vitamins, including vitamin K Vill. Fragments of destroyed platelets may activate r e m a i n i n g platelets, leading to thrombosis. Pathologic activation of the coagulation cascade 1. Widespread m i c r o t h r o m b i result in ischemia and infarction, 2. C o n s u m p t i o n of platelets and factors results in bleeding, especially f r o m IV sites and mucosal surfaces bleeding f r o m body orifices.
Almost always secondary to a n o t h e r disease process 1. Obstetric complications—Tissue t h r o m b o p l a s t i n in the amniotic fluid activates coagulation. Sepsis especially w i t h F, Colt or N ttitningitidis —Endotoxins f r o m the bacterial wall and cytokines e.
Acute promyelocytic l e u k e m i a — P r i m a r y granules activate coagulation. Rattlesnake bite—Venom activates coagulation. Laboratory findings include J, I platelet count 2. Microangiopathic hemolytic a n e m i a 5.
Derived from splitting of cross-linked fibrin; D - d i m e r is not produced f r o m splitting of fibrinogen. Treatment involves addressing the underlying cause and transfusing blood products and cryoprecipitate comains coagulation factors , as necessary. Plasmin cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation.
Disorders of fibrinolysis are due to plasmin overactivity resulting in excessive cleavage of s e r u m fibrinogen. Presents with increased bleeding resembles D1C D. Increased fibrinogen split products without D - d i m e r s — S e r u m fibrinogen is lysed; however, D - d i m e r s arc not formed because fibrin t h r o m b i are absent. Treatment is aminocaproic acid, which blocks activation of plasminogen. Pathologic formatiun of an intravascular blood clot thrombus 1.
Most c o m m o n location is the deep veins DVT of the leg below the knee. U and 2 attachment to vessel wall I.
Three major risk factors for thrombosis are disruption in blood low, endothelial cell damage, and hypercoagulablestate Virchow triad. Blood llow is normally continuous and laminar; keeps platelets and factors dispersed and inactivated B. Immobilization—increased risk for deep venous t h r o m b o s i s 2.
Cardiac wall dysfunction e. Aneurysm III. Endothelial damage d i s r u p t s the protective function of endothelial cells, increasing the risk for thrombosis. Endothelial cells prevent thrombosis by several mechanisms. Block exposure to subendothelial collagen and underlying tissue factor 2. Causes of endothelial cell d a m a g e include atherosclerosis, vasculitis, and high levels of homocysteine. V i t a m i n B12 and folate deficiency result in mildly elevated homocysteine levels, increasing the risk for thrombosis.
C o b a l a m i n transfers methyl to homocysteine resulting in methionine, iv. Cystathionine beta synthase CBS deficiency results in high homocysteine levels with homocystinuria, i. CBS converts homocysteine to cystathionine; e n z y m e deficiency leads to h o m o c y s t e i n e buildup.
Characterized by vessel thrombosis, mental retardation, lens dislocation, and long slender fingers. Due to excessive procoagulant proteins or defective anticoagulant proteins; may be inherited or acquired B.
Usually occurs in the deep veins of the leg; o t h e r sites include hepatic and cerebral veins. Protein C or S deficiency autosomal d o m i n a n t decreases negative feedback on the coagulation cascade.
Increased risk for w a r f a r i n skin necrosis i. In preexisting C or S deficiency, a severe deficiency is seen at the onset of warfarin therapy increasing risk for thrombosis, especially in the skin. Factor V Leiden is a m u t a t e d form of factor V that lacks the cleavage site for deactivation by proteins C and S. Most c o m m o n inherited cause of hypercoagulable state E. P r o t h r o m b i n A is an inherited point mutation in p r o t h r o m b i n that results in increased gene expression, I.
ATIII deficiency decreases the protective effect of heparin-I ike molecules p r o d u c e d by the endothelium, increasing the risk for t h r o m b u s. High doses of h e p a r i n activate limited ATIII; Coumadin is t h e n given to m a i n t a i n an anlicoagulated state.
Oral contraceptives are associated with a hypercoagulable state. Intravascular mass that travels and occludes d o w n s t r e a m vessels; symptoms depend on the vessel involved. Atherosclerotic embolus is d u e to an atherosclerotic plaque that dislodges. Characterized by the presence of cholesterol clefts in the embolus Fig.
Far embolus is associated with bone fractures, particularly long bones, and soft tissue t r a u m a. Develops while f r a c t u r e is still present or shortly after repair 2. Characterized by dyspnea fat, often with b o n e m a r r o w elements, is seen to p u l m o n a r y vessels, Fig.
