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Patho Essay Revision > General Pathology > Flashcards

General Pathology Flashcards

1
Q

What is hypertrophy?

A

Increased cell size
Due to increased functional demand or hormonal stimulation

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2
Q

Physiological examples for hypertrophy

A

Sex organs: testosterone and oestrogen during pregnancy
Breast tissue: oestrogen and prolactin for lactation
Uterine muscle: oestrogen during puberty
Skeletal muscle: increased muscle activity (exercise)
Cardiac muscle: sustained outflow increased (athletes)

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3
Q

Pathological examples of hypertrophy

A

LV cardiac muscle: increased outflow pressure (systemic hypertension, aortic valve disease)
RV cardiac muscle: increased outflow pressure (pulmonary hypertension, pulmonary valve disease)
Arterial smooth muscle: hypertension

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4
Q

What is hyperplasia

A

Increased cell number due to increase in functional demand, hormonal stimulation and persistent cell injury

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5
Q

Physiological examples of hyperplasia

A

Breast tissue: oestrogen during puberty, pregnancy and lactation
Thyroid: increased metabolic demand during puberty and pregnancy
Stromal cells in endometrium: oestrogen during puberty
Red cell precursors in bone marrow: erythropoietin at high altitudes

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6
Q

Pathological examples of hyperplasia

A

Thyroid: Graves autoantibody effect on thyroid
Stromal cells in endometrium: oestrogen, may lead to endometrial carcinoma
Skin: persistent physical trauma (corns)
Skin, larynx, cervix: stimulation of GF in HPV infection
Parathyroid gland: hypocalcemia
Prostate gland

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7
Q

What is metaplasia

A

Reversible change, one adult cell type replaces another adult cell type

Direct conversion or apparent conversion (respecification of stem cell –> different phenotype of progeny)

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8
Q

Types of metaplasia

A

Squamous
Glandular
Mesenchymal

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9
Q

Examples of squamous metaplasia

A

Ciliated pseudostratified columnar –> squamous in smokers/chronic bronchitis pt respiratory tracts
Simple columnar –> squamous in injury/inflammation/pH change in endocervix
Transitional –> squamous in bladder calculi

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10
Q

Examples of glandular metaplasia

A

Stratified squamous –> simple columnar in Barrett’s oesophagus due to gastroesophageal reflux
Simple columnar –> intestinal in chronic gastritis (H pylori)

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11
Q

Examples of mesenchymal metaplasia

A

Osseous transformation of old scars
Chondroid
Myeloid: spleen, liver, LN of myeloproliferative diseases

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12
Q

Coagulative necrosis characteristics

A

Retain outline, normal tissue architecture
Eosinophilic cytoplasm
Chromatin clumping, pyknosis/karyolysis/karyorrhexis

All solid organs except brain

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13
Q

Liquefactive necrosis characteristics

A

No residual tissue architecture
Necrotic area is semi-fluid

Infarct of cells in CNS

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14
Q

Fat necrosis characteristics

A

Digestive enzymes act on adipose tissue to release FA precipitate
Pancreatitis, breast injury etc

Areas with intra-abdominal/subcutaneous fat

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15
Q

Caseous necrosis characteristics

A

Necrotic cells do not retain outline or tissue architecture
Dead cells persist as amorphous material, gray-white/soft/cheese-like necrosis

TB lesion in LN, has granuloma

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16
Q

Fibrinoid necrosis characteristics

A

Highly eosinophilic wall
Plasma proteins accumulate in BV wall
E.g. hypertension –> increase permeability to proteins –> damage to vessel walls

BV involved in immune reactions

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17
Q

Describe apoptosis

A

Programmed tiny and silent cell death, induced by intracellular programme
Cells activate enzymes to degrade cell contents, rapidly phagocytosed by neighboring cells without inflammation
> initiation phase: extrinsic and intrinsic pathways activate caspases
> execution phase: caspases mediate proteolytic cascade

