SPECIAL PATHOLOGY PEARLS

specail path

Special Pathology is an important subject for FCPS part 1. Many MCQs come from Special Pathology as well. So you have to do this subject with full concentration. Following are the Impotrant Points of Special Pathology by Dr Maryam Malik. Try to cover all these points because it will definitely help in your exam.

MOST COMMON CAUSE OF FATTY LIVER IN OUR COUNTRY IS MALNURITION. ONLY VIRUS TO BE CULTURED IS HAV. OROFECAL ROUTE OF TRANSMISSION IS FOR HAV AND HEV. MOST COMMON CAUSE OF HEPATOCELULLAR CARCINOMA IA HEP B > HEP C. MOST COMMON ROUTE OF TRANSMISSION OF HBV AND HCV IS BLOOD TRANSFUSION. VIRUS COMMONLY TRANSMITTED IN DIALYSIS IS HBV. FIRST TO COME AND LAST TO GO IN HBV IS HBsAg. INDICATORS OF INFECTIVE CARRIER IS ANTI HBcIgG, HBeAg, HBV DNA, HBsAg. LESS ONCOGENIC VIRUS IS HDV.

Unconjugated Bilirubin(UCB) is the end product of heme Degradation and is lipid soluble (indirect biliurin). UCB is conjugated to glucuronic acid and produce Conjugated Bilirubnin”CB” (Direct Bilirubin). Intestinal Bacteria converts, UCB to CB. Urobilin give colour of stool and urine. Viral Hepatitis Most Common Cause of Jaundice. Gilbert’s Disease is the 2nd most Common Cause of Jaundice. Gall bladder Inflammation is known as Cholecystitis. Billary tree Inflammation is known as Cholangitis. Tansaminases is at peak brfore Jaundice.

INDICATOR OF LIVER NECRORSIS IS ALT (SPECIFIC ENZYME FOR LIVER NECROSIS) , PRESENT IN CYTOSOL, ALT > AST. INDICATOR OF ALCOHOLIC HEPATITIS IS GGT > AST > ALT. INDICATOR OF  EXTRAVASCULAR HEMOLYSIS IS INCRESE AST. INDICATOR OF CHOLESTASIS IS ALP (ALKALINE PHOSPHATASE). INDICATOR OF PRIMARY BILIARY CIRRHOSIS IS INC SERUM IgM & ANTI MITOCHONDRIAL ANTIBODY. INDICATOR OF ACUTE PANCREATITIS IS AMYLASE > LIPASE. INDICATOR OF HEPTAOCELLULAR CARCINOMA IS ALPHA FETO PROTEIN.

PERSON WITH TYPE A BLOOD HAVE ANTI B ANTIBODIES, SO IF PATIENT SERUM CLUMPS ONLY WHEN B CELLS ARE ADDED THEN BLOOD GROUP IS A. PERSON WITH TYPE B BLOOD HAVE ANTI A ANITBODIES, SO IF PATIENT SERUM CLUMPS ONLY WHEN A CELLS ARE ADDED THEN BLOOD GROUP IS B. Erthropoises is the process of Production of RBCs in bone marrow, dependent on relase of erythropoietin from kidney. Erythropoietin acts as stimuli hypoxemia,severe anemia, left shift of OBC, high altitude, ectopic production in RCC AND HCC.
RETICULOCYTE COUNT IS THE MEASURE OF EFFECTIVE EYTHROPOISIS. COUNT OF >3%(EFFECTIVE ERTHYOPOISIS) GOOD BONE MARROW RESPONSE TO ANEMIA. COUNT OF <3% (IN EFFECTIVE ERTHYOPOISIS) POOR BONE MARROW RESPONSE TO ANEMIA. MEN HAVE HIGHER VALUE OF Hb THAN WOMEN DUR TO INCREASE TESTOSTERONE WHICH IN TURN STIMULATES ERYTHROPOISIS.