Gas embolus is classically seen in decompression sickness. Nitrogen gas precipitates out pf blood due torapid ascent by a diver. Presents with joint and muscle pain 'bends' and respiratory symptoms 'chokes'. Chronic form Caisson disease is characterized by multifocal ischemic necrosis of bone. Gas embolus may also o c c u r d u r i n g laparoscopic surgery air is p u m p e d into the abdomen , F. Amniotic fluid embolus enters maternal circulation d u r i n g labor or delivery!. Presents with shortness of breath, neurologic symptoms, and DIC due to the thrombogenic nature of amniotic fluid 2.
Characterized by s q u a m o u s cells and keratin debris, f r o m fetal skin, in embolus Fig. Usually d u e to t h r o m b o e m b o l u s ; the most c o m m o n source is deep venous t h r o m b u s DVT of the lower extremity, usually involving the femoral, iliac, or popliteal veins. Most often clinically silent because 1 the lung has a dual blood supply via p u l m o n a r y and bronchial arteries and 2 the embolus is usually small self- resolves C.
B Fat embolus with bone marrow elements. C, Amniotic fluid embolus with squamous cells and keratin debris from fetal skin. Presents with shortness of breath, hemoptysis, pleuritic chest pain, a n d pleura! Spiral CT shows a vascular tilling defect in the lung. Lower extremity Doppler ultrasound is useful to detect DVT. Gross e x a m i n a t i o n reveals a hemorrhagic, wedge-shaped infarct, D. Sudden death occurs with a large saddle embolus that blocks b o t h left and right p u l m o n a r y arteries or with significant occlusion of a large p u l m o n a r y a r t e r y Fig.
P u l m o n a r y hypertension may arise with chronic emboli that are reorganized over time. Travel down systemic circulation to occlude flow to organs, most c o m m o n l y be- lower extremities Fig. S Saddle embolus involving pulmonary artery. Reduction in circulating red blood cell RBC mass B. Presents with signs and s y m p t o m s of hypoxia L Weakness, fatigue, and dyspnea 2.
Pale conjunctiva and skin 3. Headache and lightheadedness 4. Angina, especially with preexisting coronary artery disease C. Microcytic anemias are due to decreased production of hemoglobin.
Microcytosis is due to an "extra" division which occurs to m a i n t a i n hemoglobin concentration. Hemoglobin is m a d e of heme and globin: heme is c o m p o s e d of iron a n d protoporphyrin. A decrease in any of these c o m p o n e n t s leads to microcytic anemia.
Microcytic anemias include 1 iron deficiency a n e m i a , 2 a n e m i a of chronic disease, 3 sideroblastic anemia, and 4 thalassemia. Due to decreased levels of iron 1. Iron is c o n s u m e d in heme meat-derived and n o n - h e m e vegetable-derived forms. Absorption o c c u r s in the d u o d e n u m , Enterocytes have h e m e and n o n - h e m e DMT1 transporters; the heme form is m o r e readily absorbed. Enterocytes t r a n s p o r t iron across the cell m e m b r a n e into blood via ferroportin, 3.
Transferrin t r a n s p o r t s iron in the blood and delivers it to liver and b o n e m a r r o w macrophages for storage.
Stored intracellular iron is b o u n d to ferritin, which prevents iron f r o m f o r m i n g free radicals via the Pcnton reaction. Laboratory measurements of iron status 1. Serum iron—measure of iron in the blood 2. Total iron-binding capacity TIBC —measure of transferrin molecules in the blood 3. S e r u m ferritin—reflects iron stores in macrophages and the liver E. Iron deficiency is usually caused by dietary lack or blood loss. Infants—breast-feeding h u m a n milk is low in iron 2.
Children—poor diet 3. Adtilts years —peptic ulcer disease in males and menorrhagia or pregnancy in females 4. Stages of iron deficiency 1. Normocytic anemia—Bone m a r r o w makes fewer, but normal-sized, RBCs, 4. Microcytic, hypochromic anemia—Bone m a r r o w makes smaller and fewer RBCs.
G, Clinical features of iron deficiency include anemia, koilonychia, and pica. Laboratory findings include I. Treatment involves supplemental iron ferrous sulfate. Plu miner-Vinson s y n d r o m e is iron deficiency anemia with esophageal web and atrophic glossitis; presents with a n e m i a , dysphagia, and beefy-red tongue III. A n e m i a associated with chronic inflammation e. Chronic disease results in production o f a c u t e phase reactants f r o m the liver, including hepcidln.
