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2 Pathology Flashcards

1
Q 
Describe necrosis types:
Coagulative
Colliquitive
Caseous
Fat
A

Coagulative - firm, maintains structure
>Haemorrhagic - blocked venous drainage
>Gangrenous

Colliquitive - liquefies (e.g. infarct/ abscess)
Caseous - mixture of both, “cheese-like” appearance
(e.g. granulomatous disease aka TB)
Fat - action of lipases to break down fatty tissue

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2
Q

How would hemorrhagic coagulative necrosis look in an organ (straight after damage and after necrosis occurred)

A

Straight away: bright red and haemorrhagic

After necrosis: yellow/scarred

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3
Q

What is the main difference between necrosis and apoptosis?

A

Necrosis releases cell contents and has membrane (and nuclear) breakdown. Apoptosis does not.

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4
Q

What is characteristic to pancreatic necrosis?

A

Fat deposition in pancreas

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5
Q

Physiological apoptosis situations (5)

A

1- Embryogenesis - deletion of cell populations
2- Autoimmune T/B cells - in thymus/marrow self-ag
3- Hormone dept involution - uterus/ovaries/breast
4- After inflammatory response - delete inflam cells
5- Deletion of cells in constantly renewing tissues

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6
Q

Pathological apoptosis situations (3)

A

1- Virus (cytotoxic T cells)
2- DNA damage
3- ischemia/ hypoxia

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7
Q

Stages of apoptosis (4)

A

1) Cell shrinkage
2) Chromatin condenses
3) Membranes intact
4) Cytoplasmic blebs -> phagocytosis

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8
Q

Stages of necrosis (4)

A

1) Cell swelling - reversible
2) Cell swelling - irreversible
3) Nuclear chromatin dissolution, shrinkage and fragmentation
4) Rupture of membranes

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9
Q

Characteristic microscopic appearance and stain of amyloid

A

Congo red stain - pink

Under polarised light - apple green birefringence

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10
Q 
Histological appearance of depositions and organs:
Steatosis
Carbon
Iron
Haemosiderin
Lipofuscin
A

> Steatosis - fat lobules in liver
Carbon - black lines in lung (mucosa) , blobs in macrophages (lymphatics)
Iron - brown depositions in liver, stains blue
Haemosiderin - brown staining in macrophages
Lipofuscin - brown pigment in liver/ heart etc

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11
Q

Dystrophic and metastatic calcification definition

A 
Dystrophic = deposition in ABNORMAL tissues with normal blood calcium level
Metastatic = deposition in normal tissues with RAISED blood calcium level
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12
Q

Causes of raised serum calcium

A

1y parathyroidism - tumour
2y parathyroidism - kidney disease
systemic - cancer

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13
Q

3 main changes to cells/vasculature in acute inflammation

A

1) Vasodilation - by histamine, prostaglandins, nitric oxide

2) Neutrophil activation - by complement, leukotrienes, bacterial products
- Activation, chemotaxis and phagocytosis

3) Endothelial activation - by complement, 5HT, bradykinin, histamine, leukotrines
- Increase vascular permeability for fluid/ inflammatory markers -> swelling

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14
Q

5 cardinal signs of inflammation and causes

A 
Red - hyperaemia
Heat - hyperaemia
Swelling - hyperaemia and fluid exudate
Pain - bradykinin and prostaglandins
Loss of function - due to pain and swelling
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15
Q

Definition of exudate

A

Fluid leaking out from blood vessels, through endothelium to extracellular space in tissues

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16
Q

How granulomatous chronic inflammation is defined (3)

A

1) Granulomas
2) Epithelioid macrophages
3) Multinucleate giant cells

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17
Q

What cells are present in chronic inflammation (4)

+ what other substance is present

A

Lymphocytes (T/B/NK cells)
Macrophages
Eosinophils
Plasma cells

Fibrin

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18
Q

3 wound types

A

Abrasion
Incision
Laceration

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19
Q

2 things required for wound healing/repair

A

Granulation tissue

Fibrous scar

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20
Q

Difference between 1y and 2y wound healing/repair

A

1y - little granulation tissue and small neat scar, edges of would neat

2y - lots of granulation tissue, scab and large scar, edges of wound jaggy

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21
Q

Outcomes of acute inflammation (3)

A

1- complete resolution
2- healing by fibrosis
3- progression to chronic

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22
Q

Stages of a post-mortem examination

A

(background info - history, cause of death, clinical care etc.)
1) external - general exam

2) internal
a) Excavation - incision sternal notch-> symphysis pubis & remove thoracic/abdo/pelvic organs, incision posterior skull & remove brain
b) Organ dissection - macroscopic and sometimes microscopic (lab)

3) After
Close up/ restore body and replace organs
Write MCCD if not done so
Report to PF/ GP & clinician
Release body to family
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23
Q

How is a death certificate laid out

A

1a - disease/ condition directly causing death
1b/c/d - as a result/ consequence of …

2 - other diseases/ conditions contributing to death but not directly related to COD

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24
Q

Types of embolism (4)

A

air
thrombus
fat
amniotic fluid

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25
Q

Method of haemorrhage occurring (4) and e.g.

