GENERAL PATHOLOGY PEARLS BY Dr MARYAM MALIK!!

In the exam of FCPS Part1, MCQs of General Pathology is on the third number if we distribute the MCQs subject vise. So you have to prepare well for the MCQs of General Pathology. There are many Books for General Pathology, select the Book according to the MCQs. Never forget to cover important points as well.

Below are the Importane Points of General pathology. Try to cover all these points as it will be beneficial for you in order to solve the MCQs for FCPS Part 1 Exam.

HYPOXIA: Inadequate Oxygenation of tissue.
Tissue susceptible to hypoxia: Area b/w anterior and middle cerebral arteries, splenic flexure, In Renal Cortex straight portion of proximal Tubule & Co transport channel in thick Ascending Limb of Medulla, Hepato cytes(ZONE 3), Purkinje cells in cerebellum, Neurons in layers 3, 5, 6 of cerebral cortex. Note: Neuron Most adversely Affected cell in tissue Hypoxia

ANAEROBIC GLYCOLYSIS PRIMARY SOURCE OF ATP IN HYPOXIA.
SMOKERS HAVE DECREASE LEVELS OF VITAMIN-C TO NEUTRALIZE FREE RADICALS.
PRIMARY LYSOSOME ARE DERIVE FROM GOLGI APPARATUS.
MALLORY BODIES(CYTOKERATIN INTERMEDIATE FILAMENT) –>ALCOHOLIC LIVER DISEASE.
LEWY BODIES(DAMAGED NEURO FILAMENT) —> PARKINSON’S DISEASE.
MOST COMMON CAUSE OF
FATTY CHANGE —-> ALCOHOL.
AMYLOID STAINS RED WITH CONGO RED & APPLE GREEN BIREFRINGENCE WHEN POLARIZED.
HEMOSIDERIN: —-> BREAKDOWN PRODUCT FERRITIN DEPOSITION IN PARANCHYMAL CELLS. —-> BREAKDOWN PRODUCT OF RBC DEGRADATION ON MACROPHAGES(‘’HEART FAILURE’’) CELLS.

EXAMPLES OF FREE RADICAL INJURY:

  • ACETAMINOPHEN —-> FREE RADICAL IN LIVER AND KIDNEY
  • CCL4–> LIVER CELL NECROSIS —-> FATTY CHANGE
  • ISCHEMIC/REPERFUSION INJURY IN ACUTE MYOCARDIAL INFARCTION
  • RETINOPATHY OF PREMATURITY
  • IRON OVERLOAD DISEASE —-> HEMOCHROMATOSIS, HEMOSIDEROSISà HYDROXY FREE RADICAL DAMAGE OF TISSUE
  • COPPER OVERLOAD —-> WILSON’S DISEASE à HYDROXY FREE RADICAL DAMAGE OF TISSUE

 

HYPOXEMIA  —-> Decrease Arterial Oxygen Pressure (PaO2)

VENTILATION DEFECT —-> Intra pulmonary shunt

PERFUSION DEFECT —-> Dead Space

ANEMIA  —–> Normal  PaO2 and SaO2

Ischemia —–> Decrease in Arterial blood Inflow/ Venous Outflow

Apoptosis is Programmed cell death,  Physiological/Pathological, Shrinkage in cell size occur in Apoptosis.
Necrosis is Invariably Pathological, cell Swelling, sum of degenerative and inflammatory reaction occurring after tissue death.
Nuclear changes in necrosis —–> Pyknosis  -> Karyorrhexis -> Karyolysis.
Necrotic cells —–> more eosinophillic, appear glassy(glycogen loss), attracts calcium salt.
Coagulative Necrosis most common pattern.
Ischemic and hypoxic Injury are most common forms of cell injury in clinical medicine..
Coagulative necrosis structural outline is preserve with denaturation of enzyme and structural protein..
Primary type of necrosis in dead tissue is  Coagulative necrosis.
Dry gangrene is predominantly Coagulative necrosis.

