concise bullet point Q&A summary from pages 279 TO 283

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Concise Q&A Summary from Pages 279–283 (Cellular Injury)

1. What is cellular injury?

Cellular injury occurs when cells are exposed to harmful stimuli (e.g.,
hypoxia, toxins, infections) that disrupt their structure or function, leading
to reversible or irreversible damage.

2. What are the main causes of cellular injury?

 Hypoxia (e.g., ischemia, anemia)

 Physical agents (e.g., trauma, radiation)
 Chemical agents (e.g., toxins, drugs)
 Infections (e.g., bacteria, viruses)
 Immunologic reactions (e.g., autoimmune diseases)
 Genetic mutations
 Nutritional imbalances (e.g., vitamin deficiencies)

3. What are the key mechanisms of cellular injury?

 ATP depletion (impairs energy-dependent processes)

 Mitochondrial damage (disrupts oxidative phosphorylation)
 Loss of calcium homeostasis (activates harmful enzymes)
 Oxidative stress (free radical damage)
 Membrane permeability defects (disrupts ion balance)

4. What are the types of cellular adaptations to injury?

 Atrophy (shrinkage of cells)

 Hypertrophy (increase in cell size)
 Hyperplasia (increase in cell number)
 Metaplasia (replacement by a different cell type)
 Dysplasia (abnormal cell growth, pre-cancerous)

5. What is necrosis?
 Necrosis is irreversible cell death characterized by:

 Cellular swelling
 Membrane rupture
 Inflammation
 Types: Coagulative, liquefactive, caseous, fat necrosis.

6. What is apoptosis?

Apoptosis is programmed cell death (non-inflammatory, controlled):

 Cell shrinkage
 Membrane blebbing
 Nuclear fragmentation
 Phagocytosis without inflammation

7. What are free radicals, and how do they cause injury?

 Reactive oxygen species (ROS) with unpaired electrons.

 Damage lipids (peroxidation), proteins, and DNA.
 Neutralized by antioxidants (e.g., glutathione, vitamins C/E).

8. What is ischemia-reperfusion injury?

 Ischemia reduces blood flow, causing hypoxia.

 Reperfusion restores oxygen but worsens injury via free radicals and
inflammation.

9. How do intracellular accumulations occur?

 Lipids (e.g., fatty liver)

 Proteins (e.g., Russell bodies in plasma cells)
 Glycogen (e.g., diabetes mellitus)
 Pigments (e.g., lipofuscin, melanin)

10. What are the clinical consequences of cellular injury?

 Reversible injury (e.g., swelling, fatty change)

 Irreversible injury (necrosis → organ dysfunction)
 Chronic injury (fibrosis, atrophy)

This summary provides a quick review of key concepts in cellular injury.

For detailed explanations, refer to the full text.

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NEXT 5 PAGES

Here’s a concise bullet-point Q&A summary of the next 5 pages

(pages 284–288) from Basic Science for the MRCS:

1. What are the types of necrosis?

 Coagulative necrosis:

o Seen in ischemic injury (e.g., myocardial infarction).

o Preserved cell outlines (architecture remains).
 Liquefactive necrosis:

o Seen in brain infarcts or abscesses.

o Tissue digested into liquid.
 Caseous necrosis:

o Cheese-like appearance (e.g., tuberculosis).

 Fat necrosis:

o Enzymatic (e.g., acute pancreatitis) or traumatic (e.g., breast tissue).

 Gangrenous necrosis:

o Dry gangrene (ischemic, no infection) vs. wet gangrene (infection +

liquefaction).

2. What is apoptosis vs. necrosis?

Feature Apoptosis Necrosis

Cause Programmed Uncontrolled (e.g., ischemia,

 Feature Apoptosis Necrosis

(physiological/pathological) toxins)

Inflammation No inflammation Inflammation present

Cell membrane Intact (blebbing) Disrupted (leakage)

DNA Random (smear on

Ordered (ladder pattern)
breakdown electrophoresis)

3. What is fatty change (steatosis)?

 Accumulation of triglycerides in parenchymal cells (e.g., liver, heart).

 Causes: Alcohol abuse, obesity, diabetes, hypoxia.
 Reversible if cause is removed.

4. What is dystrophic vs. metastatic calcification?

 Dystrophic calcification:

o Occurs in dead/damaged tissue (normal serum calcium).

o E.g., atherosclerotic plaques, tuberculous lymph nodes.
 Metastatic calcification:

o Occurs in normal tissues due to hypercalcemia (e.g.,

hyperparathyroidism, bone metastases).

5. What are free radicals, and how do they cause injury?

 Reactive oxygen species (ROS) with unpaired electrons.

 Sources:

o Mitochondrial respiration, radiation, inflammation.

 Effects:

o Lipid peroxidation (membrane damage).

o Protein cross-linking (enzyme dysfunction).
o DNA breaks (mutations).
 Defenses:

o Antioxidants (vitamins E, C, glutathione).

 6. What is reperfusion injury?

 Paradoxical worsening of cell damage after blood flow is restored (e.g.,

post-ischemia).
 Mechanisms:

o Free radical burst.

o Calcium overload.
o Inflammation (neutrophil infiltration).

7. What are intracellular accumulations?

 Lipids: Fatty liver (hepatic steatosis).

 Proteins: Russell bodies (plasma cells in chronic inflammation).
 Glycogen: Diabetes mellitus (glycogen-rich nuclei in liver).
 Pigments:

o Endogenous: Bilirubin (jaundice), melanin.

o Exogenous: Tattoo ink, coal dust (anthracosis).

8. What is hyaline change?

 Glass-like eosinophilic material in tissues.

 Examples:

o Hyaline arteriolosclerosis (hypertension, diabetes).

o Alcoholic hyaline (Mallory bodies) in liver.

9. What is amyloidosis?

 Extracellular deposition of misfolded proteins (β-pleated sheets).

 Types:

o AL amyloid (plasma cell dyscrasias).

o AA amyloid (chronic inflammation, e.g., rheumatoid arthritis).
 Stains: Congo red (apple-green birefringence under polarized light).

10. What are the clinical effects of cellular aging?

 Telomere shortening → replicative senescence.

 Accumulated DNA damage (e.g., oxidative stress).
 Reduced protein turnover (e.g., dysfunctional organelles).

Key Takeaways:

 Necrosis is uncontrolled and inflammatory; apoptosis is controlled and

physiological.
 Free radicals play a major role in reperfusion injury and aging.
 Calcification and amyloidosis are examples of pathological protein
deposition.

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NEXT 5 PAGES

Here’s a concise bullet-point Q&A summary of the next 5 pages

(pages 289–293) from Basic Science for the MRCS:

1. What is inflammation?

 Definition: A protective response to injury/infection aimed at removing

harmful stimuli and initiating healing.
 Cardinal signs:

o Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio

laesa (loss of function).

2. What are the types of inflammation?

 Acute inflammation:

o Rapid onset (minutes/hours), short duration.

o Key features: Vasodilation, increased vascular
permeability, neutrophil infiltration.
 Chronic inflammation:

o Prolonged (weeks/years).
o Key features: Lymphocytes/macrophages, fibrosis, granuloma
formation.

3. What are the vascular changes in acute inflammation?

1. Transient vasoconstriction (seconds).

2. Vasodilation (↑ blood flow → redness/heat).
3. Increased permeability (protein-rich exudate → swelling).

o Mechanisms: Endothelial contraction, direct injury, leukocyte-mediated

damage.

4. What are the cellular events in acute inflammation?

 Leukocyte recruitment:

1. Margination: Neutrophils move to vessel edges.

2. Rolling: Weak adhesion (selectins).
3. Adhesion: Firm attachment (integrins, ICAM-1).
4. Transmigration: Diapedesis (via chemotaxis).
 Phagocytosis:
o Opsonization (IgG/C3b) → engulfment → killing (ROS, lysosomal enzymes).

5. What are chemical mediators of inflammation?

Mediator Source Action

Mast cells,
Histamine Vasodilation, ↑ permeability
basophils

Prostaglandins Arachidonic acid Vasodilation, pain, fever

Leukotrienes Arachidonic acid ↑ permeability, chemotaxis

Cytokines (e.g., TNF-α, IL-1) Macrophages Fever, endothelial activation

 Mediator Source Action

Bradykinin Kinin system Pain, ↑ permeability

6. What are the outcomes of acute inflammation?

 Resolution: Complete return to normal (e.g., mild sunburn).