In Pregnancy there is two times greater increase in plasma volume than RBC Mass which decreases in Hb (dilutional Effect). IN ANEMIA there is OXYGEN SATURATION AND ARTERIAL Po2 is normal with decrease oxygen content. MCV is the AVERAGE VOLUME OF RBC.  we can CLASSIFY ANEMIA as 1) MICROCYTIC (<80, NORMOCYCTIC80-100) 2) MACROCYCTIC(>100). IN ALL MICROCYTIC ANEMIAS THERE IS DECREASE MCHC. IN SPHEROCYTOSIS THERE IS INCREASE MCHC. MICROCYTIC (<80) ANEMIA ARE IRON DEFICIENCY, ANEMIA OF CHRONIC DISEASE, THALASSEMIA, SIDEROBLASTIC ANEMIA. IRON DEFICIENCY ANEMIA MOST COMMON OF OVERALL ANEMIAS.




Plummer-vinson syndrome is caused by chronic iron deficiency
1) Dysphagia for solids
2) Iron deficiency
3) Achlorhydria
MOST COMMON ANEMIA IN HOPITALIZED PATIENTS IS ANEMIA OF CHRONIC DISEASE. MOST COMMON OVERALL ANEMIA IN ALCOHOLISM IS ANEMIA OF CHRONIC DISEASE.  Serum Ferritin Increases in ANEMIA OF CHRONIC DISEASE. Cooley’s ANEMIA IS PRESENT IN BETA THALASSEMIA MAJOR. MOST COMMON CAUSE OF SIDEROBLASTIC ANEMIA IS CHRONIC ALCOHOLISM. OTHER CAUSES OF SIDEROBLASTIC ANEMIA ARE VIT B6 DEFICIENCY AND X-LINKED RECESSIVE INHERITANCE. DEFECT IN HEME SYNTHESIS IN MITOCHONDRIA LEADS TO SIDEROBLASTIC ANEMIA. PEPSIN FREES VITAMIN B12 FROM INGESTED PROTEIN. VITAMIN B12 + INTRINSIC FACTOR BOTH REEABSORBED IN TERMINAL ILEUM. AUTOIMMUNE DESTRUCTION OF PARIETAL CELL(PERNICIOUS ANEMIA) MOST COMMON CAUSE OF VITAMIN B12 DEFICIENCY. MOST COMMON CAUSE OF FOLATE DEFICIENY IS ALCOHOLISM. VITAMIN B12/ FOLATE DEFICIENCY LEADS TO DELAYED NUCLEAR MATURATION; MEGALOBLASTS. VITAMIN B12/ FOLATE DEFICIENCY LEADS TO INCREASE PLASMA HOMOCYSTEINE(DAMAGES ENDOTHELIAL CELLS LEADING TO VESSEL THROMBOSIS). IN VITAMIN B12 DEFICIENCY THERE IS INVOLVEMENT OF POSTERIOR COLUMNS, LATERAL CORTICOSPINAL TRACT, DORSAL SPINOCEREBELLAR TRACT.
MACROCYTIC ANEMIA LEADS TO NEUROLOGIC DISEASE. METHYLMALONIC ACID IS THE MOST SENSITIVE TEST FOR VITAMIN B12 DEFICIENCY. INDICATORS OF VITAMIN B12/ FOLATE DEFICIENCY IS PANCYTOPENIA, OVAL MACROCYTES, HYPERSEGMENTED NEUTROPHIL. ADDITIONAL FINDINGS ONLY IN VITAMIN B12(PERNICIOUS) DEFICIENCY IS ACHLORHYDRIA, AUTOANTIBODIES , CHRONIC ATROPHIC GASTRIRITS, SERUM GASTRIN LEVEL & URINE METHYMALONIC ACID INCREASE. IN EXTRAVASCULAR HEMOLYSIS THERE IS  RBC PHAGOCYTOSIS BY MACROPHAGES IN SLEEPN, LIVER, UNCONJUGATED HYPERBILIRUBINEMIA. IN INTRAVASCULAR HEMOLYSIS THERE IS WITH IN BLOOD VESSELS , G6PD DEFICIENCY, COMPLEMENT DESTRUCTION(IgM MEDIATED HEMOLYSIS), MECHANICAL Damage, DECREASE SERUM HAPTOGLOBIN, HEMOGLOBINURIA. HS AND HE ARE AUTOSOMAL DOMINANT. IN HS THERE IS INCREASE RBC OSMOTIC FRAGILITY, LOSS OF RBC MEMBRANE AND SPHEROCYTE FORMATION.
PNH IS SCREENING TEST (SUCROSE HEMOLYSIS TEST), CONFIRMATORY TEST (ACIDIFIED SERUM TEST). SICKLE CELL ANEMIA IS INYRINSIC DEFECT, EXTRAVASCULAR HEMOLYSIS, MISSENSE MUTATION, AUTO SPLEENOMEGALY, INCREASE HbS AND DEOXY Hb. KEY PATHOLOGIC PROCESSES IN HbSS IS SEVERE HEMOLYTIC ANEMIA, PAINFUL VASO-OCCLUSIVE CRISES. HOWELL JOLLEY BODIES ARE SIGN OF SPLEENIC DYSFUNCTION. G6PD deficiency is the most common enzyme deficiency causing hemolysis
Intrinsic defect, primarily intravascular hemolysis, Heinz bodies and bite cells.