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18
Q

Examples of apoptosis

A

Physiological:
Endometrial breakdown during menstruation
In embryogenesis to prevent malformation
Killing DNA damaged cells to prevent mutations and cancer
Killing virus/infected cancer cells

Pathological:
Atrophy of parenchymal tissues after duct obstruction

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19
Q

What are the two types of pathological calcification

A

Dystrophic and metastatic calcification

20
Q

What is dystrophic calcification

A

Abnormal deposition of CaPO4 in dead/dying tissues
Intra and extracellular, in areas of necrosis
Component of atherosclerotic and valvular heart diseases

21
Q

What is metastatic calcification

A

Deposition of Ca in normal tissues due to hypercalcemia

Due to:
Increased PTH secretion
Bone resorption
Vit D-related disorders
Renal failure (secondary hyper PTH, kidney reabsorbs too much phosphate –> forms insoluble CaPO4, calcium ion levels drop –> PTH increases)

22
Q

Acute inflammation signs

A

Red, swelling, warm, pain, loss of function

23
Q

Acute inflammation causes

A

Infection
Physical agent (mechanical trauma, heat/cold, ionising radiation)
Chemical agent
Ischemia
Immunological reaction

24
Q

Acute inflammation pathway

A

Hyperemia (increased blood flow)
Exudation of fluid and plasma proteins
Emigration of leukocytes (WBC)

25
Q

Effects of hyperemia in acute inflammation

A

Vasodilation, reflex action by chemical mediators like histamine
Increased BV wall permeability –> contraction, damage, transport of fluids and proteins through endothelial cells
Lewis’ triple response:
> Flush: arteriolar dilation, red line
> Flare: capillary dilation, surrounding redness
> Weal: edema

26
Q

Effects of exudation of fluid and plasma proteins in acute inflammation

A

Vasodilation, increased permeability, osmotic pressure
Protein exudation of immunoglobulin and fibrinogen causing fibrin network formation
Increased lymphatic outflow causing edema of inflamed tissue

27
Q

Effects of emigration of leukocytes (WBC) in acute inflammation

A

Transmigration across endothelium and chemotaxis towards fibrin meshwork
Margination, rolling, adhesion via integrins to decrease blood flow speed
Recognise foreign bodies via opsonization by complements and antibodies, phagocytosing bacteria and debris
Kill and degrade ingested material, ROS, degradative enzymes
Secrete chemical mediators like cytokines
Produce growth factor to initiate tissue repair

28
Q

Sequelae of acute inflammation

A

Complete resolution
Healing by scarring
Suppuration/abscess formation (necrotic tissue softens and liquifies due to proteolytic enzymes, with neutrophil infiltration and pus made of leukocytes, necrotic tissue, fluid, fibrin, microorganisms, and abscess formed by pus accumulation and pyogenic lining membrane)
Chronic inflammation
Granulomatous infection (aggregates of epithelioid macrophages and multinucleated Langhans giant cells, surrounded by lymphocytes, plasma cells and fibrosis)

29
Q

What causes granulomatous infection

A

Cellular attempt to remove offending agents that are difficult to eradicate

Infection: TB
Foreign body
Autoimmune disease: sarcoidosis
Crohn’s disease

30
Q

1st vs 2nd intention healing

A

Skin edges: 1st closed, 2nd open
Granulation tissue: 1st minimal, 2nd extensive
Suturing: 1st early, 2nd absent
Scarring: 1st minimal, 2nd extensive
Tissue loss: 1st minimal, 2nd extensive
Healing: 1st rapid, 2nd delayed
Risk of infection: 1st minimal, 2nd extensive
Defect size: 1st smaller, 2nd larger
Wound contraction: 1st no, 2nd yes for larger SA wound

31
Q

Systemic factors affecting wound healing

A

Old age, malnutrition, trauma
Smoking, vasoconstriction, atherosclerosis, decreased O2 delivery
Valvular disease
Chronic disease, e.g. diabetes
Immunosuppressant with excess steroids –> inhibit macrophages, fibroblasts, collagen synthesis, and decreases wound tensile strength
Cancer
CT disorder