 Abscess formation: Pus (neutrophils + debris) walled off by fibrosis.
 Chronic inflammation: If stimulus persists (e.g., tuberculosis).
 Fibrosis: Scarring (e.g., chronic hepatitis → cirrhosis).

7. What is chronic inflammation?

 Causes: Persistent infection (TB, H. pylori), autoimmune disease (RA),

foreign bodies.
 Key cells:

o Macrophages (secrete cytokines, growth factors).

o Lymphocytes (B/T cells).
o Plasma cells (antibody production).
 Granuloma:

o Caseating (e.g., TB) vs. non-caseating (e.g., sarcoidosis).

8. What is the difference between transudate and

exudate?

Feature Transudate Exudate

↑ hydrostatic pressure (e.g.,

Cause Inflammation (e.g., infection)
CHF)

Protein Low (<2.5 g/dL) High (>3 g/dL)

Specific gravity <1.012 >1.020

Cells Few Neutrophils/macrophages

9. What is pyrexia (fever)?

 Mechanism: Cytokines (IL-1, TNF-α) → hypothalamus ↑ prostaglandins

(PGE₂).
 Causes: Infection, inflammation, malignancy.

10. What are systemic effects of inflammation?

 Fever (pyrogens).
 Leukocytosis (↑ neutrophils in bacterial infection).
 Acute-phase proteins (e.g., CRP, fibrinogen).
 Sepsis: Systemic inflammatory response (SIRS) to infection.

Key Takeaways:

 Acute inflammation is neutrophil-driven; chronic

inflammation involves macrophages/lymphocytes.
 Chemical mediators (histamine, prostaglandins) regulate
vascular/cellular responses.
 Granulomas indicate chronic inflammation (e.g., TB, sarcoidosis).

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NEXT 5 PZGES

Here’s a concise bullet-point Q&A summary of the next 5 pages

(pages 294–298) from Basic Science for the MRCS:

1. What are the key features of chronic inflammation?

 Prolonged duration (weeks to years)

 Dominant cells: Macrophages, lymphocytes, plasma cells
 Tissue destruction and fibrosis (scarring)
 Granuloma formation in some cases (e.g., TB, sarcoidosis)
 2. What is a granuloma?

 Definition: Focal collection of epithelioid macrophages surrounded by

lymphocytes.
 Types:

o Caseating (necrotic center, e.g., tuberculosis)

o Non-caseating (no necrosis, e.g., sarcoidosis)
 Causes:

o Infections (TB, leprosy, syphilis)

o Foreign bodies (silicosis, suture material)
o Autoimmune (Crohn’s disease)

3. What are giant cells, and how do they form?

 Formed by fusion of macrophages (multinucleated).

 Types:

o Langhans giant cells (peripheral nuclei, e.g., TB)

o Foreign-body giant cells (random nuclei, e.g., around sutures)
o Touton giant cells (lipid-laden, e.g., xanthomas)

4. What are the systemic effects of chronic inflammation?

 Fever (cytokine release, e.g., IL-1, TNF-α)

 Weight loss (cachexia due to TNF-α)
 Anemia of chronic disease (↑ hepcidin → ↓ iron absorption)
 Amyloidosis (long-term AA amyloid deposition)

5. What is wound healing, and what are the phases?

1. Hemostasis: Platelet plug + fibrin clot.

2. Inflammation: Neutrophils (24–48h) → macrophages (cleanup).
3. Proliferation:

o Fibroblasts (collagen synthesis)

o Angiogenesis (new blood vessels)
o Epithelialization (skin regrowth)
4. Remodeling: Collagen cross-linking (weeks-months).
 6. What is the difference between primary and secondary
intention healing?

Feature Primary Intention Secondary Intention

Wound Clean, approximated (e.g., surgical Separated, irregular (e.g., burn,

edges incision) ulcer)

Healing time Faster (days-weeks) Slower (weeks-months)

Scarring Minimal Significant (granulation tissue)

7. What factors impair wound healing?

 Local: Infection, ischemia, foreign bodies, radiation.

 Systemic:

o Diabetes (↓ neutrophil function, microangiopathy)

o Malnutrition (↓ protein for collagen)
o Steroids (↓ inflammation, collagen synthesis)
o Vitamin C deficiency (impaired collagen cross-linking)

8. What is fibrosis, and when does it occur?

 Excessive collagen deposition replacing normal tissue.

 Causes:

o Chronic inflammation (e.g., cirrhosis, pulmonary fibrosis)

o Ischemic injury (e.g., myocardial infarction scar)

9. What are keloids vs. hypertrophic scars?

Feature Keloid Hypertrophic Scar

Extends beyond wound

Growth Stays within wound boundaries
margins

Recurrence High Low

Common sites Earlobes, sternum, shoulders Flexor surfaces (e.g., knees)

10. What is the role of macrophages in healing?

 Early phase: Phagocytose debris, release cytokines (TGF-β, PDGF).
 Late phase: Stimulate fibroblast proliferation and angiogenesis.

Key Takeaways:

 Chronic inflammation involves macrophages, fibrosis,

and granulomas.
 Wound healing progresses through hemostasis → inflammation →
proliferation → remodeling.
 Keloids (excessive scar growth) vs. hypertrophic scars (confined to
wound).

Would you like a deeper dive into granulomatous diseases or fibrotic

disorders?

next 10 pages

Here’s a high-yield bullet-point Q&A summary covering the next 10

pages (pages 299–308) from Basic Science for the MRCS:

1. What are the types of tissue repair?

 Regeneration: Replacement with identical functional tissue (e.g.,

liver after partial resection).
 Fibrosis: Replacement with scar tissue (e.g., myocardial infarction).
 Key factor: Depends on tissue’s proliferative
capacity (labile/stable/permanent cells).

2. How are cells classified by regenerative ability?

 Type Examples Regenerative Capacity

Labile cells Skin, GI epithelium, bone marrow High (constant turnover)

Stable cells Liver, kidney, endothelial cells Moderate (regenerate if stimulated)

Permanent
Neurons, cardiac myocytes None (replaced by scarring)
cells

3. What are growth factors in healing?

 EGF (Epidermal Growth Factor): Stimulates epithelial proliferation.

 TGF-β (Transforming Growth Factor-beta): Promotes fibrosis (↑
collagen synthesis).
 VEGF (Vascular Endothelial Growth Factor): Drives angiogenesis.
 PDGF (Platelet-Derived Growth Factor): Attracts fibroblasts.

4. What is angiogenesis, and how does it occur?

 Formation of new blood vessels from pre-existing ones.

 Steps:

1. Vasodilation (NO-mediated).
2. ECM degradation (MMPs).
3. Endothelial cell migration/proliferation (VEGF-driven).

5. What are the complications of wound healing?

 Dehiscence: Wound reopening (e.g., due to infection or tension).

 Contracture: Excessive scar contraction (e.g., burns → joint immobility).
 Stricture: Fibrosis narrowing a lumen (e.g., esophageal stricture post-
alkali burn).
 Fistula: Abnormal connection between organs (e.g., enterocutaneous
fistula).

6. What is the extracellular matrix (ECM) composed of?

 Collagen (Type I in skin/bone, Type II in cartilage).

 Elastin (provides elasticity to vessels/lungs).
 Proteoglycans (e.g., hyaluronan – retains water).
 Adhesive glycoproteins (e.g., fibronectin, laminin).

7. What are matrix metalloproteinases (MMPs)?

 Zinc-dependent enzymes that degrade ECM components.

 Role: Tissue remodeling, wound healing, cancer metastasis.
 Inhibitors: TIMPs (Tissue Inhibitors of Metalloproteinases).

8. What is the difference between healing in bone vs. soft

tissue?

 Bone healing:

o Primary (direct): Rigid fixation → osteonal bridging (no callus).

o Secondary (indirect): Callus formation (soft → hard).
 Soft tissue healing: Relies on collagen deposition (Type III → Type I).