A

Weakness by disease (atherosclerosis > AAA > rupture)
Congenital weakness (berry aneurysm > SAH)
High pressure (hypertension > cerebral haemorrhage)
Erosion (bleeding from perforated gastric ulcer)

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26
Q

Most common sites of:
1- thrombus development
2- thrombus travel

A

1) leg veins, heart, carotid arteries

2) lungs, brain, other

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27
Q

Function of Von Willebrand factor in coagulation

A

Coagulation factor which helps attach fibrin to vessel wall with collagen

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28
Q

Difference between arterial and venous thrombus

A

Arterial - lots of platelets, little fibrin, fast flowing blood
Venous - lots of fibrin trapping RBCs, static blood

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29
Q

Classes of risk factors for abnormal thrombus (3)

A

Circulatory stasis
Hypercoagulative state
Vascular wall injury

30
Q

Hypercoagulative state risk factors for abnormal thrombus (8)

A 
Oestrogen therapy
Pregnancy/ post-partum
Malignancy
Thrombophilia
Trauma/ surgery of lower body
Nephrotic syndrom
IBD
Sepsis
31
Q

Circulatory stasis risk factors for abnormal thrombus (5)

A

Immobility/ paralysis
AF
LV dysfunction
Venous occlusion - tumour, pregnancy, obesity
Venous insufficiency/ varicose/ faulty valve

32
Q

Vascular wall injury risk factors for abnormal thrombus (6)

A 
Heart valve disease/ replacement
Surgery/ trauma
IV access (venepuncture)
Atheroscleorsis
Chemical irritation
Indwelling catheter
33
Q

What are the main deep leg veins (which DVTs form in) (4)? –> other veins (3)?

A 
Posterior tibial
Anterior tibial
Popliteal
Superficial femoral
(Common femoral > Internal iliac > common iliac)
34
Q

Causes of a DVT/ how it forms (2)

A

Slow blood flow

Faulty valves

35
Q

How to confirm diagnosis of DVT (3 steps)

A

Clinical history/ exam - Well’s Score
Biochemical: D-Dimer
Imaging - Compression ultrasound, venography

36
Q

What is D-dimer

A

Breakdown product of fibrin, containing parts (D2xD, 1xE) of fibrinogen

37
Q

Difference between thrombus and post-mortem clots

A

Thrombus - attached to vessel wall, granular, maintains vessel shape

PM - slippy, shiny “chicken fat”, easy to remove

38
Q

Risks after VTE (4)

A

PE
Recurrent VTE
Post thrombotic syndrome
Venous insufficiency - varicose veins, residual thrombus

39
Q

What is a:

1) saddle embolism
2) paradoxical embolism

A

1) at pulmonary junction

2) transfers to arterial circulation e.g. by patent foramen ovale (>stroke)

40
Q

Treatment of VTE (4)

A

Anti-coagulation 3-6 moths - warfarin, LMWH, direct factor Xa/IIa inhibitor
Compression stockings
Pain relief
Remove risk factors

41
Q 
Action of:
Warfarin
Herparins
Adoxaban/Rivaroxaban/ Enoxaban
Dibagatran
A

Warfarin - inhibits factors 7, 9, 10 and 2 (thrombin)

Heparins - indirect inhibitor of factors 2 (thrombin) and 10

Adoxaban/Rivaroxaban/ Enoxaban - direct factor 10 inhibitors

Dibagatran - direct factor 2 (thrombin) inhibitor

42
Q

Diagnosis of MI/ACS (3 steps)

A

Clinical history/ exam
Biochemical marker - troponin levels
ECG - ST elevation/depression, T wave inversion
Imaging - cardiac catheterisation

43
Q

What is acute coronary syndrome (3)?

A

Unstable angina (ST dep)
NSTEMI (ST dep/ T wave inv/ troponin)
STEMI (ST elev/ T wave inv/ troponin)

44
Q

Treatment of acute coronary syndrome (atherosclerosis) (4)

A

1) Prevention of clot getting bigger - anti platelets (clopidogrel/aspirin), anticoagulant (heparin)
2) Removal of clot - catheter angiography, thrombolysis (-teplases)
3) Widen stenosis - balloon, stent
4) Prevent further clots - anti-platelet (clopidogrel/aspirin), statin

45
Q

How does normal vs post-MI myocardium appear on H&E stain?

A

Normal: long light pink cells with central nuclei

Post-MI: dark pink cells (hyper-eosinophilic) with lots of inflammatory infiltrate (+ haemorrhaged oedema)

46
Q

How long until micro/ macroscopic changes can be seen following MI?

A

Micro - 12 hrs

Macros - at least 24hrs

47
Q

Investigation of suspected stroke (1)

A

CT of brain

48
Q

Treatment of stroke (4)

A

1) Removal of cause of thrombus - correct AF (cardioversion), replace valve
2) Anticoagulation
3) Removal of other CVD risk factors
4) (Rarely remove clot - cardiac end-arterectomy, thrombolysis)

49
Q

What is troponin?

