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MBBS 2nd Year Pathology - 10-Day Exam Survival Plan

Goal: Pass the university exam | Books: Robbins Basic Pathology (primary)

10-Day Daily Study Plan

Overview of Distribution

Days	Focus Area
Day 1-2	Cell Injury, Adaptations, Cell Death
Day 3-4	Inflammation & Repair
Day 5-6	Neoplasia & Carcinogenesis
Day 7	Blood Disorders (Anemias, Leukemias)
Day 8	Lymph Node Disorders + Thrombosis/Embolism/Shock
Day 9	Organ Pathology - Heart, Lung, Kidney
Day 10	Organ Pathology - Liver, GIT + Revision + PYQs

DAY 1 - Cell Injury & Cell Death

Key Concepts to Cover

Cell Injury Types:

Reversible: cellular swelling, fatty change - eosinophilic, swollen cells with clumped chromatin
Irreversible: cell death (necrosis or apoptosis)
Causes: hypoxia (#1), toxins, immunologic, genetic, infections, nutritional

Necrosis vs. Apoptosis - THE MOST IMPORTANT TABLE:

Feature	Necrosis	Apoptosis
Cause	Pathologic	Physiologic or pathologic
ATP	Not required	Required
Inflammation	YES	NO
Cell size	Swells	Shrinks
Membrane	Disrupted	Intact (blebs)
DNA	Random digestion	Ladder pattern (internucleosomal)
Chromatin	Clumped at periphery	Condensed, fragmented
Histology	Ghost outlines, pink cytoplasm	Apoptotic bodies

Types of Necrosis (high-yield for spotters and MCQs):

Type	Appearance	Classic Example
Coagulative	Cell outlines preserved, "ghost cells"	MI, infarcts (all organs except brain)
Liquefactive	Pus, liquid	Brain infarct, bacterial abscess
Caseous	Cheese-like, white, amorphous	TB (granuloma center)
Fat	Chalky white deposits (calcium soaps)	Acute pancreatitis, breast trauma
Fibrinoid	Immune complexes + fibrin in vessel walls	Malignant hypertension, vasculitis
Gangrenous	Coagulative + liquefactive	Diabetic limb

Mechanisms of Cell Injury (Important for essays):

Mitochondrial dysfunction → ATP depletion
Oxidative stress / ROS → lipid peroxidation, DNA damage
Calcium influx → activates phospholipases, proteases
Membrane damage
ER stress
DNA damage

Apoptosis Pathways:

Intrinsic (mitochondrial): DNA damage → p53 ↑ → BAX ↑, BCL-2 ↓ → cytochrome c release → caspase 9 → caspase 3
Extrinsic (death receptor): FasL binds Fas (CD95) → FADD → caspase 8 → caspase 3

DAY 2 - Cellular Adaptations + Intracellular Depositions

Cellular Adaptations

Adaptation	Definition	Example
Hypertrophy	↑ cell size (not number)	Cardiac hypertrophy in HTN
Hyperplasia	↑ cell number	Endometrial hyperplasia (estrogen), BPH
Atrophy	↓ cell size and function	Disuse, denervation, ischemia
Metaplasia	One adult cell type → another	Barrett's esophagus (squamous → columnar), smoking (columnar → squamous in bronchi)
Dysplasia	Disordered growth - pre-neoplastic	CIN in cervix

Key: Metaplasia is reversible. Dysplasia may be reversible. Neoplasia is irreversible.