PERSON WITH TYPE O BLOOD HAVE BOTH ANTI A AND ANTI B ANTIBODIES, SO IF PATIENT SERUM CLUMPS WITH BOTH THEN BLOOD GROUP IS O. PERSON WITH TYPE AB BLOOD HAVE NEITHER A OR B ANTIBODIES, SO IF PATIENT SERUM DOESN’T CLUPMS THEN NLOOD GROUP IS AB. COMMON SITE OF EXTRA HEMATOPOISIS IS LIVER AND SPLEEN. TREPHINE BIOPSY OF BONEMARROW IN DONE FOR APLASTIC ANEMIA.  CRYO is used for FACTOR 8. IN HODGKIN’S there is REED- STRENBERG CELLS.
HEMOLYTIC DISORDER BEST RESPOND TO SPLEENECTOMY —> HEREDITARY SPHEROCYTOSIS > AUTOIMMUNE HEMOLYTIC ANEMIA
PLATELET TRANSFUSION NOT INDICATED IN —> PATIENT WITH SPLEENOMEGALY > TTP > ITP
MOST COMMON ORGAN INVOLVED IN TTP —> KIDNEY AND BRIAN
LEAST DONE IN DIC —> CLOTTING TIME
ANTICOAGULANT NOT GIVEN IN THROMBOCYTOPENIA
35 YEARS OLD FEMALE WITH GENERALIZED LYMPHADENOPATHY —> MON HODGKIN LYMPHOMA
INHERITED CAUSE OF HYPER COAGUBILITY —> MUTATION OF FACTOR 5
BLOOD COMPONENT MOST USEFUL TO PREVENT EXCESSIVE BLOOD LOSS IS —> FRESH FROZEN PLASMA
PT TEST FUNCTION OF COMMON & EXTRINSIC PATHWAY (FACTOR 1,2,5,7,10)
PTT TEST FUNCTION OF COMMON & INTRINSIC PATHWAY ( ALL FACTORS EXCEPT 7 & 13)
DISEASE NOT ASSOCIATED WITH INCREASE RISK OF CLOTTING —> PROTHROMBIN DEFICIENCY
COAGULATIVE DISORDER —> HEMOPHILLIA A /B, VITAMIN K DEFICIENCY
PLATELET DISORDER —> BERNARD-SOULIER SYNDROME, GLANZ MANN’S SYNDROME, ITP, TTP
MIX COAGULATIVE & PLATELET DISORDERS —> VONWILLEBRAND’S DISEASE, DIC
STORAGE OF FERRITIN —> BONE MARROW MACROPHAGES
SERUM IRON —> SYNTHESIZE IN LIVER
VWFACTOR IS SYSNTHESIZE BY —> ENDOTHELIAL CELLS AND MEGAKARYOCYTES
FACTOR 8:C IS ACTIVATED BY THROMBIN(INTRINSIC PATHWAY)
FACTOR 8:C IS SYNTHESIZE IN LIVER AND RETICULO SYSTEM
TISSUE THROMBOPLASTIN ACTIVATES —> EXTRINSIC PATHWAY
COMMON FINAL PATHWAY FACTORS —> 1,2,5,10
FIBRIN STABILIZING FACTOR —> 13
THROMBIN ACTIVATES FACTOR 13 AND 8
EXTRINSIC SYSTEM —> 7
INTRINSIC SYSTEM —> 8,9,11,12
VITAMIN-K DEPENDENT FACTOR —> 9,2,7,10 PROTEIN C AND S
VITAMIN K IS SYNTHESIZE BY COLONIC BACTERIA
VITAMIN K IS ACTIVATED IN LIVER BY EPOXIDE REDUCTASE
ACTIVATED VITAMIN K ALPHA CARBOXYLATE EACH FACTOR
FACTORS IN FIBRIN CLOT —> 1,2,5,8
FIBRINOGEN —> FIBRIN ( + CLOT)
PLASMINOGEN —> PLASMIN ( – CLOT)
ANTICOAGULANTS —> AT3, PROTEIN C AND S
FIBRINOLYTIC —> PLASMINOGEN
FDP AND D-DIMERS —> INTERFERE WITH PLATELET AGGREGATION AND INTERFERE WITH POLYMERIZATION OF FIBRIN
MOST COMMON CAUSE OF DIC —> SEPSIS
DIC —> ACTIVATION OF COAGULATION CASCADE AND CLOT FORMATION STARTS
HEMOPHILLIA A —> FACTOR 8 DEFICIENCY
HEMOPHILLIA B —> FACTOR 9 DEFICIENCY
VONWILLEBRAND DISEASE MOST COMMON HEREDITARY BLEEDING DISORDER, COMBINE PALTELET AND COAGULATION DISORDER.
VONWILLEBRAND FACTOR DEFICIENCY —> DEFICEINT PLATELET PLUG FORMATION, FAILURE OF PALTELET ADHESION
BLEEDING TIME INCREASE —> DEFECT IN PLATELET PLUG FORMATION
GP 1b :- PLATELET ADHESION —> BERNARD,VWF DEFICIENCY
GP2b3a:- PLATELET AGGREGATION —> GLANZMAN’S DISEASE, ASPIRIN, RENAL FAILURE
HEPARIN NEUTRALIZING FACTOR —> PLATELET FACTOR 4
HEPARIN —> GIVEN I/V, SC), t1/2 = 2 hr, safe in pregnancy, catalyzes the binding of antithrombin 3 to factors 2a, 9a, 10a, 11a,12a. Monitor by PTT, rapid anticoagulation
WARFARIN —> GIVEN ORALLY, t1/2= 30+hrs, cross placenta (teratogenic), Decrease hepatic synthesis of K-dependent factor(2,7,9,10), Monitor PT;INR, Long term anticoagulant
AORTIC STENOSIS —> EJECTION SYSTOLIC MURMUR
MITRAL REGURGITATION —> PAN-SYSTOLIC MURMUR
AORTIC REGURGITATION —> EARLY DIASTOLIC MURMUR
MITRAL STENOSIS —> MID-DIASTOLIC MURMUR
IN PREGNANT LADY, WHAT WILL WORSEN —> MITRAL STENOSIS
WIDE SPLITTING —> PULMONARY STENOSIS, RIGHT BUNDLE BRANCH BLOCK
FIXED SPLITTING —> ASD
PARADOXICAL SPLITTING —> AORTIC STENOSIS, LEFT BUNDLE BRANCH BLOCK
MOST SENSITIVE CARDIAC MARKER —> TROPONIN-T
COR-PULMONALE —> PULMONARY HYPERTENSION + RIGHT VENTRICLE HYPERTROPHY
HOLOSYSTOLIC MURMUR, HARSH SOUNDING ACCENTUATED WITH HAND GRIP —> ASD
ACUTE TUBULAR NECROSIS (ATN) —> MOST COMMON CAUSE OF ACUTE RENAL FAILURE
ACUTE TUBULAR NECROSIS MOST COMMON TYPE —> ISCHEMIC ATN
CAUSE OF ISCHEMIC ATN —> PRERENAL AZOTEMIA
NEPHROTIC SYNDROME (GENERALIZED EDEMA) DUE TO DECREASE COLLOID OSMOTIC PRESSURE(HYPOALBUMIN)