A

Protein released by damaged myocytes, indicating ischemia/ trauma

50
Q

What are the 3 components of cellular pathology

A

Autopsy
Histology
Cytology

51
Q

Difference types of biopsy (and subtypes)

A

Small biopsy - mucosal, needle core, incision
Excisions biopsy
Ressection

52
Q

What can special stains be used for (4)?

A

Mucin
Deposition
Infection
Normal elastic tissue

53
Q

Uses of immunohistochemistry (4)

A

Tumour staging/ classification
Cancer prognosis estimates
Cancer treatment estimates (receptors)
Identification/ diagnosis of infectious disease

54
Q

What is immunohistochemistry?

A

Staining technique which strains certain proteins brown (cytoplasmic/membranous/nuclear)

55
Q

How is FISH used to determine gene over expression in tumour?

A

1) DNA denatured by heating
2) DNA separates exposing nucleotides
3) Fluorescent tag to mark gene is added (e.g. HER2)
4) Fluorescent tag to mark chromosome is added (e.g. cr17)
5) Compare dots for number of genes vs number of chromosomes, if there are more genes than chromosomes (by a lot), there is over expression

56
Q

Define congenital and developmental anomalies

A

Congenital = any abnormality present at or before birth, can be structural or functional/metabolic

Developmental = congenital structural

57
Q

How to VSDs go from L>R shunts to R>L shunts?

A

Increased pressure in low-pressure system > pul. hypertention > stenosis > higher pressure

Pressure then equalises and blood goes both ways

58
Q

What is spina bifida?

A

Failure of complete closure of neural tube so contents of spinal canal protrude from back

59
Q

Symptoms of spina bifida (5 & 3)

A

Motor interruption - muscle weakness/ limb paralysis
Autonomic interruption - bowel/ bladder problems
Hydrocephalus
Seizures
Orthopaedic problems - lower body

Syndactyly
Polydactyly
Cleft palate

60
Q

Define Hamartoma

A

Disordered growth of normal tissue within an organ, growing at the same rate as surrounding tissues

61
Q

Define Chondroid hamartoma

A

In the lung, on imaging as a “coin lesion”

Composition = epithelium, cartilage, fat, smooth muscle

Need to investigate as malignancy, can cause obstruction, and can mimic malignancy if endobronchial

62
Q

Define ectopia cordis

A

Growth of heart outside the body

63
Q

Define a diverticulum and state the 2 main types

A

Diverticulum = out pouching caused by herniation of mucosa through muscle wall

Diverticular Disease
Meckel’s Diverticulum

64
Q

Describe diverticular disease/ diverticulitis and complications

A

Out pouching of intestine, usually in sigmoid colon
Can become inflamed (feral material) = diverticulitis
This can perforate/bleed/ fistulate
Or can heal by fibrosis > muscle hypertrophy > stenosis

Similar signs to malignancy - PR bleeding and altered bowel habit

65
Q

Describe Meckel’s diverticulum and complications

A

Congenital - failure of complete obliteration of vitelline duct
2 inches, in terminal ileum

66
Q

Difference between neoplastic and non-neoplastic growth

A

Neoplastic - uncontrolled and irreversible

Non-neoplastic - controlled and reversible

67
Q

What are the grade and staging of a tumour based on?

A

Grade = level of differentiation of cells

Stage = how advanced aka size/invasion, involved nodes, mets

68
Q

What cell/nuclear changes are present in dysplasia (3)?

A

Hyperchromatic nuclei (dark)
Increased nuclear:cytoplasmic ratio (bigger nuclei)
Irregular nuclear membranes

69
Q

Define carcinoma in situ

A

> Full thickness epithelial dysplasia what has not yet invaded past the basement membrane (non-invasive)
Risk of mets is zero just now as there is no blood or lymphatics in epithelium above BM
Can progress to malignant

70
Q

3 methods of metastatic spread and examples

A

Lymphatic - carcinoma
Haematogenous - sarcoma
Transcoelemic

71
Q

Local effects of malignant tumours (6)

A 
SOL
Pressure effects - compression
Nerve innervation - pain
Ulceration/ bleeding (> anaemia)
Local destruction
Stromal reaction/ fibrosis - stenosis/obstruction
72
Q 
Raised tumour markers may suggest:
CEA (carcinoembryonic antigen) 
AFP (a-feto protein)
hCG (human chorionic gonadotropin
PSA (prostate specific antigen)
Ca125
Ca19.9
Ca15.3
A

> CEA (carcinoembryonic antigen) = various/ generic
AFP (a-feto protein) = liver, (& germ cells, testicular)
hCG (human chorionic gonadotropin) = germ cell tumours
PSA (prostate specific antigen) = prostate
Ca125 = ovarian (& uterine)
Ca19.9 = pancreatic
Ca15.3 = breast

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