Hepcidin sequesters iron in storage sites by 1 limiting iron transfer from macrophages to erythroid precursors and 2 suppressing erythropoietin KPO Fig.
White Blood Cell Disorders 43 production; a i m is to prevent bacteria f r o m accessing iron, which is necessary for their survival. Treatment involves addressing the underlying cause; exogenous E P O is useful in a subset of patients, especially those w i t h cancer. Anemia due tor-defective protoporphyrin synthesis 1. P r o t o p o r p h y r i n is synthesized via a series of reactions. Additional reactions convert porphobilinogen to p r o t o p o r p h y r i n , 4.
Ferrochelatase attaches p r o t o p o r p h y r i n to iron to make h e m e final reaction; o c c u r s in the mitochondria. Iron is transferred to erythroid precursors and enters the m i t o c h o n d r i a to form heme. Iron-laden m i t o c h o n d r i a f o r m a ring a r o u n d the nucleus of e r y t h r o i d precursors; these cells are called ringed sideroblasts hence, the term sideroblastic a n e m i a , Fig, 5. Sideroblastic anemia can be congenital or acquired.
Congenital defect most c o m m o n l y involves ALAS rate-limiting enzyme. Acquired causes include i. Alcoholism—mitochondrial poison ii. Lead poisoning—inhibits A L A D and ferrochelatase iii. V i t a m i n B6 deficiency—required cofactor for ALAS; most c o m m o n l y seen as a side effect of isoniazid t r e a t m e n t for tuberculosis E. Anemia d u e to decreased synthesis of the globin c h a i n s of hemoglobin 1. Inherited mutation; carriers are protected against Plasmodium falciparum malaria.
Divided into a- a n d [3-thalassemia based on decreased production of alpha or beta globin chains. Table 5. One gene deleted—asymptomatic 2. Two genes deleted—mild anemia with t RBC count; eis deletion is associated with an increased risk of severe thalassemia in offspring. Cis deletion is when both deletions o c c u r on the same chromosome; seen in Asians ii.
Trans deletion is when one deletion occurs on each chromosome; seen in Africans, including African Americans 3. Microcytic, h y p o c h r o m i c RBCs and target cells are seen on blood smear Fig. Massive erythroid hyperplasia ensues resulting in 1 expansion of hematopoiesis into the skull reactive bone formation leads to 'crewcut' appearance on x-ray.
Chronic t r a n s f u s i o n s are often necessary; leads to risk for secondary hemochromatosis iv. Smear show r s microcytic, hypochromic RBCs with target cells and nucleated red blood cells. Folate and v i t a m i n B12 are necessary tor synthesis of DNA precursors, 1. Folate circulates in the serum as methyltetrahydrofolate methyl THF ; removal of the methyl g r o u p allows for participation in the synthesis of DNA precursors. Methyl group is transferred to vitamin B12 eobalamin , 3.
V i t a m i n B12 then transfers it to homocysteine, producing m e t h i o n i n e. Lack of folate or vitamin B12 impairs synthesis of DNA precursors, 1. Impaired division and enlargement of RBC precursors leads to megaloblastic anemia, 2. Impaired division of granulocytic precursors leads to hyper segmented neutrophils. Megaloblastic change is also seen in rapidly-dividing e. O t h e r causes of macrocytic anemia without megaloblastic change include alcoholism, liver disease, and d r u g s e.
Dietary folate is obtained f r o m green vegetables and some fruits. Folate deficiency develops within m o n t h s , as b o d y stores are minimal, C. Causes include p o o r diet e. Clinical and laboratory findings include 1. Glossitis 3. I serum folate 4. T serum homocysteine increases risk for thrombosis 5. Normal methylmalonic acid III.
Dietary v i t a m i n B12 is complexed to animal-derived proteins. Salivary gland enzymes e. Pancreatic proteases in the d u o d e n u m detach vitamin B12 f r o m R-binder. V i t a m i n BI2 binds intrinsic factor made by gastric parietal cells in the small bowel; the intrinsic factor-vitamin B12 complex is absorbed in the ileum.
Vitamin B12 deficiency is less c o m m o n t h a n folate deficiency and takes years to develop due to large hepatic stores 6 f v i t a m i n B Pernicious anemia is the most c o m m o n cause of vitamin B12 deficiency. A u t o i m m u n e destruction of parietal cells body of stomach leads to intrinsic factor deficiency D. O t h e r causes of vitamin B12 deficiency include pancreatic insufficiency and d a m a g e to the terminal ileum e.