32
Q

Local factors affecting wound healing

A

Infection, decreasing O2 content, collagen lysis and prolonging inflammation
Poor blood supply and ischemia
Foreign body, necrotic tissue retarding granulation tissue
Tension/movement in injured area
Irradiation causing abnormal collagen synthesis and vessel fibrosis

33
Q

Complications of wound healing

A

Wound dehiscence (rupture)
Inadequate vascularisation (ulceration)
Denervation areas like in diabetic myopathy (non-healing wounds)
Excessive contraction like in severe burns
Excessive scar formation (keloid)

34
Q

What is an embolism

A

Detached intravascular solid/liquid/gas mass, carried by blood to distant site from point of origin

35
Q

Effects of embolism

A

Vascular occlusion at distant site –> necrosis, death
Septic emboli spreading infection
Tumour dissemination

36
Q

Types of embolism

A

Pulmonary (solid): hypertension –> DVT –> pulmonary hypertension/infarction

Fat (liquid): femoral/pelvic fracture, bone marrow rich in fat –> vascular occlusion/tissue damage

Amniotic fluid (liquid): enter maternal bloodstream

Air (gas): decompression sickness, air in pulmonary vessels preventing gas exchange –> difficulty breathing –> choking, air in muscles/bones –> bends, air in cerebral vessels –> cerebral ischemia, staggering

37
Q

Benign vs Malignant tumours: gross features

A

Benign: smooth surface with fibrotic capsule. Compressed surrounding tissues. Small to large, can be very large

Malignant: irregular surface without encapsulation. Destruction of surrounding tissues. Small to large.

38
Q

Benign vs Malignant tumours: microscopic features

A

Benign: Highly differentiated, resembling normal tissue of origin. Uniform appearance. Few and normal mitotic figures. Unlikely to have necrosis, does not have metastasis

Malignant: Well/poorly differentiated, most do not resemble normal tissue of origin. Enlarged hyperchromatic irregular nuclei with large nucleoli. Marked variation in size and shape of cells (pleomorphism). Increased mitotic activity with abnormal, bizarre mitotic figures. Necrosis and haemorrhage are common, metastasis may occur.

39
Q

Benign vs Malignant tumours: clinical findings

A

Benign: high survival rate after successful surgical removal

Malignant: poor survival rate, tendency for local and distant recurrence

40
Q

Staging of malignant neoplasms

A

TNM staging

T: tumour in primary site, T0: no invasion, T1 - T4: increasing degrees of tumour invasion

N: Local LN metastasis, N0: none, N1: 1-3, N2: >3

M: Distant metastasis, M0: none, M1: present

41
Q

Effects of benign tumours

A

Mass: Present as tissue lump
Haemorrhage: Ulcerated, eroded vessels
Pain: Compression of sensory nerve endings
Seizures: Growth in brain, increased ICP
Obstruction: bile duct obstruction causes jaundice
Inflammation
Oedema: venous/lymphatic obstruction

Can cut off blood flow to cause ischemia, necrosis and death
Can compress brainstem to cause death

42
Q

What is dysplasia

A

Presence of abnormal cells within tissue/organ, may eventually progress to cancer
Abnormal cells are confined by an epithelial basement membrane: pre-invasive neoplasm
No invasion into underlying tissues

43
Q

Microscopic features of dysplasia

A

Loss of architectural order
Loss of maturation
Loss of uniformity
Nuclear pleomorphism
Increased mitotic activity

44
Q

Types of cancers

A

Carcinoma: malignant, epithelial origin
Sarcoma: malignant, connective tissue origin
Adenoma: benign, glandular/endocrine origin
Adenocarcinoma: malignant, glandular/endocrine origin

45
Q

Paraneoplastic syndromes

A

Cushing: ACTH secretion by small cell lung cancer
Inappropriate ADH secretion: ADH by small cell lung cancer
Hypercalcemia: PTH-related protein by small cell lung cancer
Hypoglycemia
Polycythemia

Patho Essay Revision (12 decks)

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