Intracellular Deposits

Fatty change (steatosis): liver - alcohol, obesity, DM - Oil Red O stain
Cholesterol deposits: atherosclerotic plaques, foam cells
Hemosiderin: iron overload - Prussian blue stain
Lipofuscin: "wear and tear" brown pigment - perinuclear in old cells
Melanin: neural crest origin, melanocytes
Bilirubin: jaundice
Pathologic calcification:
- Dystrophic: in dead/dying tissue, serum calcium NORMAL (TB, atherosclerosis, infarcts)
- Metastatic: in normal tissue, serum calcium ELEVATED (hyperparathyroidism, vitamin D toxicity)

DAY 3 - Acute Inflammation

General Features

Signs (Celsus): Rubor, Calor, Tumor, Dolor + Functio laesa (5th, Virchow)
Purpose: Eliminate cause + initiate repair

Vascular Changes

Transient vasoconstriction
Vasodilation (histamine, NO) → redness and heat
Increased vascular permeability → exudate
Stasis → leukocyte margination

Mechanisms of Increased Permeability

Endothelial contraction (histamine, bradykinin) - immediate, transient
Direct endothelial injury - immediate, sustained
Leukocyte-mediated injury - delayed
Angiogenesis-related leakage

Leukocyte Recruitment (Step-by-step - essay favorite)

Margination - leukocytes move to periphery
Rolling - selectins (P-selectin, E-selectin) + PSGL-1
Adhesion/Activation - integrins (LFA-1, Mac-1) + ICAM-1, VCAM-1; chemokines activate
Transmigration (Diapedesis) - through vessel wall via PECAM-1 (CD31)
Chemotaxis - movement toward C5a, LTB4, IL-8, bacterial products
Phagocytosis - opsonization (IgG, C3b) → engulfment → killing (O2-dependent and independent)

O2-dependent killing: NADPH oxidase → O2•- → H2O2 → HOCl (myeloperoxidase) - most important O2-independent killing: lysozyme, defensins, lactoferrin, major basic protein (eosinophils)

Inflammatory Mediators (HIGH YIELD TABLE)

Mediator	Source	Action
Histamine	Mast cells, basophils	Vasodilation, permeability ↑ (immediate)
Serotonin	Platelets	Permeability ↑
PGE2, PGI2	Arachidonic acid (COX)	Vasodilation, fever, pain
LTB4	Arachidonic acid (LOX)	Chemotaxis of neutrophils
LTC4, LTD4, LTE4	Arachidonic acid (LOX)	Bronchoconstriction, permeability ↑
PAF	Leukocytes, endothelium	Platelet aggregation, permeability ↑
C3a, C5a	Complement	C5a: chemotaxis, opsonization; C3a, C5a: mast cell degranulation
C3b	Complement	Opsonization
IL-1, TNF	Macrophages	Fever, acute phase response, endothelial activation
IL-8 (CXCL8)	Macrophages, endothelium	Neutrophil chemotaxis
IL-6	Macrophages	Fever, acute phase proteins
NO	Endothelium	Vasodilation
Bradykinin	Kinin system	Pain, vasodilation, permeability ↑

Outcomes of Acute Inflammation

Resolution (complete restoration)
Abscess formation
Organization/Fibrosis
Progression to chronic inflammation

DAY 4 - Chronic Inflammation, Granulomas & Tissue Repair

Chronic Inflammation

Characterized by: mononuclear infiltrate (lymphocytes, macrophages, plasma cells), tissue destruction, attempts at repair occurring simultaneously
Causes: persistent infections (TB, syphilis), autoimmune (RA, SLE), foreign body, prolonged exposure to toxins

Granulomatous Inflammation (VERY HIGH YIELD)

Definition: Focal accumulation of activated macrophages (epithelioid cells) + Langhans giant cells (nuclei at periphery) + lymphocytes
Mechanism: CD4+ T cells → IFN-γ → activates macrophages

Types of Granulomas:

Type	Caseation	Example
Caseating	YES (cheesy necrosis center)	TB, Histoplasmosis, Coccidioidomycosis
Non-caseating	NO	Sarcoidosis, Crohn's disease, Foreign body, Leprosy (tuberculoid), Cat scratch disease