9. What is the pathophysiology of chronic wounds?

 Causes: Ischemia (e.g., diabetic ulcers), pressure (decubitus ulcers),

venous stasis.
 Features:

o Persistent inflammation (↑ TNF-α, IL-1).

o Impaired angiogenesis (↓ VEGF).
o Bacterial biofilms.

10. What are stem cells, and how do they contribute to

repair?

 Types:

o Embryonic (pluripotent – all cell types).

o Adult (multipotent – tissue-specific, e.g., hematopoietic stem cells).
 Roles:

o Replace damaged cells (e.g., intestinal crypt stem cells).

o Modulate inflammation (MSCs suppress immune responses).

11. What is the role of fibroblasts in fibrosis?

 Activated by TGF-β → differentiate into myofibroblasts (express α-
SMA).
 Secrete collagen (Types I/III) → ECM deposition → scar formation.

12. What is the difference between resolution and

regeneration?

 Resolution: Complete restoration of original tissue (e.g., mild

pneumonia).
 Regeneration: Replacement with similar functional tissue (e.g., liver
regeneration).

13. What are the stages of bone fracture healing?

1. Hematoma formation (clot at fracture site).

2. Inflammation (neutrophils/macrophages clear debris).
3. Soft callus (fibroblasts/chondrocytes → provisional matrix).
4. Hard callus (osteoblasts → woven bone).
5. Remodeling (osteoclasts/osteoblasts → lamellar bone).

14. What is the difference between primary and secondary

union in skin wounds?

Feature Primary Union Secondary Union

Example Surgical incision Large wound (e.g., burn)

Granulation tissue Minimal Prominent

Contraction None Significant (myofibroblasts)

15. What is the role of vitamin C in healing?

 Cofactor for prolyl hydroxylase → stabilizes collagen triple helix.

 Deficiency (scurvy): Fragile capillaries, poor wound healing, gingival
bleeding.
 Key Takeaways:

 Labile/stable/permanent cells dictate regenerative capacity.

 Fibrosis is driven by TGF-β and myofibroblasts.
 Bone healing involves callus formation (unless rigidly fixed).
 Chronic wounds fail due to ischemia, infection, or biofilms.

Would you like to focus on specific clinical scenarios (e.g., diabetic

ulcers) or molecular mechanisms (e.g., TGF-β signaling)?

next 10 pages

Here's a concise bullet-point Q&A summary of the next 10 pages

(pages 309-318) from Basic Science for the MRCS:

1. What are the key components of the immune system?

 Innate immunity (non-specific):

o Physical barriers (skin, mucous membranes)

o Phagocytes (neutrophils, macrophages)
o Complement system
o NK cells
 Adaptive immunity (specific):

o B cells (humoral immunity → antibodies)

o T cells (cell-mediated immunity)

2. What are the major histocompatibility complexes

(MHC)?

 MHC Class I: Present on all nucleated cells → present endogenous

antigens to CD8+ T cells
 MHC Class II: Present on APCs (macrophages, B cells, dendritic cells) →
present exogenous antigens to CD4+ T cells
 3. What are the 5 classes of antibodies?

1. IgG: Most abundant (80%), crosses placenta

2. IgM: First responder (pentamer), activates complement
3. IgA: Secretory (mucosal immunity)
4. IgD: B cell receptor
5. IgE: Allergies, parasites

4. What is the complement system?

 3 activation pathways:

o Classical (antigen-antibody complexes)

o Alternative (microbial surfaces)
o Lectin (mannose-binding lectin)
 Functions:

o Opsonization (C3b)
o Cell lysis (MAC: C5b-9)
o Chemotaxis (C5a)

5. What are hypersensitivity reactions?

Type Mechanism Example

I (Immediate) IgE → mast cell degranulation Anaphylaxis, asthma

II (Cytotoxic) IgG/IgM vs cell surface antigens Autoimmune hemolytic anemia

III (Immune Ag-Ab complexes deposit in

SLE, vasculitis
complex) tissues

IV (Delayed) T-cell mediated Contact dermatitis, TB test

6. What is autoimmunity?

 Breakdown of self-tolerance → immune attack on self-antigens

 Mechanisms:

o Molecular mimicry (e.g., rheumatic fever)

o Release of sequestered antigens (e.g., post-traumatic uveitis)
 Examples: RA, SLE, Type 1 DM
 7. What are primary vs secondary immunodeficiencies?

 Primary (congenital):

o B-cell: Bruton's agammaglobulinemia (↓ all antibodies)

o T-cell: DiGeorge syndrome (thymic aplasia)
o Combined: SCID ("bubble boy" disease)
 Secondary (acquired):

o HIV/AIDS (CD4+ T cell depletion)

o Malnutrition, immunosuppressants

8. What is transplant rejection?

 Hyperacute: Pre-formed antibodies → minutes/hours

 Acute: T-cell mediated → days/weeks
 Chronic: Fibrosis → months/years
 GVHD: Donor T cells attack recipient (bone marrow transplants)

9. What are tumor antigens?

 Tumor-specific antigens (TSAs): Unique to cancer cells (e.g., MAGE in

melanoma)
 Tumor-associated antigens (TAAs): Overexpressed in cancer (e.g.,
CEA in colon CA)

10. How does the immune system fight cancer?

 Immune surveillance:

o NK cells (innate)
o CD8+ cytotoxic T cells (adaptive)
o Macrophages
 Evasion mechanisms:

o Downregulation of MHC I
o PD-L1 expression (inhibits T cells)

11. What are vaccines?

 Live attenuated (MMR, varicella) - strongest/longest immunity

 Inactivated/killed (polio, rabies)
 Subunit/recombinant (Hep B, HPV)
 Toxoid (tetanus, diphtheria)

12. What are cytokines?

 Pro-inflammatory:

o TNF-α, IL-1, IL-6 (fever, acute phase response)

o IFN-γ (macrophage activation)
 Anti-inflammatory:

o IL-10, TGF-β
 Chemokines (e.g., IL-8 → neutrophil chemotaxis)

13. What is septic shock?

 Pathogenesis: LPS (Gram -ve) or superantigens (Gram +ve) → massive

cytokine release (TNF-α, IL-1) → vasodilation, DIC, MODS
 Treatment: Fluids, vasopressors, antibiotics

14. What are the blood groups?

 ABO system:

o Type A: A antigens, anti-B antibodies

o Type B: B antigens, anti-A antibodies
o Type AB: both antigens, no antibodies (universal recipient)
o Type O: no antigens, both antibodies (universal donor)
 Rh system: Anti-D antibodies cause hemolytic disease of newborn

15. What is the difference between active and passive

immunity?

Feature Active Immunity Passive Immunity

Source Exposure to antigen Pre-formed antibodies

Duration Long-lasting Temporary

Examples Vaccination, Maternal IgG, antitoxin

 Feature Active Immunity Passive Immunity

infection

Key Takeaways:

1. Innate vs adaptive immunity work together for defense

2. Hypersensitivity reactions range from immediate (Type I) to delayed
(Type IV)
3. Autoimmunity results from loss of self-tolerance
4. Transplant rejection mechanisms differ by timing
5. Cancer immunology involves immune surveillance and evasion

Would you like me to elaborate on any specific topic (e.g., HIV

pathogenesis or monoclonal antibodies)?

next 10 pages

Here's a concise bullet-point Q&A summary of the next 10 pages

(pages 319-328) from Basic Science for the MRCS:

1. What are neoplasms?

 Definition: Abnormal mass of tissue with excessive, uncoordinated

growth persisting after stimulus removal
 Key features:

o Clonal expansion (derived from single mutated cell)

o Autonomous growth (independent of normal regulatory mechanisms)

2. What's the difference between benign and malignant

tumors?
 Feature Benign Malignant

Growth rate Slow Rapid

Invasion No Yes (infiltrates)

Metastasis Never Common

Differentiation Well-differentiated Poorly differentiated

Examples Lipoma, fibroadenoma Carcinoma, sarcoma

3. What are the hallmarks of cancer?

1. Sustained proliferative signaling (e.g., RAS mutations)

2. Evading growth suppressors (e.g., p53 loss)
3. Resisting cell death (e.g., BCL-2 overexpression)
4. Enabling replicative immortality (telomerase activation)
5. Inducing angiogenesis (VEGF secretion)
6. Activating invasion/metastasis (EMT)
7. Genome instability
8. Avoiding immune destruction
9. Deregulating cellular metabolism (Warburg effect)
10. Tumor-promoting inflammation