Macrocytic RBCs with hypersegmented neutrophils 2. V i t a m i n B12 deficiency results in increased levels of methylmalonic acid, which impairs spinal cord myelinization, iii. Damage results in poor proprioception a n d vibratory sensation posterior c o l u m n and spastic paresis lateral corticospinal tract. T serum homocysteine similar to folate deficiency , which increases risk for thrombosis 6. Due to increased peripheral destruction or u n d e r p r o d u c t i o n 1, Reticulocyte count helps to distinguish between these two etiologies.
Young RBCs released f r o m the bone m a r r o w 1. Identified on blood smear as larger cells with bluish cytoplasm due lo residual RNA, Fig. RC, however, is falsely elevated in anemia. Divided into extravascular and intravascular hemolysis; both result in anemia with a good m a r r o w response.
Extravascular hemolysis involves RBC destruction by the reticuloendothelial system macrophages of the spleen, liver, a n d l y m p h nodes. White Blood Cell Disorders 47 1. Macrophages c o n s u m e RBCs and break down hemoglobin, i. Globiu is broken d o w n inlo a m i n o acids.
A n e m i a with splenomegaly, jaundice d u e to u n c o n j u g a t e d bilirubin, and increased risk for bilirubin gallstones ii. Intravascular hemolysis involves d e s t r u c t i o n of RBCs w i t h i n vessels. Hemoglobinemia ii. Hemoglobinuria iii. Hemosiderinuria-—Renal t u b u l a r cells pick up some of the hemoglobin that is filtered into the u r i n e and break it down into iron, which accumulaies as hemosiderin; t u b u l a r cells are eventually shed resulting in hemosiderinuria.
M e m b r a n e blebs are formed and lost over time. Loss of m e m b r a n e renders cells r o u n d spherocytes instead of disc-shaped. Spherocytes are less able to m a n e u v e r t h r o u g h splenic sinusoids and are c o n s u m e d by splenic macrophages, resulting in a n e m i a.
Clinical and laboratory findings include 1, Spherocytes with loss of central pallor Fig, 5. Diagnosed by osmotic fragility test, which reveals increased spherocyte fragility in hypotonic solution E. Treatment is splenectomy; a n e m i a resolves, bui spherocytes persist and Howell Tolly bodies fragments of nuclear material in RBCs emerge on blood s m e a r Fig. Autosomal recessive mutation in 5 c h a i n of hemoglobin; a single a m i n o acid change replaces n o r m a l glutamic acid hydrophilic with valine hydrophobic.
HbS polymerizes when deoxygenated; polymers aggregate i n t o needle-like structures, resulting in sickle cells Fig. Increased risk of sickling occurs with hypoxemia, dehydration, and acidosis. H b F protects against sickling; high H b F at b i r t h is protective for the first few m o n t h s of life. Treatment with hydroxyurea increases levels of HbF.
Cells continuously sickle and de-sickle while passing t h r o u g h the microcirculation, resulting in complications related to RBC m e m b r a n e damage. I n t r a v a s c u l a r hemolysis—Reticuloendothelial system removes RBCs with d a m a g e d m e m b r a n e s , leading to anemia, jaundice with unconjugated hyperbilirubinemia, and increased risk for bilirubin gallstones.
Intravascular hemolysis—RBCs with damaged m e m b r a n e s dehydrate, leading to hemolysis with decreased haptoglobin and target cells on blood smear, 3. Massive erythroid hyperplasia ensues resulting in i. Expansion of hematopoiesis into the skull 'crewcut' appearance oil x-ray and facial bones ' c h i p m u n k fades' ii.
E x t r a m e d u l l a r hematopoiesis with hepatomegaly iii. Risk of aplastic crisis with p a r v o v i r u s B19 infection of erythroid precursors F. Irreversible sickling leads to complications of vaso-occlusion. Dactylitis—swollen hands and feet d u e to vaso-occlusive infarcts in bones; c o m m o n presenting sign in infants 2. Autosplenectomy—shrunken, fibrotic spleen. Consequences include i. Increased risk of infection with encapsulated o r g a n i s m s such as Streptococcus pneumoniae and Haemophilus influenzae most c o m m o n cause of death in children ; affected children should be vaccinated by 5 years of age.