Varient of Coagulative necrosis is caseous necrosis ( Acellular, cheese material ).
Most common cause of Caseous necrosis is Tuberculosis.
Wet gangrene, Abscess in bacterial infection & brain infarction is predominantly —–> Liqueficative necrosis.
Traumatic Fat Necrosis —–> not enzyme Mediated .
Enzymatic Fat necrosis —–> Acute Pancreatitis.
Fibrinoid Necrosis —–> small muscular arteries, arterioles, venules & glomerular capillaries. Infarction is gross manifestation of coagulative necrosis secondary to sudden occlusion of vessel.
Ischemic —–> heart kidney spleen.
Red —-> lung small bowel.
Extrinsic pathway Of Apoptosis —–> Binding of TNF to its receptors.
Intrinsic Pathway Of Apoptosis —–> Mitochondrial Leakage of cytochrome c into cytosol.
BCL2 gene —–> Anti apoptosis gene( located at chromosome 18)

REVERSIBLE CELL INJURY:-

  • Decrease systhesis of ATP
  • Decrease Function of Na+ K+ ATPase Pump
  • K+ Eflux
  • Cell Swelling(Hydropic)
  • ER Swelling
  • Influx of Na+ and Water

 

  • Switch to glycolysis
  • Decrease Intracellular PH
  • Decrease Glycogen
  • Increase Lactic Acid
  • Detachment Of Ribosome From RER

 

IR-RVERSIBLE INJURY:-1 ( Membrane damage Play critical role)

  • Massive Influx of Calcium into cell

2) Marked Mitochondrial dysfunctionà swelling + no ATP

3) Rupture of Lysosome

4)Nuclear changes —–> Pyknosis  -> Karyorrhexis -> Karyolysis

 

DYSPLASIA    —–> PRECURSOR TO CANCER

  • DISODERED CELL GROWTH
  • MAY PROGRESS TO CANCER

 

Redness,colour,tumor —-> Histamine mediated

Mast cell Release —–> Pre-formed Histamine

Histamin —–> Most Important Chemical Mediator of Acute Inflammation

Neutrophil primary cell of acute Inflamation

In Acute Inflammation Vasoconstriction of arterioles —–> first Sequential Vascular event

In Acute Inflammation Margination —–> first sequential cellular event

Types of Acute Inflammation —–> Purulent, Fibrinous, serous, Pseudo membranous Inflammation

Necrosis is present in Acute Inflammation with no scar tissue formation

Most common cause of skin abcess —–> S.Aureus

Selectins —–> ROLLS!! (rolling of neutrophil)

Integrins —–> Neutrophil Adhesion Molecules

Neutrophil Leukocytosis —–> Catecholamine, Corticosteroids, Lithium

Neutropenia —–> Endotoxins

Chemotaxis

—-> Directed Migration Of Neutrophils

—–>Mediated by C5a, LTB4, IL-8

Anaphylatoxin —-> C3a + C5a

Opsonin —–> IgG + C3b .

Opsonization Defect —–> Bruton’s Agammaglobulinemia

 

Produce Pain —-> PGE2 + Bradykinin

Produce Fever —–> PGE2 + IL-1 + TNF

Vasodilators —-> Histamine, Nitric Oxide, PGI2

 

Most Common cause Of Chronic Inflammation —–> Infection

Specialized type of Chronic Inflammation —-> Granulomatus Inflammation

Primary Leukocytes in Chronic Inflammation —-> Monocytes & Macrophages

Seen in Chronic Inflammation —–> Scar Tissue Formation, disability, Amyloidosis

Main Immunoglobulin in Acute Inflammation —-> IgM

Main Immunoglobulin in Chronic Inflammation —-> IgG

Caseation is due to lipid release from cell wall of dead pathogens.

Main Immunoglobulin is IgM for Acute and IgG for chronic Inflammation

Cell types in TB Granuloma à Macrophages & CD4 Helper T cells

Important in formation & Maintenance  of granulomaà TNF- alpha

G1Phase —->Most Variable Phase in cell cycle

G1-S Phase —-> Most Critical Phase in cell cycle

Collagen is Major Fibrous Component of Connective Tissue

Tropocollagen —–> Structural Unit of Collagen

In Wound Healing Ascorbic Acid —–> required for Hydroxylation of Proline & lysine

In Wound Healing Ascorbic Acid Deficiency —–> decrease Tensile Strength of wound

Keloid —–> Excess type 3 Collagen

In Wound Healing Strength —-> due to type 3 Collagen

Scar tissue Strength —-> due to Type 1 collagen

Persistent Infection —-> Most common cause of Impaired wound healing.

