Fundamentals of pathology sattar pdf download

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Notify me of follow-up comments by email. Notify me of new posts by email. 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. Intravascular hemolysis leads to hemoglobinemia a n d hemoglobinuria especially in the m o r n i n g ; h e m o s i d e r i n u r i a is seen days after hemolysis. Sucrose test is used to screen for disease; c o n f i r m a t o r y test is the acidified s e r u m test or flow c y t o m e t r y to detect lack of C D 5 5 DAF on blood cells, D.

M a i n cause of death is t h r o m b o s i s of the hepalic, portal, or cerebral veins. Destroyed platelets release cytoplasmic contents into circulation, inducing th rombosis. X-llnked recessive disorder resulting in reduced half-life of G6PD; renders cells susceptible to oxidative stress 1. RBCs are normally exposed to oxidative stress, in p a r t i c u l a r H , 0 ,. Glutathione an antioxidant neutralizes F1,0,, but becomes oxidized in the process. G 6 P D deficiency has two m a j o r variants.

African variant—mildly reduced half-life of G 6 P D leading to mild intravascular hemolysis with oxidative stress 2.

Mediterranean variant—markedly reduced half-life of G 6 P D leading to marked intravascular hemolysis with oxidative stress 3. H i g h carrier frequency in b o t h populations is likely d u e to protective role against f a l c i p a r u m malaria. Oxidative stress precipitates Hb as Heinz bodies. Causes of oxidative stress include infections, d r u g s e. Heinz bodies are removed f r o m RBCs by splenic macrophages, resulting in bite cells Fig.

Leads to p r e d o m i n a n t l y intravascular hemolysis D. Presents with hemoglobinuria and back pain hours after exposure to oxidative stress E. Heinz preparation is used to screen for disease precipitated hemoglobin can only be seen with a special Heinz stain, Fig. IgG-mediated disease usually involves extravascular hemolysis. IgG binds RBCs in the relatively w a r m temperature ol the central body warm agglutinin ; m e m b r a n e of antibody-coated RBC is c o n s u m e d by splenic macrophages, resulting in spherocytes.

Drug may induce production of autoantibodies e. Treatment involves cessation of the offending d r u g , steroids, IV1G, a n d , if necessary, splenectomy.

IgM-mediared disease usually involves intravascular hemolysis. IgM binds RBCs and fixes complement in the relatively cold temperature of the extremities cold agglutinin. Associated with Mycoplasma pneumoniae and infectious mononucleosis D.

C o o m b s test is used to diagnose IHA; testing can be direct or indirect. Direct C o o m b s test c o n f i r m s the presence of antibody-coated RBCs. This is the most important test lor IHA. Indirect C o o m b s test c o n f i r m s the presence of antibodies in patient s e r u m. Anti- IgG and test RBCs are mixed with the patient serum; agglutination occurs if s e r u m antibodies are present.

Intravascular hemolysis that results f r o m vascular pathology; RBCs are destroyed as they pass t h r o u g h the circulation. Fig, 5. Iron deficiency anemia o c c u r s with chronic hemolysis, B. RBCs r u p t u r e as a part of the Plasmodium life cycle, resulting in intravascular hemolysis and cyclical fever. Pfalciparum—daily fever 2. J 1 vivax and P ovale—fever every o t h e r day C. Decreased production of RBCs by bone marrow; characterized by low corrected reticulocyte c o u n t B. Causes of microcytic and macrocytic a n e m i a 2.

Renal failure—decreased production of E P O by p e r i t u b u l a r interstitial cells 3. Damage to bone m a r r o w precursor cells may result in a n e m i a or pancytopenia II. Infects progenitor red cells and temporarily halts erythropoiesis; leads to significant anemia in the setting of preexisting m a r r o w stress e. Treatment is supportive infection is self-limited.

D a m a g e to hematopoietic stem cells, resulting pancytopenia anemia, t h r o m b o c y t o p e n i a , and leukopenia with low reticulocyte count B. Etiologies include drugs or chemicals, viral infections, and a u t o i m m u n e d a m a g e. Biopsy reveals an empty, fatty m a r r o w Fig. I m m u n o s u p p r e s s i o n may be helpful as some idiopathic cases are due to a b n o r m a l T-cell activation with release of cytokines.

May require b o n e m a r r o w transplantation as a last resort Fig. Pathologic process e. Hematopoiesis o c c u r s via a stepwise maturation of C O M ' hematopoietic stem cells Fig. A low or high VVBC c o u n t is usually d u e to a decrease or increase in one particular ceil lineage.