Increased risk of Salmonella paratyphi osteomyelitis iii, Howell-Jolly bodies on blood smear 3. Acute chest syndrome—vaso-occlusion in p u l m o n a r y microcirculation i. Presents with chest pain, shortness of breath, and lung infiltrates ii. Often precipitated by p n e u m o n i a iii. Most c o m m o n cause of death in adult patients 4. Pain crisis 5. Renal papillary necrosis—results in gross hematuria and proteinuria G.
Laboratory findings 1. Sickle cells and target cells are seen on blood s m e a r in sickle cell disease, but not in sickle cell trait. Metabisulfite screen causes cells with any a m o u n t of HbS to sickle; positive in b o t h disease and trait 3.
Jolly body within RBC. White Blood Cell Disorders 49 i. Autosomal recessive mulalion in J c h a i n of hemoglobin 1. N o r m a l glutamic acid is replaced by lysine. Presents with mild a n e m i a d u e to extravascular hemolysis C. A c q u i r e d defect in myeloid stem cells resulting in absent g ly cosy 1 phosphatidyl inositol GPI ; renders cells susceptible to destruction by complement 1.
Blood cells coexist with c o m p l e m e n t. Decay accelerating factor DAF on the surface o f b l o o d cells protects against c o m p l e m e n t - m e d i a t e d d a m a g e by inhibiting C3 convertase. Intravascular hemolysis o c c u r s episodically, often at night d u r i n g sleep, 1. Sign-Up Today! Full access to 35 hours of online videos by Dr.
Videos highlight key concepts and highly-tested material. Covers all 19 chapters of Fundamentals of Pathology.
Create a Free trial account today! Click here to read more student reviews I do online tutoring for Step 1 and Step 2 CK see www. I would have spent even more time on the NBMEs and potentially made Anki cards for all the questions.
I would have started skimming First Aid a couple of days earlier say 5 days before my test rather than 3 because it was stressful to have to read it all in 3 days. Dedicated Time : 6 weeks. Cram Fighter- Literally saved my ass by making my entire schedule for me so I stayed on topic and focused. Obviously, all of the CBSE practice tests. I took all of those. I ended up doing about 7 from then on. I think I also would have done some more review during my blocks.
About : Qcount, non-traditional US MD who has a grad degree and worked as a research scientist before medicine. Dedicated Time : 6. All blocks were timed random. I Took handwritten notes this was key for my success! Re-watched some of the cardiology videos. Read the text 1x during weeks I took notes while I watched the videos.
Sketchy Pharm 0. Goljan Audio 1x : Listened on my walks to and from campus during the fall of M2. Somewhat dated, but great for integrating concepts. General Advice : Develop a plan to build confidence leading up to your exam day. I specifically saved UWorld self assessment 2 as my last practice test since it is relatively accurate but also is slightly generous with the score as opposed to NBMEs which tend to under-predict.
I also graphed the average of the past 10 days of UWorld blocks to help remind myself that I was trending the right way even if I happened to score poorly on one block. The questions on the real exam were most similar to UWorld questions, with long stems and multiple steps required to get to the answer, they were not similar at all to NBME questions.
I felt terrible after I finished the test, and pretty flat for the next few days. I knew I passed, but beyond that I had no idea what my score would be. I would also make a pass through First Aid following along with class material during M1 and M2. Pre-dedicated during classes: All of bros anki, sketchy videos, boards and beyond prn, and about questions between Kaplan and Rx I did about 70 questions a week for a year.
General Advice : Study longitudinally and put in a few hours a week during the school year to give yourself a foundation for dedicated.
Also do as many different questions as you can, it can be expensive but you only get one shot at this. Its worth seeing as many of those as possible cause it can get you free points.
I read first aid once before dedicated. During dedicated I did uworld once, then did the marked questions when I ran out of new questions.
I read first aid twice while sometimes following along with DIT videos. I also used sketchy micro for bugs I had a hard time remembering. I read pathoma 3 times during dedicated. Then every day I did 40 Uworld questions, mixed-untimed-tutor mode. Somethings I would try to memorize but others I would try to understand very well. At the end of the day I would do another 40 uworld questions.
You will finish going through first aid in about 4 weeks this way. Next I did the same thing over again but in a more concentrated fashion whole first aid chapter in one day, along with 1 pathoma unit and 80 uworld questions. I felt sick because I ate too much junk food. Resources : UWorld 1x : Untimed, random. Took notes on incorrect questions and tried to review these when I had time. In retrospect, I found Pathoma to be much more useful during dedicated than any other time. Relatively concise and really nails down the high-yield points of pathology.
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