4. What are oncogenes vs tumor suppressor genes?

Feature Oncogenes Tumor Suppressors

Function Accelerate growth Brake cell division

Mutation
Gain-of-function Loss-of-function
effect

Inheritance Not inherited Often inherited (e.g., RB1)

Examples RAS, MYC, HER2 p53, RB, APC

5. What are carcinogens?

 Chemical:
o Direct (alkylating agents)
o Indirect (benzopyrene → requires metabolic activation)
 Radiation: UVB (melanoma), ionizing (leukemia)
 Viral:

o HPV (cervical CA)

o EBV (Burkitt's lymphoma)
o HBV/HCV (hepatocellular CA)
 Bacterial: H. pylori (gastric CA/MALT lymphoma)

6. What is the TNM staging system?

 T: Tumor size/depth (T1-T4)

 N: Lymph node involvement (N0-N3)
 M: Metastasis (M0/M1)
 Example: T2N1M0 = Tumor invades muscularis propria, 1-3 regional
nodes, no mets

7. What are tumor markers?

Marker Associated Cancer

PSA Prostate

CEA Colorectal

CA-125 Ovarian

Hepatocellular, germ
AFP
cell

hCG Choriocarcinoma

8. What are paraneoplastic syndromes?

 Remote effects of tumors not caused by mass effect/metastases

 Examples:

o Cushing's (ACTH from small cell lung CA)

o Hypercalcemia (PTHrP from squamous cell CA)
o Lambert-Eaton myasthenic syndrome (anti-voltage-gated Ca2+ channels)
 9. What are the routes of metastasis?

1. Lymphatic (carcinomas → regional nodes)

2. Hematogenous (sarcomas → lungs/liver)
3. Transcoelomic (ovarian CA → peritoneal cavity)
4. Seeding (surgical incision sites)

10. What is cachexia?

 Cancer-associated wasting syndrome (unlike starvation):

o Severe muscle loss

o Anorexia
o Elevated metabolic rate
 Mediators: TNF-α ("cachectin"), IL-6

11. What are the differences between carcinoma and

sarcoma?

Feature Carcinoma Sarcoma

Origin Epithelial cells Mesenchymal cells

Metastasis Lymphatic first Hematogenous first

Common sites Lung, breast, colon Bone, soft tissues

Incidence 80% of cancers 1% of cancers

12. What is the Warburg effect?

 Aerobic glycolysis: Cancer cells metabolize glucose to lactate even with

O₂ present
 Advantages:

o Rapid ATP generation

o Provides intermediates for biosynthesis
 Clinical use: FDG-PET scans detect increased glucose uptake

13. What are the steps in chemical carcinogenesis?

1. Initiation: DNA mutation (irreversible)

2. Promotion: Clonal expansion of initiated cells (reversible)
3. Progression: Malignant conversion (genomic instability)

14. What are the common inherited cancer syndromes?

Syndrome Gene Cancers

Li-
p53 Breast, brain, sarcoma
Fraumeni

FAP APC Colorectal (100%)

BRCA1/2 BRCA1/2 Breast, ovarian

MEN2 RET Medullary thyroid, pheo

15. How do viruses cause cancer?

 Mechanisms:

o Insertional mutagenesis (HPV E6/E7 degrade p53/RB)

o Chronic inflammation (HBV/HCV)
o Immunosuppression (EBV in transplant patients)
 Vaccine-preventable: HPV (cervical CA), HBV (hepatocellular CA)

Key Takeaways:

1. Neoplasia involves autonomous, clonal growth

2. Malignant tumors invade/metastasize via multiple pathways
3. Oncogenes (gas pedal) vs tumor suppressors (brakes)
4. TNM staging guides prognosis/treatment
5. Paraneoplastic syndromes are systemic effects of tumors

Would you like me to focus on any specific cancer type (e.g., colorectal
carcinogenesis) or diagnostic methods (e.g., immunohistochemistry)?

next 10 pages
 Here's a concise bullet-point Q&A summary of the next 10 pages
(pages 329-338) from Basic Science for the MRCS:

1. What is thrombosis?

 Definition: Formation of a blood clot (thrombus) within intact vessels

 Virchow's triad (3 predisposing factors):

1. Endothelial injury (e.g., atherosclerosis, trauma)

2. Stasis/turbulent flow (e.g., AF, immobility)
3. Hypercoagulability (e.g., Factor V Leiden, malignancy)

2. What are arterial vs venous thrombi?

Feature Arterial Venous

Composition Platelet-rich (white) RBC/fibrin-rich (red)

Common
Coronary, cerebral DVT, pulmonary arteries
sites

Main risk Ischemia/infarction Embolism

3. What is embolism?

 Definition: Detached thrombus or other material traveling through

bloodstream
 Types:

o Thromboembolism (95% of cases)

o Fat (fractures), air (decompression sickness), amniotic fluid

4. What is DIC?

 Disseminated intravascular coagulation:

o Widespread microthrombi → organ ischemia

o Concurrent bleeding (consumption of platelets/clotting factors)
 Triggers: Sepsis, trauma, obstetric complications

5. What are the outcomes of thrombosis?

1. Lysis (complete resolution)

2. Organization (fibrosis → recanalization)
3. Propagation (clot enlarges)
4. Embolization (detachment → pulmonary/systemic embolism)

6. What is infarction?

 Definition: Tissue necrosis due to ischemia

 Types:

o White infarct (arterial occlusion in solid organs - heart, spleen)

o Red infarct (venous occlusion/dual blood supply - lung, intestine)

7. What is shock?

 Definition: Systemic hypoperfusion → cellular hypoxia

 Types:

1. Hypovolemic (hemorrhage, burns)

2. Cardiogenic (MI, arrhythmia)
3. Distributive (septic, anaphylactic)
4. Obstructive (PE, cardiac tamponade)

8. What are the stages of shock?

1. Compensated: BP maintained (tachycardia, vasoconstriction)

2. Progressive: Organ dysfunction (oliguria, confusion)
3. Irreversible: Multi-organ failure (refractory hypotension)

9. What are the genetic hypercoagulable states?

 Factor V Leiden (resistance to protein C)

 Prothrombin G20210A (↑ thrombin)
 Antithrombin III deficiency
 Protein C/S deficiency
 10. What is atherosclerosis?

 Pathogenesis:

1. Endothelial injury → LDL accumulation

2. Macrophage uptake → foam cells
3. Smooth muscle migration → fibrous cap
4. Plaque rupture → thrombosis
 Risk factors: HTN, smoking, diabetes, hyperlipidemia

11. What are aneurysms?

 Definition: Abnormal dilation of vessel >50% normal diameter

 Types:

o True (all 3 vessel layers) - atherosclerotic, syphilitic

o False (pseudoaneurysm) - trauma, post-surgical
 Rupture risks: Size >5cm, rapid expansion, smoking

12. What is vasculitis?

 Definition: Vessel wall inflammation

 Examples:

o Giant cell arteritis (temporal artery → blindness)

o Polyarteritis nodosa (medium vessels → renal infarcts)
o Granulomatosis with polyangiitis (c-ANCA, pulmonary/kidney)

13. What are venous ulcers vs arterial ulcers?

Feature Venous Arterial

Locatio
Medial malleolus Toes, pressure points
n

Pain Mild Severe (rest pain)

Edema Present Absent

Pulses Present Absent

14. What is the coagulation cascade?

 Extrinsic pathway: Tissue factor (TF) + VIIa → Xa
 Intrinsic pathway: XII → XI → IX + VIII → Xa
 Common pathway: Xa + Va → thrombin (IIa) → fibrin

15. What are anticoagulants?

 Heparin (activates antithrombin III)

 Warfarin (vitamin K antagonist → ↓ II, VII, IX, X)
 DOACs (direct Xa/thrombin inhibitors)

Key Takeaways:

1. Thrombosis requires Virchow's triad components

2. Embolism often originates from DVTs (→ PE) or left heart (→ stroke)
3. Shock progresses from compensated to irreversible stages
4. Atherosclerosis underlies most arterial thrombotic events
5. Hypercoagulability can be inherited (Factor V Leiden) or acquired
(malignancy)