Type 2 Pneumocytes —-> Key repair cell of lung

Astrocytes —–> Proliferate in response to injury

Muscle undergoes Atrophy in 15 days

Corticosteroids Increases Neutrophil and decreases Lymphocytes & Eosinophils

Innate Immunity —–> First Defense against Pathogen

IgG & IgM synthesis —–> Begins After Birth

Class 1 Antigen —-> Recognized by CD8 T Cells and Natural Killer Cells

Class 2 Antigen —–> Recognized by CD 4 T Cells

CD8 T cell Mediated —-> Altered Class 1 Antigens (Contact Dermatitis)

CD 8 T Cells Interact With Altered MHC Class 1 Antigens on Neoplastic, Virus Infected or Donor Graft Cells , causing Cell Lysis

ABO BLOOD GROUP COMPATIBILITY ——> MOST IMPORTANT REQUIREMENT FOR SUCCESSFUL TRANSPLANTATION

FETUS IS AN ALLOGRAFT THAT IS NOT REJECTED BY THE MOTHER

Hyper Acute Rejection (with in Minutes) —-> Irreversible Type 2 HSR

GRAFT VERSUS HOST REACTION —-> Jaundice, Diarrhea, Dermatitis

Best Allograft Survival Rate —–> Cornea

Most Common Cardiac Finding in SLE —–> Fibrinous Percarditis with Effusion

Screening Test for SLE —> Serum ANA

Confirmatory Test for SLE —> Anti dsDNA and Anti Sm Antibodies

Screening Test / Sensitivity Test for AIDS —-> ELISA

Confirmatory Test/ Specific  Test for AIDS —-> WESTERN BLOT

Most Sensitive Test for Diagnosis Of Acute HIV before Seroconversion —-> HIV Viral Load

Most Common Malignancy in AIDS —-> Kaposi’s Sarcoma(HHV-8)

Most Common Cause of Blindness in AIDS —-> CMV

CNS Fungal Infection In Aids Is Cause by —-> Cryptococcus

C2 Deficiency —–> Most Common Complement Deficiency

AMYLOID —-> Fibrillar Protein that forms deposits in interstitial tissue( organ dysfunction)

Adult Diarrhea &   Loss whole Blood —-> Isotonic Loss with ECF Contraction

Excessive Isotonic Saline —-> Isotonic Gain with ECF Expansion

Loop diuretics, Addison’s Disease and 21-Hydroxylase Deficiency —-> Hypertonic loss with ECF Contraction and ICF Expansion

SIADH, Compulsive Water Drinker —-> Net gain in only water (Hypo osmotic) Volume Expansion involving               both  ECF and ICF

Right Heart Failure, Cirrhosis, Nephrotic Syndrome —-> Net gain in water in excess of Sodium

Hypokalemia Increase Risk Of Metabolic Alkalosis

Hyperkalemia  Increase Risk of Metabolic Acidosis

ADDISON’S Disease —-> Hyponatermia, Hyperkalemia, Metabolic Acidosis

PRIMARY ALDOSTERONISM —-> Hypernatremia,Hypokalemia, Metabolic Alkalosis, LOW RENIN type hypertension, absence of pitting edema

BARTTER’S SYNDROME —-> Hypokalemia, Metabolic Alkalosis, Increase Aldosterone

SIADH —-> Small cell Carcinoma of lung Most Common Cause

  • Serum Sodium <120 m Eq/L, Dilution Disorder

 

