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Pathology > Histopathology > Flashcards

Histopathology Flashcards

1
Q

What is the Z line

A

The junction between oesophageal epithelium and columnar in the stomach.

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2
Q

What are some complications of GORD

A

Ulceration, fibrosis, haemorrhage, perforation (Boerrhave’s), Barrett’s oesophagus

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3
Q

What is the pathophysiology of Barrett’s oesophagus

A

Metaplasia of the oesophageal squamous epithelium into columnar (gastric type mucosa)
+/- goblet cells (intestinal metaplasia)

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4
Q

What is the most common oesophageal carcinoma (developed countries) and developing) and Rfs

A

Developed: Adenocarcinoma RF- GORD associated.
Barrett’s -> dysplasia-> malignant.
Developing: Squamous Cell Carcinoma - RFs HPV, alcohol, smoking - mid/lower

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5
Q

What are the causes of gastritis

A 
Acute: 
chemical - NSAIDs, alcohol, corrosives.
Infective- H.pylori, CMV, strongyloides.
Chronic:
AI eg anti-parietal, Bacterial -H.pylori, Chemical - same + bile reflux (ABC), +IBD (Crohn's)
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6
Q

What are the risks associated with H.pylori

A

Acute+ Chronic gastritis, CLO-IM->dysplasia>adenocarcinoma/ MALToma.
H.pylori injects cag-A- postive/negative into epithelium (it only sits on the surface)

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7
Q

Whats the difference between a gastric ulcer and erosion

A

An erosion only goes through the surface epithelium +/- lamina propria. Ulcers go the whole way through.

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8
Q

What is the epidemiology of gastric cancer

A

95% are adenocarcinoma.
<5% - squamous cell carcinoma, MALToma, GI stromal tumour, neuroendocrine.
Poor survival -15%
Most common in males.
Japan, Italy, Chile, Portugal have high burdens of disease.

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9
Q

How can MALTomas be treated

A

If caught early H.pylori antibiotic treatment can reverse (even though it’s malignant )

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10
Q

What are the causes of duodenitis

A

Increased acid from the stomach -> duodenum. Duodenum epithelium will look like gastric (metaplasia)
H.pylori, endoscopy
Immunosuppressed, CMV, cryptosporidiosis, Giardia Lamblia, Whipple’s disease.

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11
Q

How does the histology of the fundus, body, antrum and duodenum differ?

A

The body and fundus - are responsible for acid and enzyme production so have a larger lamina propria with specialised glands.
Whereas the antrum and pylorus have a small area with gastric pits - more commonly associated with H.pylori.
Duodenum- villous: crypt 2:1. Goblet cells are found here (not usually in the stomach).

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12
Q

What is the histology of squamous cell carcinoma of the oesophagus

A

invasion of the submucosa, squamous cells at the bottom, producing keratin, with intracellular bridges

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13
Q

What are histological changes associated with gastritis

A

Lymphocytes (Chronic) +/- neutrophils (acute inflammation)

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14
Q

What are the surgical options for neurooncology

A

Maximal safe recession (depends on size, location and number of lesions)
Craniotomy or (debulking subtotal but as much as possible)
Inoperable:

Open biopsies, small needle (sterostatic) biopsy

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15
Q

What are the 2 types of cerebral oedema

A

Vasogenic- BBB issue

cytotoxic- cellular injury eg hypoxia, ischaemia -> damaged astrocytes

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16
Q

What are the two types of hydrocephalus?

A

Communicating - obstructed CSF outflow (eg neonates)

Non-communicating - reabsorption issues eg meningitis

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17
Q

What’s the normal range of ICP

A

7-15mmHg

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18
Q

What are the different types of brain herniation

A

Subfalcine- cortex pushed under Falx cerebri SOL
Transtentorial (Uncal)- medial tentorial lobe through tentorial notch (due to superficial pressure)
Tonsillar- cerebellar through foramen magnum global ^ICP. (Can be iatrogenic - LPs -> can be fatal)

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19
Q

What vascular events are classified as stroke (and which are excluded)?

A

Cerebral infarction
Primary intracerebral haemorrhage
Intraventricular haemorrhage
Subarachnoid haemorrhage

(not subdural, epidural, intracerebral haemorrhage or infarction caused by infection or tumour)

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20
Q

Why are TIAs an important prognostic factor for patients?

A

1/3 of people with a TIA have a significant infarction within 5 years

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21
Q

What’s the most common pathophysiology of cerebral intraparenchymal haemorrhage?

A

Haemorrhage due to rupture of small intraparenchymal vessels.
Usually basal ganglia
hypertension associated

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22
Q

How do arteriovenous malformations present?

A

often congenital but nil til 30-50s
haemorrhagic stroke - headache, focal neuro deficit.
Major pressure bleed and can be seen on angiography

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23
Q

Describe the flow of CSF through the ventricular system

A

lateral-> intraventricular foramina-> 3rd-> 4th -> exits to subarchnoid (small amount to spinal cord) -> circulates via arachnoid granulations that pierce superior sagital sinus

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24
Q

What is a cavernous Angioma?

A

closely packed vessels with (no brain substance just vessels) - low-pressure bleed

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25
Q

Where are the most common sites for aneurysms that cause subarachnoid haemorrhage (thunderclap)?