Here's a high-yield Q&A summary of pages 339-348 from Basic Science

for the MRCS:

1. What is hemodynamic instability?

 Definition: Inadequate perfusion pressure (SBP <90mmHg, MAP

<65mmHg) with end-organ dysfunction
 Key signs:

o Tachycardia (>100 bpm)

o Oliguria (<0.5 mL/kg/hr)
o Altered mental status
o Lactate >2 mmol/L

2. What are the types of hemorrhage?

Class Blood Loss Clinical Features

<15%
I Mild tachycardia
(750mL)

II 15-30% (1.5L) Tachycardia, tachypnea, anxiety

III 30-40% (2L) Hypotension, confusion

IV >40% Profound shock, coma

3. What is the trauma triad of death?

1. Hypothermia (<35°C → coagulopathy)

2. Acidosis (pH <7.2 → impaired clotting)
3. Coagulopathy (↑PT/APTT, ↓fibrinogen)

4. What are the stages of acute inflammation?

1. Vasodilation (histamine → redness/heat)

2. Increased permeability (bradykinin → edema)
3. Leukocyte recruitment (margination → diapedesis)
4. Phagocytosis (opsonization → ROS/lysozymes)

5. What are the systemic effects of inflammation?

 Fever (IL-1/TNF → hypothalamic PGE₂)

 Leukocytosis (↑WBCs, left shift)
 Acute-phase proteins (CRP, fibrinogen)
 Metabolic (↑catabolism → negative nitrogen balance)

6. What are the types of wound healing?

 Primary intention: Surgical wounds (minimal granulation)

 Secondary intention: Large defects (extensive granulation)
 Tertiary intention: Delayed closure (infected wounds)
 7. What are the phases of bone healing?

1. Inflammatory (hematoma → 72hr)

2. Reparative (soft callus → 3wks; hard callus → 3mo)
3. Remodeling (Wolff's law → years)

8. What is compartment syndrome?

 Definition: ↑Intracompartmental pressure (>30mmHg) → ischemia

 5 Ps: Pain (out of proportion), Pallor, Paresthesia, Paralysis, Pulselessness
(late)
 Treatment: Emergency fasciotomy

9. What are the types of fractures?

Type Description

Open Bone exposed through skin

Comminuted >2 fracture fragments

Greenstick Incomplete (pediatric)

Pathologic Tumor/metabolic disease

10. What is fat embolism syndrome?

 Triad: Hypoxia (PaO₂ <60), neurologic changes, petechiae (chest/axilla)

 Mechanism: Long bone fractures → marrow fat enters circulation
 Timing: 12-72hr post-injury

11. What is crush syndrome?

 Pathophysiology: Muscle compression → rhabdomyolysis →

myoglobinuria → AKI
 Treatment: Aggressive IV fluids (target urine >300mL/hr), alkalinization

12. What are the types of burns?

 Degre
Depth Features
e

1st Epidermis Erythema, pain

2nd Partial dermis Blisters, wet appearance

3rd Full thickness Leathery, insensate

13. How is burn severity calculated?

 Rule of 9s:

o Head 9%, Arm 9%, Leg 18%, Torso 18% (front/back)

 Lund-Browder chart (more accurate for children)

14. What is the Parkland formula?

 Fluid resuscitation: 4mL × %TBSA × kg (1st 24hr)

o ½ in first 8hr, ½ next 16hr

o Example: 70kg patient with 30% burns → 4×30×70 = 8400mL

15. What are the complications of burns?

 Early: Hypovolemia, airway edema, compartment syndrome

 Late: Infection (Pseudomonas), contractures, hypertrophic scarring

Key Clinical Pearls:

1. Hemorrhage control takes priority over definitive management in

trauma
2. Compartment syndrome requires immediate surgical decompression
3. Burn resuscitation uses crystalloids (LR) - avoid hypotonic solutions
4. Fat embolism presents with respiratory/neurologic symptoms 1-3 days
post-fracture
5. Crush syndrome mandates aggressive fluid therapy to prevent renal
failure

Here’s a concise Q&A format based on key points from pages 349–
358 (assuming this section covers haematopoietic and
lymphoreticular pathology):

1. Bone Marrow & Haematopoiesis

Q: Where does haematopoiesis occur in adults?

A: Primarily in red bone marrow (flat bones, vertebrae, pelvis, and ends
of long bones).

Q: What are the two lineages derived from haematopoietic stem cells?
A: Myeloid (RBCs, platelets, granulocytes) and lymphoid (B/T/NK cells).

2. Anaemias

Q: What distinguishes iron-deficiency anaemia?

A: Microcytic, hypochromic RBCs (low MCV/MCH) due to iron
deficiency.

Q: What causes megaloblastic anaemia?

A: Deficiency of vitamin B12 or folate, leading to macrocytic
RBCs and hypersegmented neutrophils.

Q: How does haemolytic anaemia present?

A: Jaundice, reticulocytosis, and elevated LDH (due to RBC
breakdown).
3. Leukaemias

Q: What is the hallmark of acute lymphoblastic leukaemia (ALL)?

A: Proliferation of immature lymphoblasts (common in children).

Q: What genetic abnormality is seen in CML?

A: Philadelphia chromosome (t(9;22)), producing *BCR-ABL1* fusion
gene.

Q: How does AML differ from ALL?

A: AML involves myeloid blasts (Auer rods may be seen), while ALL
involves lymphoblasts.

4. Lymphomas

Q: What cell type is pathognomonic for Hodgkin lymphoma?

A: Reed-Sternberg cells (CD15+, CD30+).

Q: What is the most common non-Hodgkin lymphoma?

A: Diffuse large B-cell lymphoma (DLBCL).

5. Bleeding Disorders

Q: What is the inheritance pattern of haemophilia A?

A: X-linked recessive (Factor VIII deficiency).

Q: What defect causes von Willebrand disease?

A: Deficient or dysfunctional von Willebrand factor (vWF), impairing
platelet adhesion.
6. Thrombosis

Q: What are risk factors for DVT?

A: Virchow’s triad: Stasis, hypercoagulability, endothelial injury (e.g.,
surgery, immobilization).

Q: What is a life-threatening complication of DVT?

A: Pulmonary embolism (PE).

7. Immunodeficiency

Q: What is SCID?
A: Severe combined immunodeficiency (defective T/B cells; "bubble
boy" disease).

Q: What virus causes secondary immunodeficiency (AIDS)?

A: HIV (targets CD4+ T cells).

8. Transfusion Medicine

Q: Why is the Rh system important in pregnancy?

A: Anti-Rh(D) antibodies in Rh-negative mothers can cause haemolytic
disease of the newborn.

Q: What is a haemolytic transfusion reaction?

A: Mismatched blood → complement-mediated RBC lysis (fever, pain,
hypotension).

NEXT 10 PAGES
 Here are the key Q&A bullet points from the next 10 pages (359–
368) of Basic Science for the MRCS, focusing on basic microbiology and
system-specific pathology:

1. Microbiology Fundamentals

Q: What are the four main types of microorganisms?

A:

1. Bacteria (prokaryotes; e.g., Staphylococcus).

2. Viruses (obligate intracellular; e.g., HIV).
3. Fungi (eukaryotes; e.g., Candida).
4. Parasites (protozoa/helminths; e.g., Plasmodium).

Q: How are bacteria classified by Gram stain?

A:

 Gram-positive (thick peptidoglycan; purple; e.g., Staphylococcus).

 Gram-negative (thin peptidoglycan + outer membrane; pink; e.g., E.
coli).

2. Bacterial Pathogens

Q: What are pyogenic bacteria? Give examples.

A: Pus-forming bacteria (e.g., Staph. aureus, Strep. pyogenes).

Q: Which bacteria cause surgical site infections (SSIs)?

A:

 Skin flora: Staph. aureus, Staph. epidermidis.

 Gut flora: E. coli, Bacteroides fragilis.
 Q: What toxin causes tetanus?
A: Tetanospasmin (Clostridium tetani; inhibits GABA/glycine → spastic
paralysis).

3. Viral Pathogens

Q: Which viruses are oncogenic?

A:

 HPV (cervical cancer).

 EBV (Burkitt’s lymphoma).
 HBV/HCV (hepatocellular carcinoma).