MOST COMMON CAUSE OF UPPER UUTI OBSTRUCTION —> RENAL STONE
GOLD STANDARD TO EVALUATE RENAL DISEASE —> URINEANALYSIS
HEMOPTYSIS + GLOMERULONEPHRIRTIS+ IgA DEPOSITE —> Dx GOOD PASTURE SYNDROME
DYSTROPHIC CALCIFICATION —> CALCIUM DEPOSITE IN NECROTIC TISSUE AND SERUM CALCIUM/PHOSPHATE NORMAL
EAMPLE: CHRONIC PANCREATITIS, ATHEROSCLEROTIC PLAQUE, PERIVENTRICULAR CALCIFICATION, TB, DEAD FEATUS, HYDATID CYST
METASTATIC CALCIFIACTION—> CALCIUM DEPOSITE IN NORMAL TISSUE AND SERUM CALCIUM/PHOSPHATE INCREASE
EXAPMLE: INCREASE CALCIUM —> PRIMARY HYPERPARATHYROIDISIM, MALIGANNACY INDUCE HYPERCALCEMIA
INCREASE PHOSPHATEMIA —> RENAL FAILURE, NEPHROCALCINOSIS
DECRAESE PROTEIN INTAKE —> KWASHIORKOR
TOTAL CALORIES DEPRIVIATION —> MARASMUS
SARCOIDOSIS —> GRANULOMA WITH ASTEROID
CHARACTERISTIC FEATURE OF MESOTHELOMA —> PLEURAL PLAQUE
SIGNIFICANT REGARDING CHRON’S DISEASE —> INVOLVE BOTH SMALL AND LARGE INTESTINE
PECULIAR FOR CHRON’S DISEASE —> PERIANAL LESION
HEPATIC HEMANGIOMA —> VINYL CHLORIDE
HEPATOCELLULAR CARCINOMA —> AFLATOXIN
ACUTE ABDOMINAL PAIN WITH MIGRATORY THROMBOPHILIBITIS —> PANCREATIC CARCINOMA
Risk FACTOR FOR CHIROSIS —> ALCOHOL >HEP C> HEP B