Sarcoidosis granuloma: non-caseating + Schaumann bodies + asteroid bodies

Tissue Repair

Labile cells (continuously dividing): skin, GI epithelium, bone marrow - best regeneration Stable cells (quiescent but can divide): liver, kidney, pancreas - moderate regeneration Permanent cells (cannot divide): neurons, cardiac muscle, skeletal muscle - no regeneration

Healing by primary intention (clean wound) vs secondary intention (gaping wound):

1° intention: minimal scar, re-epithelialization in 24-48 hrs
2° intention: wound contraction (myofibroblasts), more granulation tissue, larger scar

Wound Healing Sequence:

0-24 h: Neutrophils (first responders)
24-48 h: Monocytes → macrophages (#1 cell for healing)
3-5 days: Granulation tissue (fibroblasts + new blood vessels)
Week 2+: Collagen deposition, wound strength ↑
Months: Scar maturation (type III collagen → type I collagen)

DAY 5 - Neoplasia Part 1 (Basics & Carcinogenesis)

Benign vs. Malignant

Feature	Benign	Malignant
Growth rate	Slow	Fast
Borders	Well-defined, encapsulated	Ill-defined, invasive
Differentiation	Well differentiated	Varies (poorly diff. = worse)
Mitoses	Rare, normal	Frequent, abnormal
Metastasis	NO	YES (hallmark of malignancy)
Necrosis	Rare	Common
Nuclear features	Normal N:C ratio	High N:C, hyperchromatism, prominent nucleoli

Nomenclature

Origin	Benign	Malignant
Epithelium	Adenoma / Papilloma	Adenocarcinoma / Squamous cell carcinoma
Mesenchyme (fibrous)	Fibroma	Fibrosarcoma
Mesenchyme (fat)	Lipoma	Liposarcoma
Mesenchyme (muscle)	Leiomyoma (smooth) / Rhabdomyoma (skeletal)	Leiomyosarcoma / Rhabdomyosarcoma
Blood vessels	Hemangioma	Angiosarcoma
Bone	Osteoma	Osteosarcoma
Nerve tissue	Neuroma	Neuroblastoma, Glioma
Melanocytes	Nevus	Melanoma

Carcinogenesis - Hallmarks of Cancer (Hanahan & Weinberg)

Self-sufficiency in growth signals
Insensitivity to anti-growth signals
Evasion of apoptosis
Limitless replicative potential (telomerase)
Angiogenesis (VEGF)
Invasion and metastasis
Reprogramming energy metabolism
Evading immune destruction

Oncogenes vs. Tumor Suppressor Genes

	Oncogene	TSG
Normal gene	Proto-oncogene	Anti-oncogene
Effect of mutation	Gain-of-function	Loss-of-function
Alleles needed	1 (dominant)	2 (recessive - Knudson two-hit)
Examples	RAS, MYC, HER2/neu, BCR-ABL	p53, RB, APC, BRCA1/2

High-yield Oncogene mnemonics:

RAS: mutated in ~30% of all cancers; GTPase mutation
MYC: Burkitt lymphoma t(8;14)
BCR-ABL: CML, t(9;22) Philadelphia chromosome
HER2/neu (c-erbB2): breast cancer amplification → target of Herceptin
RET: MEN2A, MEN2B, papillary thyroid cancer

Tumor Suppressor Genes:

RB (13q14): Retinoblastoma - two-hit hypothesis - controls G1/S checkpoint
p53 (17p13): "guardian of the genome" - mutated in >50% of cancers; Li-Fraumeni syndrome
APC: Familial adenomatous polyposis (colon cancer)
BRCA1/2: Breast and ovarian cancer
VHL: Renal cell carcinoma, hemangioblastoma
NF1/NF2: Neurofibromatosis

DAY 6 - Neoplasia Part 2 (Spread & Tumor Markers)

Routes of Metastasis

Lymphatic (carcinomas): most common route for carcinomas → regional nodes first
Hematogenous (sarcomas): liver and lungs are most common sites
Seeding of body cavities: ovary, GI tumors → peritoneal spread (Krukenberg tumor)
Perineural spread: prostatic, pancreatic carcinomas