Q: How does HIV progress to AIDS?

A: Depletes CD4+ T cells → opportunistic infections
(e.g., Pneumocystis pneumonia).

4. Antibiotics & Resistance

Q: What is the mechanism of MRSA resistance?

A: Altered penicillin-binding protein (PBP2a) → resistance to β-
lactams (e.g., methicillin).

Q: Which antibiotic treats MRSA?

A: Vancomycin (or linezolid/daptomycin).

Q: What is ESBL?
A: Extended-spectrum β-lactamase (resists penicillins/cephalosporins;
seen in E. coli/Klebsiella).
 5. Fungal & Parasitic Infections

Q: What fungal infection is common

in diabetics/immunocompromised?
A: Candidiasis (oral/thrush, invasive C. albicans).

Q: Which parasite causes malaria?

A: Plasmodium spp. (transmitted by Anopheles mosquito).

6. System-Specific Pathology

Q: What causes peptic ulcer disease?

A:

 H. pylori (90%).
 NSAIDs (disrupt mucosal barrier).

Q: What is the pathology of Crohn’s disease?

A: Transmural inflammation (skip lesions, granulomas, fistulae).

Q: Which liver disease is linked to Mallory bodies?

A: Alcoholic hepatitis (also seen in NASH).

7. Neoplasia

Q: What are Hallmarks of Cancer?

A:

1. Sustained proliferation.
2. Evading growth suppressors.
3. Metastasis.
4. Angiogenesis.

Q: What is cachexia?
A: Cancer-induced muscle wasting (due to TNF-α/IL-6).

8. Immunology

Q: What is Type I hypersensitivity?

A: IgE-mediated (e.g., anaphylaxis, asthma).

Q: What causes autoimmune diseases?

A: Loss of self-tolerance (e.g., RA, SLE).

Key Clinical Correlations

Q: What is Waterhouse-Friderichsen syndrome?

A: Adrenal hemorrhage due to meningococcal sepsis (DIC + shock).

Q: Which bug causes gas gangrene?

A: Clostridium perfringens (α-toxin → myonecrosis + crepitus).

Here are the key Q&A bullet points from the next 10 pages (369-
378) of Basic Science for the MRCS, covering system-specific
pathology and clinical microbiology:

1. Cardiovascular Pathology
 Q: What are the three layers of arterial walls?
A:

1. Intima (endothelium + subendothelial layer)

2. Media (smooth muscle + elastic fibers)
3. Adventitia (connective tissue)

Q: What pathological change occurs in atherosclerosis?

A:

 Fatty streaks → fibrous plaques → complicated

plaques (calcification/ulceration/thrombosis)

Q: What is the most common site for atherosclerosis?

A: Abdominal aorta > coronary > carotid > femoral arteries

2. Respiratory Pathology

Q: What are the histological changes in COPD?

A:

 Emphysema: Destruction of alveolar walls (↑ air spaces)

 Chronic bronchitis: Goblet cell hyperplasia, mucus plugs

Q: What characterizes asthma pathologically?

A:

 Bronchial smooth muscle hypertrophy

 Eosinophilic inflammation
 Curschmann's spirals (mucus plugs)
 3. Gastrointestinal Pathology

Q: What are the differences between ulcerative colitis (UC) and

Crohn's disease?
A:

Feature UC Crohn's

Distribution Continuous (rectum → proximally) Skip lesions (mouth to anus)

Depth Mucosa/submucosa Transmural

Granulomas No Yes (40% cases)

Q: What are Mallory bodies seen in?

A: Alcoholic hepatitis (eosinophilic cytoplasmic inclusions in
hepatocytes)

4. Renal Pathology

Q: What are the key features of nephrotic syndrome?

A:

 Proteinuria (>3.5g/day)
 Hypoalbuminemia
 Edema
 Hyperlipidemia

Q: What causes acute tubular necrosis (ATN)?

A:

 Ischemic (hypotension, sepsis)

 Nephrotoxic (aminoglycosides, contrast dye)
 5. CNS Pathology

Q: What is the most common primary brain tumor in adults?

A: Glioblastoma multiforme (Grade IV astrocytoma)

Q: What are Lewy bodies characteristic of?

A: Parkinson's disease (α-synuclein aggregates in substantia nigra)

6. Endocrine Pathology

Q: What is the most common cause of hyperthyroidism?

A: Graves' disease (TSH receptor antibodies)

Q: What are Hürthle cells seen in?

A: Hashimoto's thyroiditis (oncocytic follicular cells)

7. Musculoskeletal Pathology

Q: What are the three zones of osteosarcoma on X-ray?

A:

1. Sclerotic (tumor bone formation)

2. Radiolucent (bone destruction)
3. Codman's triangle (periosteal elevation)

Q: What is the histology of rheumatoid arthritis?

A:

 Pannus formation (inflamed synovium)

 Lymphocytic infiltration
 Cartilage/bone erosion
 8. Clinical Microbiology

Q: What are ESKAPE pathogens?

A: Multi-drug resistant hospital-acquired pathogens:

 Enterococcus faecium
 Staphylococcus aureus (MRSA)
 Klebsiella pneumoniae
 Acinetobacter baumannii
 Pseudomonas aeruginosa
 Enterobacter spp.

Q: What is the treatment for C. difficile colitis?

A:
1st line: Oral vancomycin or fidaxomicin
2nd line: Metronidazole (for mild cases)

9. Antimicrobial Stewardship

Q: When should post-operative antibiotics be stopped?

A: Within 24 hours after clean surgery (48h for cardiac surgery)

Q: What is antibiotic prophylaxis for splenectomy?

A: Penicillin V (lifelong prophylaxis against encapsulated organisms - S.
pneumoniae, H. influenzae, N. meningitidis)

10. Emerging Infections

 Q: What are prion diseases?
A:

 CJD (Creutzfeldt-Jakob disease)

 vCJD (variant CJD from BSE)
 Caused by misfolded PrP^Sc protein

Q: What virus causes COVID-19?

A: SARS-CoV-2 (spike protein binds ACE2 receptors)

Key Mnemonics:

 COPD histology: BEAM

o Bronchiolitis
o Emphysema
o Airway remodeling
o Mucus hypersecretion
 Nephrotic syndrome: PEHO

o Proteinuria
o Edema
o Hypoalbuminemia
o Hyperlipidemia

Here are the key Q&A bullet points from the next 10 pages (379-
388) of Basic Science for the MRCS, covering advanced pathology and
surgical microbiology:

1. Vascular Pathology
 Q: What are the two main types of aortic dissection?
A:

 Type A (ascending aorta, surgical emergency)

 Type B (descending aorta, often managed medically)

Q: What is Takayasu arteritis?

A: Granulomatous vasculitis of large vessels ("pulseless disease")
affecting young women

2. Breast Pathology

Q: What are the key differences between DCIS and LCIS?

A:

Feature DCIS (Ductal) LCIS (Lobular)

Malignant High grade may progress to Lower grade, marker for bilateral
Potential invasive risk

Often present (mammographic

Calcifications Rare
finding)

Treatment Excision + radiotherapy Surveillance (bilateral risk)

Q: What receptor status must be checked in breast cancer?

A: ER/PR (hormone therapy) and HER2 (trastuzumab target)

3. Hepatobiliary Pathology

Q: What is the MELD score used for?

A: Prioritizing liver transplantation (based on bilirubin, INR, creatinine)
 Q: What are Councilman bodies in liver pathology?
A: Eosinophilic apoptotic hepatocytes seen in viral hepatitis

4. Pancreatic Pathology

Q: What is the most common pancreatic cancer?

A: Ductal adenocarcinoma (head of pancreas → obstructive jaundice)

Q: What are the classic histology findings?

A:

 Desmoplastic stroma
 Perineural invasion
 Gland formation with mucin

5. Skin Pathology

Q: What are the ABCDE criteria for melanoma?

A:

 Asymmetry
 Border irregularity
 Color variation
 Diameter >6mm
 Evolving

Q: What is Bowen's disease?

A: Squamous cell carcinoma in situ (full-thickness epidermal
dysplasia)
 6. Trauma Pathology

Q: What is the lethal triad of trauma?