Most Common cause of Endocarditis Over all —> Viridans Group

Most Common Cause of Acute endocarditis —> Staph Aureus

Most Common cause of subacute Endocarditis —> Viridans Group

NEUTROPHILIC LEUKOCYTOSIS (>7000CELLS/mm3)
 Infection( Acute appendicitis)
 Sterile inflammation necrosis(acute MI)
 Corticosteroid, Lithium, Catecholamine

NEUTROPENIA(<1500CELLA/mm3)
 Aplastic Anemia
 SLE
 Septic shock
 Endotoxin

EOSINOPHILIA (>700CELLS/mm3)
 Asthma
 Hayfever
 Oenicillin reaction
 Invasive helminth infection
 Polyarteritis Nodosa
 Addison’s disease(cortisol deficiency)

EOSINOPENIA
 Hypercortisolism (Cushing syndrome)

LYMPHOCYTOSIS
VIRAL (INFECTION MONONUCLEOSIS, CMV, VIRAL HEP, TOXOPLASMOSIS
DRUG(PHENYTOIN)
GRAVE’S DISEASE
ACUTE AND CHRONIC LYMPHOCYTIC LEUKEMIA

LYMPHOPENIA
 HIV, DIGEORGE SYNDROM

MONOCYTOSIS
 TB
 SUBACUTE INFECTIVE ENDOCARDITIS

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