Virchow's node: Left supraclavicular lymph node - metastasis from gastric/GI cancer

Tumor Markers (VERY HIGH YIELD for MCQs)

Marker	Associated Cancer	Notes
AFP (alpha-fetoprotein)	Hepatocellular carcinoma, Yolk sac tumor	Also elevated in pregnancy
CEA	Colorectal, pancreatic, gastric	Non-specific
CA-125	Ovarian carcinoma
CA 19-9	Pancreatic carcinoma
CA 15-3	Breast cancer
PSA	Prostate cancer	Best tumor marker for screening
hCG	Choriocarcinoma, testicular (choriocarcinoma component)
LDH	Lymphoma, testicular germ cell	Non-specific
Calcitonin	Medullary thyroid carcinoma (C-cell tumor)
S-100	Melanoma, neural tumors, Langerhans cells
Chromogranin A	Neuroendocrine tumors, carcinoids
TRAP	Hairy cell leukemia
CD markers	Leukemia/lymphoma classification

Special Stains for Tumor Histology

Stain	What it identifies
PAS	Glycogen, fungi
Prussian Blue	Iron, hemosiderin
Congo Red + polarized light	Amyloid (apple-green birefringence)
Mucicarmine	Mucin (adenocarcinoma, Cryptococcus)
Ziehl-Neelsen (acid-fast)	Mycobacterium TB
Silver stain	Fungi, H. pylori, reticulin

DAY 7 - Blood Disorders (Anemias & Leukemias)

Anemias - Classification

By MCV:

Microcytic (MCV <80): IDA, thalassemia, sideroblastic, lead poisoning
Normocytic (MCV 80-100): Aplastic anemia, hemolytic anemia (acute), ACD (anemia of chronic disease)
Macrocytic (MCV >100): B12 deficiency, folate deficiency, liver disease, hypothyroidism

Iron Deficiency Anemia (IDA) - Most Common

Finding	IDA	Anemia of Chronic Disease
Serum iron	↓	↓
TIBC	↑	↓ or N
Ferritin	↓	↑ (acute phase reactant)
Transferrin saturation	↓	↓
Smear	Microcytic hypochromic, pencil cells	Normocytic or microcytic

Thalassemia

	Alpha	Beta
Gene	HBA1/HBA2 (chr 16)	HBB (chr 11)
Hydrops fetalis	4 gene deletion (severe, fatal)	N/A
HbH disease	3 gene deletion	N/A
Trait	2 gene deletion	One gene mutated (β+/β or β0/β)
Major	N/A	β0/β0 - severe, transfusion dependent
Treatment	Supportive	Transfusions, stem cell transplant

Sickle Cell Disease

HbS: Glu → Val at position 6 of beta-globin chain
Triggers: hypoxia, dehydration, acidosis, cold, infection
Complications: vaso-occlusion (bone pain, dactylitis), splenic sequestration, aplastic crisis (parvovirus B19), acute chest syndrome, stroke, priapism
Peripheral smear: sickle cells, target cells, Howell-Jolly bodies (functional asplenia)

Leukemias - Key Distinctions

	ALL	CLL	AML	CML
Age	Children (#1 childhood cancer)	Elderly	Adults (>60)	Middle-aged adults
Cell	Pre-B/T lymphoblast	Mature B-cells	Myeloblasts	Mature myeloid + stem cell
Marker	TdT+, CD10 (CALLA), CD19	CD5+, CD19+, CD23+	Auer rods in blast (pathognomonic)	Philadelphia chr (BCR-ABL)
Translocation	t(12;21) - best prognosis	-	t(15;17) - M3 (APL) → ATRA treats	t(9;22)
Treatment	Chemo (high cure rate)	Watch-wait/chlorambucil	Chemo; ATRA for APL	Imatinib (Gleevec)

Key: Auer rods = AML (myeloperoxidase+ granular rods in blasts)