A:

1. Hypothermia
2. Acidosis
3. Coagulopathy

Q: What causes fat embolism syndrome?

A: Bone fracture → marrow fat enters circulation → pulmonary/CNS
symptoms (tachycardia, petechiae, confusion)

7. Transplant Pathology

Q: What is hyperacute rejection?

A: Pre-formed antibodies → graft failure within minutes (e.g., ABO
mismatch)

Q: What is GVHD?
A: Graft-versus-host disease (donor T-cells attack recipient tissues)

8. Surgical Infections

Q: What defines necrotizing fasciitis?

A:

 "Dishwater pus"
 Gas in tissues (crepitus)
 Systemic toxicity
 Surgical emergency

Q: What are Fournier's gangrene?

A: Necrotizing fasciitis of perineum/scrotum (polymicrobial)

9. Antibiotic Pearls

Q: When to use piperacillin-tazobactam (Tazocin®)?

A: Hospital-acquired intra-abdominal infections (covers anaerobes +
pseudomonas)

Q: What is MIC?
A: Minimum Inhibitory Concentration (lowest antibiotic dose that
inhibits visible bacterial growth)

10. Emerging Resistance

Q: What is VRE?
A: Vancomycin-Resistant Enterococcus (treated with
linezolid/daptomycin)

Q: What causes carbapenem resistance?

A: KPC (Klebsiella pneumoniae carbapenemase) or NDM-1 (New Delhi
metallo-β-lactamase)

Key Mnemonics:
 Aortic Dissection Types: Ascending = Acute surgery
 Necrotizing Fasciitis Signs: Pain Out of Proportion + Pallor
+ Paresthesia + Poikilothermia

Clinical Correlation:

 ER+ breast cancer responds to tamoxifen/aromatase inhibitors

 HER2+ tumors need trastuzumab (Herceptin®)

Here are the key Q&A bullet points from the next 10 pages (389-
398) of Basic Science for the MRCS, covering surgical anatomy,
physiology, and critical care principles:

1. Surgical Anatomy Essentials

Q: What are the boundaries of the femoral triangle?

A:

 Superior: Inguinal ligament

 Lateral: Sartorius
 Medial: Adductor longus
 Floor: Iliopsoas + pectineus
 Contents (lateral to medial): NAV (Nerve, Artery, Vein)

Q: What structures pass through the sciatic foramen?

A:

 Greater sciatic foramen: Sciatic nerve, pudendal nerve, superior gluteal

vessels
 Lesser sciatic foramen: Pudendal nerve (re-entering pelvis)
 2. Gastrointestinal Physiology

Q: What stimulates gastric acid secretion?

A:

 Cephalic phase: Vagus (ACh → parietal cells)

 Gastric phase: Gastrin (G cells) + histamine (ECL cells)
 Intestinal phase: Inhibited by somatostatin

Q: What is the difference between segmentation and peristalsis?

A:

 Segmentation: Mixing contractions (circular muscles)

 Peristalsis: Propulsive contractions (longitudinal + circular muscles)

3. Wound Healing

Q: What are the three phases of wound healing?

A:

1. Inflammatory (0-5 days): Neutrophils → macrophages

2. Proliferative (3-21 days): Fibroblasts → granulation tissue
3. Remodeling (21 days-1 year): Collagen cross-linking

Q: What factors impair wound healing?

A:

 Local: Infection, ischemia, tension

 Systemic: Diabetes, malnutrition, steroids

4. Shock Physiology
 Q: What are the four types of shock?
A:

1. Hypovolemic (hemorrhage)
2. Cardiogenic (MI)
3. Distributive (sepsis, anaphylaxis)
4. Obstructive (PE, tamponade)

Q: What is the Frank-Starling mechanism?

A: Increased preload → increased stroke volume (until myocardial
overstretch)

5. Fluid Management

Q: What is the difference between crystalloids and colloids?

A:

 Crystalloids (e.g., 0.9% saline): Low cost, short intravascular half-life

 Colloids (e.g., albumin): Expensive, stays intravascular longer

Q: What are signs of fluid overload?

A: JVP ↑, crackles, peripheral edema, ↑ CVP

6. Blood Transfusion

Q: What are TRALI vs TACO?

A:

 TRALI (Transfusion-Related Acute Lung Injury): Immune-mediated

pulmonary edema
 TACO (Transfusion-Associated Circulatory Overload): Volume overload
 Q: What is the maximum surgical blood order schedule (MSBOS)?
A: Standardized blood ordering for common procedures (e.g., 2 units for
cholecystectomy)

7. Surgical Nutrition

Q: When is TPN indicated?

A: When enteral feeding impossible >7 days (e.g., bowel obstruction,
high-output fistula)

Q: What is refeeding syndrome?

A: Electrolyte shifts (↓ K⁺/Mg²⁺/PO₄³⁻) after prolonged starvation →
cardiac arrhythmias

8. Critical Care Principles

Q: What is ARDS diagnostic criteria?

A:

 Acute onset
 PaO₂/FiO₂ <300
 Bilateral infiltrates
 No cardiac failure

Q: What is the SOFA score?

A: Sequential Organ Failure Assessment (predicts ICU mortality)

9. Surgical Pharmacology
 Q: What are adverse effects of NSAIDs?
A: GI ulcers, AKI, platelet dysfunction

Q: What is the reversal agent for warfarin?

A: Vitamin K (slow) or PCC (Prothrombin Complex Concentrate - rapid)

10. Perioperative Management

Q: What is the Revised Cardiac Risk Index (RCRI)?

A: Predicts cardiac risk in non-cardiac surgery (variables: HF, CAD, CVA,
DM, Cr >2, high-risk surgery)

Q: When to restart antiplatelets post-stent?

A:

 BMS: 4-6 weeks

 DES: 6-12 months

Key Mnemonics:

 Femoral triangle contents: NAVEL (Nerve, Artery, Vein, Empty space,

Lymphatics)
 Shock types: H-C-D-O (Hypovolemic, Cardiogenic, Distributive,
Obstructive)

Clinical Correlations:

 Early enteral feeding reduces septic complications

 Goal-directed fluid therapy improves outcomes in major surgery
 Here are the key Q&A bullet points from the next 10 pages (399-
408) of Basic Science for the MRCS, focusing on surgical oncology,
trauma management, and perioperative care:

1. Surgical Oncology Principles

Q: What are the TNM staging system components?

A:

 Tumor size/depth (T1-T4)

 Node involvement (N0-N3)
 Metastasis (M0/M1)

Q: What is sentinel lymph node biopsy?

A: Mapping first draining node (e.g., in breast cancer/melanoma) to avoid
full lymphadenectomy

2. Cancer Biology

Q: What are proto-oncogenes vs tumor suppressor genes?

A:

 Proto-oncogenes (e.g., RAS, MYC): Promote growth → mutated →

oncogenes
 Suppressors (e.g., p53, Rb): Inhibit growth → lost in cancer

Q: What is Lynch syndrome?

A: HNPCC (hereditary non-polyposis CRC) - defects in MMR
genes (MSH2/MLH1)
 3. Trauma Management

Q: What is the ATLS primary survey sequence?

A: ABCDE:

1. Airway (+ C-spine)
2. Breathing
3. Circulation
4. Disability (GCS)
5. Exposure

Q: What defines massive hemothorax?

A: >1.5L blood or >200mL/hr drainage

4. Burns Management

Q: How calculate burn surface area (BSA)?

A: Rule of 9's:

 Head 9%, Arm 9%, Leg 18%, Front/back trunk 18% each

Q: What fluid regimen for burns?

A: Parkland formula: 4mL x %BSA x kg (1/2 in 1st 8h)

5. Perioperative Care

Q: What are SIRS criteria?

A: ≥2 of:

 Temp >38°C or <36°C

 HR >90
 RR >20
 WBC >12 or <4

Q: When to restart DOACs post-op?

A:

 Low bleed risk: 24h

 High bleed risk: 48-72h

6. Surgical Complications

Q: What causes anastomotic leak?

A: Tension, ischemia, infection, malnutrition

Q: What is ERAS protocol?

A: Enhanced Recovery After Surgery:

 Pre-op carb loading

 Minimal fasting
 Early mobilization

7. Vascular Access

Q: What is the IJ vein landmark?