Neutropenia refers to a decreased n u m b e r of circulating neutrophils. Causes include 1. Drug toxicity e. Severe infection e. Lymphopenia refers to a decreased n u m b e r of circulating lymphocytes.

Immunodeficiency e. High Cortisol state e. Whole b o d y radiation—Lymphocytes are highly sensitive to radiation; lymphopenia is the earliest change to emerge alter whole body radiation. Neutrophilic leukocytosis refers to increased circulating neutrophils. Causes include I. Bacterial infection or tissue necrosis—induces release of m a r g i n a t e d pool and bone m a r r o w neutrophils, including i m m a t u r e f o r m s left shift ; i m m a t u r e cells are characterized by decreased Fc receptors CD High corlisol state—impairs leukocyte adhesion, leading to release of marginated pool of neutrophils B.

Monocytosis refers to increased circulating monocytes. Causes include chronic i n f l a m m a t o r y states e. Eosinophilia refers to increased circulating eosinophils. Causes include allergic reactions type I hypersensitivity , parasitic infections, and Hodgkin lymphoma, Eosinophilia is driven by increased eosinophil chemotactic factor. Basophilia refers to increased circulating basophils; classically seen in chronic myeloid leukemia E.

Lymphocytic leukocytosis refers to increased circulating lymphocytes. Viral infections—T lymphocytes undergo hyperplasia in response to virally infected ceils, 2.

Bordetella pertussis infection—Bacteria produce lymphocytosis-promoling factor, which blocks circulating lymphocytes f r o m leaving the blood to enter the lymph node. EBV primarily infects 1. O r o p h a r y n x , resulting in pharyngitis 2. Liver, resulting in hepatitis with hepatomegaly and elevated liver enzymes 3. B cells C. Generalized lymphadenopathy LAD due to T-cell hyperplasia in the lymph n o d e paracortex 2. The monospot lest is used for screening.

Detects IgM antibodies that cross-react with horse or sheep red blood cells heterophile antibodies 2. Usually t u r n s positive within 1 week after infection 3. Definitive diagnosis is made by serologic testing for the EBV viral capsid antigen. Courtesy of K. V, mononucleosis. Complications 1. Increased risk for splenic r u p t u r e Fig. Rash if exposed to ampicillin 3. D o r m a n c y of v i r u s in B cells leads to increased risk for b o t h recurrence a n d B-cell l y m p h o m a , especially if immunodeficiency e.

Increased blasts "crowd-out" n o r m a l hemalopoiesis, resulting in an "acute" presentation with a n e m i a fatigue , t h r o m b o c y t o p e n i a bleeding , or neutropenia infection.

Blasts usually enter the blood stream, resulting in a high W B C count. L Blasts are large, i m m a t u r e cells, often with p u n c h e d out nucleoli Fig. Acute leukemia is subdivided into acute lymphoblastic leukemia ALL or acute myelogenous leukemia AML based on t h e p h e n o t y p e of the blasts.

TdT is absent in myeloid blasts and m a t u r e lymphocytes. Most c o m m o n l y arises in children; associated with Down s y n d r o m e usually arises after the age of 5 years C. Prognosis is based on cytogenetic abnormalities, i, t 12;21 has a good prognosis; m o r e c o m m o n l y seen in children ii.

The blasts do not express CD Myeloblasts are usually characterized by positive cytoplasmic staining for myeloperoxidase MPO. Most commonly arises in older adults average age is years D. Subclassified based on cytogenetic abnormalities, lineage of myeloblasts, and surface markers. High-yield subtypes include 1.

Acute promyelocytic leukemia API. Characterized by l 15;J7 , which involves translocation of the retinoic acid receptor RAR on c h r o m o s o m e 17 to c h r o m o s o m e 15; RAR disruption blocks maturation and promyelocytes blasts accumulate.

Abnormal promyelocytes contain n u m e r o u s p r i m a r y granules that increase the risk for D1C. Treatment is with all-tranj-retinoic acid ATRA, a vitamin A derivative , which binds the altered receptor and causes the blasts to mature and eventually die. Acute monocytic leukemia i. Very famous among the medical students for both general and special pathology.

Can be easily and quickly revised for examination. The best way to use this book, according to Husain A. Sattar, MD, is to read the book first, then do the Pathoma video lectures and then reread the material. This method would help students building very firm concepts and reinforce whatever that is learned.

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