DAY 8 - Lymphomas + Thrombosis/Embolism/Shock

Hodgkin's vs. Non-Hodgkin's Lymphoma

	Hodgkin's	Non-Hodgkin's
Cell	Reed-Sternberg cell (CD15+, CD30+, CD45-)	B or T cell lymphocyte
Spread	Contiguous (predictable)	Non-contiguous
Extranodal involvement	Rare	Common
B symptoms	More common	Present
Bimodal age peak	Young adults + elderly	Varies by type
Prognosis	Generally good	Varies

Reed-Sternberg cell: "Owl eye" appearance - large binucleated cell with prominent nucleoli

Classic HL subtypes (by frequency):

Nodular sclerosis (most common overall, young women)
Mixed cellularity (EBV associated, HIV patients)
Lymphocyte rich (best prognosis)
Lymphocyte depleted (worst prognosis, elderly, HIV)

Important NHL entities:

Type	Feature
Diffuse large B-cell (DLBCL)	Most common NHL overall
Follicular lymphoma	t(14;18), BCL-2 overexpression; indolent
Burkitt's lymphoma	t(8;14), MYC; "starry sky" pattern; EBV (African); jaw in endemic form
Mantle cell lymphoma	t(11;14), cyclin D1; CD5+
Marginal zone (MALT)	H. pylori-associated gastric lymphoma

Thrombosis, Embolism & Infarction

Virchow's Triad:

Endothelial injury (most important)
Stasis or turbulent flow
Hypercoagulability

Emboli types:

Pulmonary embolism: DVT (leg veins) → saddle embolus → sudden death; Hampton's hump on CXR
Paradoxical embolism: DVT → arterial system through patent foramen ovale
Fat embolism: long bone fractures → petechiae, confusion, hypoxia (48-72 h)
Amniotic fluid embolism: DIC, respiratory failure, delivery
Air embolism: iatrogenic
Septic embolism: infective endocarditis

Shock

Type	Cause	CO	SVR	PCWP
Hypovolemic	Hemorrhage, dehydration	↓	↑	↓
Cardiogenic	MI, cardiac failure	↓	↑	↑
Distributive/Septic	Infection, anaphylaxis	↑ (early)	↓	↓
Obstructive	PE, cardiac tamponade	↓	↑	Varies

Stages of shock:

Compensated (tachycardia, vasoconstriction)
Progressive (tissue hypoperfusion, lactic acidosis, AKI)
Irreversible (multi-organ failure, death)

DAY 9 - Organ Pathology: Heart, Lung, Kidney

Heart

IHD (Ischemic Heart Disease) - Timeline after MI:

Time	Gross Change	Micro Change
0-4 h	None visible	None
4-12 h	Dark mottling	Waviness of fibers at border
12-24 h	Dark mottling	Coagulative necrosis, neutrophils
1-3 days	Pallor	Neutrophil infiltrate
3-7 days	Yellow-tan pallor	Macrophages, granulation tissue
1-2 weeks	Depressed yellow-tan	Granulation tissue, collagen
2 months	White fibrotic scar	Dense collagen, scar

Complications of MI: arrhythmia (#1 cause of death, first 24 h), cardiogenic shock, free wall rupture (3-7 days), papillary muscle rupture (mitral regurgitation), ventricular aneurysm, Dressler syndrome (2-10 weeks, fibrinous pericarditis)

Rheumatic Heart Disease:

Caused by: Group A beta-hemolytic Streptococcus → molecular mimicry
Jones Criteria: JONES (J-joints, O-carditis, N-nodules, E-erythema marginatum, S-Sydenham's chorea)
Aschoff bodies: pathognomonic - fibrinoid necrosis + Anitschkow cells (caterpillar cells)
Most common valve affected: Mitral (MS most common lesion)

Lung

Pneumonia:

Lobar pneumonia: S. pneumoniae (#1) - 4 stages: congestion → red hepatization → gray hepatization → resolution
Bronchopneumonia: S. aureus, Klebsiella, patchy consolidation
Atypical pneumonia (interstitial): Mycoplasma, viruses, Legionella - "walking pneumonia"

Lung cancer:

Type	Location	Marker/Feature
Squamous cell carcinoma	Central (hilar)	Keratin pearls, intercellular bridges; Cavitation; PTHrP (hypercalcemia)
Adenocarcinoma	Peripheral	Most common overall; EGFR, ALK mutations; Clara cells
Small cell (SCLC)	Central	Neuroendocrine (ACTH, ADH); worst prognosis; paraneoplastic syndromes; treat with chemo only
Large cell	Peripheral	Diagnosis of exclusion

Pleural Effusion:

Transudate: CHF, cirrhosis, nephrotic - low protein
Exudate: infection, malignancy, TB - high protein

Kidney

Glomerulonephritis Classification:

Disease	Mechanism	LM	IF	EM	Clinical
PSGN	Immune complex (post-strep)	Hypercellular, "lumpy-bumpy"	Granular (IgG, C3)	Subepithelial "humps"	Nephritic, children, 1-3 weeks post-infection
IgA nephropathy (Berger)	IgA immune complex	Focal mesangial	IgA mesangial	Mesangial	Nephritic, episodic hematuria with URTI
Membranous nephropathy	In situ immune complex	Thickened GBM, "spike and dome"	Granular IgG	Subepithelial deposits	Nephrotic, adults, #1 nephrotic in adults
Minimal change disease (MCD)	Podocyte injury (T-cell cytokines)	Normal	Negative	Podocyte foot process effacement	Nephrotic, #1 in children
FSGS	Podocyte injury	Focal sclerosis	IgM, C3 (focal)	Podocyte fusion	Nephrotic, HIV, obesity
Rapidly progressive GN (RPGN)	Various (Goodpasture, ANCA, immune complex)	Crescents	Linear IgG (Goodpasture), pauci-immune (ANCA), granular (immune complex)	Varies	Nephritic, rapidly progressive renal failure

DAY 10 - Liver + GIT + Rapid Revision + PYQs

Liver

Fatty Liver/Steatosis:

Alcohol: reversible, pericentral (zone 3) - Mallory bodies in alcoholic hepatitis
NAFLD/NASH: metabolic syndrome, obesity, DM

Hepatitis:

Viral: A & E - feco-oral, no chronic; B, C, D - blood-borne; Chronic → cirrhosis → HCC
Drug-induced: paracetamol (zone 3 necrosis), tetracycline (microvesicular steatosis)
Alcoholic hepatitis: Mallory-Denk bodies (cytokeratin), PMN infiltrate, ballooning degeneration

Cirrhosis:

End-stage liver disease: fibrosis + nodular regeneration
Macro (alcoholic): micronodular (<3mm); macro (post-viral): macronodular (>3mm)
Complications: portal hypertension → esophageal varices, splenomegaly, ascites, caput medusae; hepatic encephalopathy; SBP; hepatorenal syndrome; HCC

Hepatocellular Carcinoma (HCC):

Risk: cirrhosis (#1), Hep B/C, aflatoxin (Aspergillus)
Marker: AFP

GIT

Peptic Ulcer Disease:

H. pylori (90% of duodenal, 70% of gastric)
Gastric ulcer: pain with eating (food ↑ acid → pain), weight loss
Duodenal ulcer: pain relieved by food (food buffers acid), more common, less malignant risk

Inflammatory Bowel Disease:

	Crohn's Disease	Ulcerative Colitis
Location	Any part of GI (mouth to anus), skip lesions	Rectum + extends proximally, continuous
Depth	Transmural ("full thickness")	Mucosal only
Granulomas	Yes (non-caseating)	No
Complications	Fistulas, strictures, malabsorption	Toxic megacolon, cancer risk (10-20 yrs)
Serologies	ASCA+	pANCA+
Appearance	Cobblestone, string sign on X-ray	Lead pipe colon, pseudopolyps