A: Triangle between sternal/clavicular heads of SCM

Q: What are CVL complications?

A: Pneumothorax, arterial puncture, infection
 8. Critical Care Drugs

Q: What is noradrenaline vs vasopressin?

A:

 Norad: α1 agonist (1st line septic shock)

 Vasopressin: V1 agonist (catecholamine-sparing)

Q: How reverse heparin?

A: Protamine sulfate (1mg per 100U heparin)

9. Metabolic Response to Surgery

Q: What is the ebb vs flow phase?

A:

 Ebb: Hypometabolic (first 24h)

 Flow: Hypermetabolic (catabolic)

Q: What causes post-op hyponatremia?

A: SIADH (from pain/stress) or excess hypotonic fluids

10. Surgical Ethics

Q: What are Gillick competence criteria?

A: Child <16 can consent if understands treatment

Q: What is DNACPR?
A: Do Not Attempt Cardiopulmonary Resuscitation (clinical decision)
 Key Mnemonics:

 TNM staging: Tumor Nodes Mets

 Burn fluids: Park yourself in the land (Parkland)

Clinical Pearls:

 Sentinel node biopsy reduces lymphedema risk vs full axillary clearance

 ERAS reduces hospital stay by 30% in colorectal surgery

Here are the key Q&A bullet points from the next 10 pages (409-
418) of Basic Science for the MRCS, covering emergency surgery,
neurosurgical principles, and surgical radiology:

1. Acute Abdomen

Q: What are the 3 cardinal signs of peritonitis?

A:

1. Guarding (involuntary muscle rigidity)

2. Rebound tenderness
3. Percussion tenderness

Q: What is Boas' sign in acute cholecystitis?

A: Right subscapular pain referred from inflamed gallbladder

2. Bowel Obstruction

Q: What distinguishes simple vs strangulated obstruction?

A:

 Simple: Colicky pain, vomiting, distension

 Strangulated: Constant pain, peritonism, fever (surgical emergency)

Q: What are radiographic signs of small vs large bowel

obstruction?
A:

 SBO: Central valvulae conniventes ("stack of coins")

 LBO: Peripheral haustra, proximal dilation

3. Neurosurgical Emergencies

Q: What is the Monro-Kellie doctrine?

A: Fixed cranial volume: ↑Brain/↑CSF/↑Blood → must ↓ one (e.g., CSF
drainage)

Q: What are Cushing's triad signs of raised ICP?

A:

1. Hypertension
2. Bradycardia
3. Irregular respiration

4. Spinal Cord Injury

Q: What is spinal shock vs neurogenic shock?

A:

 Spinal shock: Flaccid paralysis + areflexia (initial phase)

 Neurogenic shock: Hypotension + bradycardia (T6+ injury)

Q: What is Brown-Séquard syndrome?

A: Hemi-cord lesion causing:
 Ipsilateral: Motor loss + proprioception loss
 Contralateral: Pain/temp loss

5. Surgical Radiology

Q: When to use CT vs MRI?

A:

 CT: Trauma, acute bleed, bone detail (faster)

 MRI: Soft tissue, spinal cord, brain tumors (no radiation)

Q: What is the "double bubble" sign?

A: Duodenal atresia on neonatal X-ray (gastric + duodenal bubbles)

6. Vascular Emergencies

Q: What are the 6 P's of acute limb ischemia?

A:

1. Pain
2. Pallor
3. Pulselessness
4. Paresthesia
5. Paralysis
6. Poikilothermia

Q: What is compartment syndrome pressure threshold?

A: >30mmHg or within 30mmHg of diastolic BP
 7. Head Injury

Q: What is the Glasgow Coma Scale (GCS) breakdown?

A:

 Eye (1-4)
 Verbal (1-5)
 Motor (1-6)

Q: When is a "talk and die" head injury concerning?

A: Lucid interval → deterioration (epidural hematoma classic pattern)

8. Urological Emergencies

Q: What is Fournier's gangrene?

A: Necrotizing fasciitis of perineum (polymicrobial, surgical emergency)

Q: What causes testicular torsion?

A: "Bell-clapper" deformity (no testis-scrotum fixation)

9. Pediatric Surgery

Q: What is Hirschsprung's disease?

A: Aganglionic megacolon (rectal biopsy shows no ganglion cells)

Q: What is malrotation with volvulus?

A: Midgut twists around SMA (bilious vomiting in neonate)

10. Surgical Instruments

 Q: What is the difference between Kelly and Mixter forceps?
A:

 Kelly: Crushing clamp (transverse serrations)

 Mixter: Right-angle clamp (for ducts/vessels)

Q: When to use Monocryl vs PDS sutures?

A:

 Monocryl: Subcuticular (absorb in 90 days)

 PDS: Fascial closure (absorb in 180 days)

Key Mnemonics:

 Peritonitis signs: Guarding Rebound Percussion (GRP)

 Bowel obstruction: SBO = Stack of coins (valvulae)

Clinical Correlations:

 "Double bubble" requires urgent pediatric surgery consult

 Fournier's gangrene needs broad-spectrum abx (piperacillin-
tazobactam + clindamycin)

Here are the key Q&A bullet points from the next 10 pages (419-
428) of Basic Science for the MRCS, covering surgical subspecialties
and advanced perioperative management:

1. Cardiothoracic Surgery

Q: What are the indications for CABG vs PCI?

A:
 CABG: Left main disease, multi-vessel CAD, diabetic patients
 PCI: Single-vessel disease, acute STEMI

Q: What is tamponade physiology?

A: Beck's triad: Hypotension, JVD, muffled heart sounds

2. Plastic Surgery

Q: What are the reconstructive ladder steps?

A:

1. Primary closure
2. Skin graft
3. Local flap
4. Free flap

Q: What is Z-plasty used for?

A: To reorient scars along tension lines (lengthens contracted scars)

3. Orthopedic Trauma

Q: What is Garden classification for hip fractures?

A:

 I: Incomplete/impacted
 II: Complete non-displaced
 III: Complete partially displaced
 IV: Complete fully displaced

Q: What is compartment syndrome treatment?

A: Emergent fasciotomy (within 6 hours to prevent necrosis)
4. Pediatric Surgery

Q: What is hypertrophic pyloric stenosis?

A: Projectile vomiting in 2-8 week olds, palpable "olive" mass,
hypochloremic alkalosis

Q: What is intussusception triad?

A: Colicky pain, currant jelly stools, palpable sausage mass

5. Urological Surgery

Q: What is TURP syndrome?

A: Hyponatremia/fluid overload from glycine absorption during prostate
resection

Q: What are staghorn calculi?

A: Struvite stones filling renal pelvis (require PCNL)

6. Bariatric Surgery

Q: What are Roux-en-Y complications?

A: Dumping syndrome, marginal ulcers, internal herniation

Q: What is dumping syndrome?

A: Early (vasomotor) and late (hypoglycemic) forms post-gastrectomy

7. Surgical Nutrition
Q: What is refeeding syndrome prevention?
A: Slow nutrition restart, thiamine pre-load, monitor K⁺/Mg²⁺/PO₄³⁻

Q: When is TPN indicated?

A: Bowel obstruction, high-output fistula, prolonged ileus (>7 days)

8. Transplant Surgery

Q: What is cold ischemia time limit for kidneys?

A: <24 hours (optimal <12h)

Q: What causes hyperacute rejection?

A: Pre-formed antibodies (ABO mismatch) → minutes-hours post-
transplant

9. Surgical Pharmacology

Q: How reverse warfarin?

A: Vitamin K (slow) or PCC (rapid)

Q: What is VTE prophylaxis for major surgery?

A: LMWH + mechanical compression (SCDs)

10. Surgical Ethics

Q: What is Montgomery ruling?

A: Doctors must disclose material risks a patient would consider
significant
 Q: What defines Gillick competence?
A: Child <16 can consent if understands treatment risks/benefits

Key Mnemonics:

 Beck's triad: JVD Hypotension Muffled sounds (JHM)

 Pyloric stenosis: PROJECTILE vomiting (Pyloric Regurgitation Olive
mass etc.)

Clinical Pearls:

 TURP syndrome requires hypertonic saline for Na⁺ <120mmol/L

 Dumping syndrome managed with small, dry, high-protein meals