Pathology Flashcards by Olivia McNee

What does VINDICATE stand for?

V – Vascular
I – Infectious/inflammatory
N – Neoplastic
D – Drugs/toxins
I – Intervention/iatrogenic
C – Congenital/developmental
A – Autoimmune
T – Trauma
E – Endocrine/metabolic

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What is an example of vascular pathology?

Blood vessels- inflammation, clot, blockage

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what is neoplasia?

New growth

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What is iatrogenic?

Caused by doctor

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Describe adaptation?

Increased demand- hyperplasia, hypertrophy

Decreased demand-atrophy

Altered stimulus- metaplasia

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What is hyperplasia?

Increase in cell number

-response to external stimulus

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What does hyperplasia result in?

Will regress on withdrawal of stimulus

Increased organ volume

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Describe hormonal hyperplasia?

Puberty- breast tissue

Pregnancy- hyperplasia of lining of uterus

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When does compensatory hyperplasia occur?

After loss of tissue

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Where does compensatory hyperplasia occur?

Liver

Bone Marrow

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Describe the mechanism of hyperplasia?

Production of increased growth factors- locally or from distant site. Hormone may be a growth factor itself.

Increased growth factor receptors

Switch on genes encoding growth factors and cell cycle regulators to promote new cell growth.

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Describe hormonally induced pathological hyperplasia?

Excess oestrogen- endometrial hyperplasia and abnormal bleeding

Prostatic hyperplasia in response to androgens

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What happens in lymph nodes as a result of infection?

Hyperplasia

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Is hyperplasia reversible?

Yes, reverse on withdrawal of stimulus

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What is the risk of hyper plastic tissue?

Risk site for development of cancer

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What is hypertrophy?

increase in cell size

Not cell number

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When does hypertrophy occur?

In conjunction with hyperplasia

In isolation in non-dividing cells e.g. cardiac myocytes, skeletal muscle

In response to mechanical stress

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When does hypertrophy of cardiac myocytes become pathological?

When heart can no longer function and requires more than is supplied

Muscle becomes less functional

Results in HF

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What is atrophy?

Reduction in cell size

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What are examples of physiological atrophy?

Embryological structures

Uterus after parturition

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What can pathological atrophy be a result of?

Decreased workload

Malnutrition

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Describe pathological atrophy?

Loss of inervation

Loss of function after nerve supply is removed

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What causes atrophy in the brain?

Blocked blood supply

In association with atherosclerosis

Ageing (also in heart)

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What causes atrophy of the kidneys?

Pressure

Due to endogenous or exogenous structures

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Describe the mechanism of atrophy?

Reduced cellular components Protein degradation Digested in lysosomes and degraded in many cases by ubiquitin proteasome pathway

Which hormones promote atrophy?

Glucocorticoids | Thyroid hormone

Which hormones oppose atrophy

Insulin

Define metaplasia

Reversible change from one mature cell type to another

What does metaplasia represent

Change in signals delivered to stem cells causing them to differentiate down a different line

What is metaplasia in response to?

Cytokines (chemical messengers, growth factors and other chemicals in the cells microenvironment) Noxious stimuli

What is squamous metaplasia a result of?

Response to injury

what is the risk of metaplasia?

Metaplastic site is at risk for cancer development

Which metaplasia cancer is common in the lung?

Squamous cell

Which metaplastic cancer is common in the oesophagus?

Adenocarcinoma (glands)

What does stress on cells cause?

Adaptation

What are the causes of inflammation?

``` Infection Trauma Foreign bodies Immune reaction Necrosis ```

What is the response to injury?

Vascular changes Cellular changes Chemical mediators Morphologic patterns

Describe vascular changes in response to injury?

Changes in flow and vessel caliber Vasodilation First involves arterioles and then capillary beds

What mediates vascular changes?

Histamine | Nitric oxide

What are the clinical manifestations of vascular changes?

Increased heat (calor) Redness/erythema (rubor)

What are the cellular changes in response to injury?

``` Stasis White cell margination Rolling Adhesions Migration ```

What are selectins?

Expressed on a variety of white cells and bind cell adhesion molecules (CAMs) on endothelial surface

What are integrins?

Over 30 types | Bind to vessel walls, cell matrix and other cells

What increases selectin expression?

Histamine and thrombin

What increases endothelial cell expression of VCAM and ICAM?

TNF and interleukin 1

What is the role of chemokines?

Chemokines from the site of injury bind to proteoglycans on endothelial cell surface

What is the role of proteoglycans?

Increase the affinity of VCAMs and ICAMs for intergrins

What happens in increased vascular permeability?

Leaky vessels- loss of protein Change in osmotic pressure Water follows protein- swelling (tumour)

What causes Endothelial contraction?

Histamine, bradykinin, substance P, leukotrienes

What causes leaky vessels

``` Endothelial contraction Direct injury White cells Transcytosis New vessel formation ```

What causes direct injury to vessels?

Toxins | Burns

What do white cells do to vessels?

Self harm

What is transcytosis mediated by?

VEGF

What forms new vessels?

VEGF

What is chemotaxis?

Cells follow a chemical gradient

What causes chemotaxis?

Bacterial components Complement Leukotrienes Cytokines- interleukins

What are the three phases of phagocytosis?

Recognition and attatchment Engulfment Killing and degradation

What is responsible for recognition and attachment?

Mannose receptors (Bacterial surface glycoproteins and glycolipids contain terminal mannose residues) Scavenger receptors Opsonins

What does not contain mannose receptors?

Mammalian glycoproteins and glycolipids do not

What are opsonins?

Coating proteins making bacteria stand out Include components of the complement cascade as well as IgG

What vesicle is formed during engulfment?

Phagosome

What is it called when a phagosome joins with lysosome?

Phagolysosome

What is responsible for killing and degradation?

Reactive oxygen species NADPH oxidase- oxygen gains an electron from it and becomes superoxide Reactive nitrogen species Nitric oxide synthase combines NO with superoxide and produces ONOO Many other cytotoxic granules

What are the five pillars of inflammation?

``` Heat Redness Swelling Pain Loss of function ```

Define rubor?

Redness >Increased perfusion. Slow flow. Increased permeability of vessels.

Define calor?

Heat >Again – increased perfusion, slow flow rate, increased vascular permeability

Define tumour?

Literal translation- swelling Due to vascular changes

Define Dolor?

Pain Mediated by prostaglandins and bradykinin

What are the microscopic changes in inflammation?

``` Neutrophils -polymorph Many lobes to nucleus Granulocyte Phagocytic and cytotoxic abilities ```