Colorectal Cancer:

Adenoma-carcinoma sequence: APC mutation → K-RAS → SMAD4/DCC → p53 → carcinoma
FAP (familial adenomatous polyposis): APC gene, 100s of polyps, prophylactic colectomy
Lynch syndrome (HNPCC): DNA mismatch repair gene mutations, right-sided colon cancer

MOST IMPORTANT EXAM QUESTIONS (Previous Year Pattern)

Essay Questions (10-15 marks each)

Describe the events in acute inflammation and role of chemical mediators
Enumerate the types of necrosis with examples - compare necrosis vs apoptosis
Discuss carcinogenesis - oncogenes, tumor suppressor genes and hallmarks of cancer
Describe morphological changes in MI at different time intervals
Compare Hodgkin's and Non-Hodgkin's lymphoma
Describe glomerulonephritis - classify and describe morphological features
Write about wound healing - primary vs secondary intention
Discuss cirrhosis of liver - etiology, pathogenesis, morphology, complications

Short Notes (5 marks each)

Reed-Sternberg cell
Granuloma (types, mechanism, examples)
Philadelphia chromosome
Auer rods
Tumor markers
Virchow's triad
DIC (Disseminated Intravascular Coagulation)
Apoptosis pathway (intrinsic and extrinsic)
Mallory bodies
Types of calcification
Metaplasia vs Dysplasia
Krukenberg tumor

Fill in the Blanks / MCQ Favorites

Most common type of necrosis: Coagulative
Cell responsible for wound healing: Macrophage
"Starry sky" pattern: Burkitt's lymphoma
Owl eye cell: Reed-Sternberg cell (Hodgkin's lymphoma)
Auer rod: AML
Psammoma bodies: Papillary thyroid carcinoma, Serous cystadenoma of ovary, Meningioma, Mesothelioma (mnemonic: PSaMMoma - Papillary thyroid, Serous ovarian, Meningioma, Mesothelioma)
Apple-green birefringence with Congo red: Amyloid
Translocation in CML: t(9;22) Philadelphia chromosome
"Indian file" pattern: Lobular carcinoma of breast
Most common childhood malignancy: ALL (Acute Lymphoblastic Leukemia)

PRACTICAL / SPOTTER TIPS (University exams often have a practical paper)

Blood smears to recognize:

IDA: hypochromic microcytic, pencil cells
Sickle cell: sickle cells, Howell-Jolly bodies
CML: left shift, all stages of myeloid cells
ALL: lymphoblasts (large nuclei, scant cytoplasm)

Histology slides commonly asked:

TB: caseating granuloma + Langhans giant cells
Amyloid: Congo red + apple-green birefringence
MI: coagulative necrosis, ghost cells (pale eosinophilic with no nuclei)
Hodgkin's: Reed-Sternberg cell (owl eye)
Burkitt's: starry sky pattern
PSGN: hypercellular glomerulus

LAST 24-HOUR REVISION CHECKLIST

All types of necrosis + examples
Necrosis vs Apoptosis table
Steps of leukocyte recruitment
Mediators table (source + action)
Granuloma types (caseating vs non-caseating)
Tumor markers table
Leukemia comparison table (ALL/CLL/AML/CML)
HL vs NHL + Reed-Sternberg cell
MI timeline
Glomerulonephritis table (LM/IF/EM)
IBD comparison (Crohn's vs UC)
Cirrhosis complications
Important translocations: t(9;22), t(8;14), t(14;18), t(15;17), t(11;14)
Psammoma bodies list
Tumor suppressor genes and their associated cancers

Study tip: Read Robbins Basic Pathology for concepts and mechanisms. For exam, pair with Harsh Mohan's "Textbook of Pathology" for Indian university-style questions. Solve at least 3-5 previous university papers. Good luck!

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