HYPOKALEMIA —-> INSULIN, BETA 2-AGONIST(ALBUTEROL)à MAY SHIFT K+ INTO CELL

MOST COMMON CAUSE OF HYPOKALEMIA—-> LOOPAND THIAZIDE DIURETICS

HYPO KALEMIA ECG —–>U WAVE

  HYPERKALEMIA—-> DIGITALIS, BETA BLOCKER,SUCCINYLCHOLINE —-> MAY SHIFT K+ OUT CELL

MOST COMMON CAUSE OF HYPERKALEMIA —-> RENAL FAILURE

HYPERKALEMIA ECG —-> PEAKED T WAVES

RESPIRATORY ACIDOSIS(PaCO2 > 45mmHg). RESPIRATORY ALKALOSIS (PaCO2 <33 mmHg). METABOLIC ACIDOSIS ( HCO-3 <22 mEq/L). METABOLIC A LKALOSIS ( HCO-3 > 28 mEq/L). CHRONIC BRONCHITIS DUE TO SMOKING COMMON CAUSE OF RESPIRATORY ACIDOSIS(PaCO2 > 45mmHg). ANXIETY MOST COMMON CAUSE OF RESPIRATORY ALKALOSIS (PaCO2 <33 mmHg). TETANY COMMONLY OCCURS IN ACUTE RESPIRATORY ALKALOSIS. LACTIC ACIDOSIS MOST COMMON INCREASE ANION GAP METABOLIC ACIDOSIS. OBSTRUCTIVE LUNG DISEASE —> CHRONIC BRONCHITIS, CYSTIC FIBROSIS, PULMONARY EDEMA, ARDS, RDS, SEVERE BRONCHIAL ASTHMA. RESTRICTIVE LUNG DISEASEà SARCOIDOSIS, ASBESTOSIS, PULMONARY EMBOLUS, MILD BRONCHIAL ASTHMA. EDEMA —–> EXCESS FLUID IN INTERSTITIAL SPACE. TRANSUDATE —–> PROTEIN AND CELL POOR FULID. EXUDATE —–> PROTEIN RICH (>3 g/dL) AND CELL RICH(Neutrophil) FLUID

—->Swelling of tissue but no pitting edema

—-> ACUTE INFLAMMATION

LYMPHEDEMA —-> PROTEIN RICH FLUID

PITTING EDEMA IN RIGHT HEART FAILUREàINCREASE HYDROSTATIC PRESSURE

PITTING EDEMA IN CIRRHOSIS —-> DECREASE ONCOTIC PRESSURE

 

HEPARIN AND WARFARIN —–> PREVENTS VENOUS THROMBOSIS

ASPIRIN —–> PRVENTS ARTERIAL THROMBOSIS

MOST COMMON SITE FOR VENOUS THOMBOSIS —-> DEEP VEIN IN LOWER EXTREMITY BELOW THE KNEE

PULMONARY THROMBOEMBOLISMà MAJORITY ORIGINATE IN FEMORAL VEINS

SHOCK:

HYPOVOLEMMIC …CARDIAC OUTPUT , PERIPHERAL VASCULAR RESISTANCE AND MIXED VENOUS OXYGEN CONTENT DECREASES

CARDIOGENIC SHOCK … CARDIAC OUTPUT DECREASE , PERIPHERAL VASCULAR RESISTANCE INCREASE AND  MIXED VENOUS OXYGEN CONTENT DECREASE

SEPTIC— CARDIAC OUTPUT Increase  , PERIPHERAL VASCULAR RESISTANCE decrease AND MIXED VENOUS OXYGEN CONTENT Increase

MOST COMMON GENETIC CAUSE OF PRIMARY AMENORRHEA —-> TURNER’S SYNDROME

MOST COMMON GENETIC CAUSE OF MENTAL RETARDATION —-> DOWN SYNDROME

TRIPLE MARKER FOR  DOWN SYNDROME —–> DECREASE AFP & URINE ESTRIOL, INCREASE HCG

 

MOST COMMON X-LINKED DISORDER —-> FRAGILE X-SYNDROME

NORMAL FEMALE HAVE ONE BARR BODY AND NORMAL MALE HAVE NONE

EDWARD’S SYNDROME —-> TRISOMY 18

PATAU’S SYNDROME —-> TRISOMY 13

TURNER SYNDROME —-> 45,X KARYOTYPE (60%)

KLINEFELTER’S SYNDROME —–> XXY KARYOTYPE (NON DISJUCTION), HYPOGONADISM, ONE BARR BODY, DECREASE TESTOSTERONE, INCREASE LH AND FSH.

ALCOHOL —-> MOST COMMON TERATOGEN (FETAL ALCOHOL SYSNDROME)

MOST COMMON PATHOGEN CAUSING A CONGENITAL INFECTION —-> CMV

TORCH SYNDROME —-> TOXOPLASMOSIS, RUBELLA, CMV, HSV

 

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