A

80% internal carotid artery bifurcation
20% vertebra-basilar circulation.
Risk at 6-10mm

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26
Q

What is the management of an unruptured berry aneurysm (it’s because of how they look)

A

endovascular coils - fill it with wire so no blood flow

Surgical - clipped (very invasive)

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27
Q

Define ischaemia

A

A loss of blood supply - hypoxia and lack of all other nutrients

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28
Q

What are the sites commonly affected by atheroma and emboli? (Brain)

A

Atheroma - internal carotid bifurcation or basilar artery

Emboli - middle cerebral artery.

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29
Q

Where does the MCA, ACA and PCA supply?

A

Middle - temporal
Anterior - strip in the middle of the brain from front to occipital
Posterior - occipital

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30
Q

What are the classification of head trauma?

A

Missle or non-missle (war zone)
Acceleration or deceleration (RTAs, assault)
Rotational (eg boxing)
Focal or diffuse

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31
Q

Which classific skull fracture signs are associated with what location of fracture?

A

Raccoon eyes and battle sign- fissure fracture extends to the base of the skull
Otorrhoea and Rhinorrhea-pass through the middle ear or anterior cranial fossa

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32
Q

What is the cause of contusions and lacerations (brain)?

A

acceleration/ deccleration
Laceration= pia mater is torn
Co and contra co (due to rebound hitting the back of the skull).

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33
Q

Explain diffuse axonal injury

A

At the moment of injury there are shearing and tensile forces of axons which mainly affects midline structures - corpus callosum, rostral brainstem and septum pellucidium

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34
Q

What is a prion infection

A

Transfer of pathological protein - conversion of host proteins to the pathological form (no DNA or RNA transfer)
Cause spongiform encephalopathy

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35
Q

Give examples of prion disease in humans?

A

Kuru (cannibalism- motor cognitive disorder)
Creutzfeldt-Jakob disease (CJD)- mad cow
Gertmann-Straussler-Sheinker Syndrome (GSS)
Fatal familial insomnia

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36
Q

What are the different structures of prion proteins

A

start as alpha helices can unfold +/- refold tightly into beta-pleated sheet (transmissible) and more susceptible to aggregation and propagation.

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37
Q

What are the clinical features of CJD

A

<45 y/o, cerebellar ataxia and dementia. diagnosed at autopsy

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38
Q

What’s the pathology of Alzheimer’s disease

A

Extracellular plaques of amyloid-beta. (can deposit in blood vessels)
Tau Neurofibrillary tangles (intraneuronal)
neuronal loss -> cerebral atrophy - wide gyri and wide ventricles

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39
Q

What are the different ways Amyloid precursor protein be processed?

A
  • Amyloidgenic - cleavage of the A-beta sequence
  • Non- amyloidgenic - cleaved at the amino terminus and a second cleavage produces A-beta (when too much is produced is kicked out the cell)
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40
Q

How can tau cause AD?

A

It is hyperphosphorylated cytoskeleton microtubule protein (accumulates intracellularly)

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41
Q

Describe the Braak staging of AD

A
  1. Tau in the temporal lobe - entorhinal cortex (next to the hippocampus)
  2. +posterior hippocampus
  3. immunostaining by eye (clinical symptoms)
  4. spreads to superior temporal gyrus
  5. peristriate cortex (around primary visual cortex)
  6. spread to the striate cortex of the occipital lobe
42
Q

What is chronic traumatic encephalopathy?

A

A tauopathy caused by chronic head trauma causing parkinsonian symptoms

43
Q

What is the pathology of Parkinson’s disease

A

Lewy bodies (smooth hyaline inclusions) in the substansia nigra in the midbrain (loss of pigment) due to loss of dopaminergic neurones (project to caudate and putamen) - important in the initiation of movement

44
Q

How can Parkinson’s disease be diagnosed histopathologically

A

Pale substansia nigra (old)
H&E stain for Lewy bodies
Alpha-synuclein immunostaining (gold standard)

45
Q

Whats the Braak staging of Parkinson’s disease

A
  1. Lower brainstem ( dorsal motor nucleus of CNX) and olfactory
  2. Raphe nuclei and gigantocellular retituclar nucleus (medulla)
  3. 70% loss symptomatic, substansia nigra, progresses to basal nuclei
  4. Pars compacta + mesocortex
  5. Neocortex + other corticical ateas
  6. motor and sensiry cortex
46
Q

What are the proposed routes for environmental triggers for Parkinson’s disease?

A
  1. retrograde from the gut -> medulla via vagus nerve

2. Nose (often anosmia as pc, often heavily affected olfactory bulb)

47
Q

What are the causes of parkinsonism?

A 
Protein issues
PD
Multiple system atrophy- cerebellar pc or parkinson (alpha synuclein at glial cells)
Tauopathies:
-Progressive supranuclear palsy (PSP)
-Corticobasal degeneration
other
Drug induced
corticobasal degeneration
vascular pseudoparkinsonism
Alheimers changes
Fronto-temporal neurodegenerative disorders
48
Q

What are the PC of frontotemporal disease

A

dysexecutive syndrome

49
Q

What is the pathology associated with Pick’s disease

A

Marked gliosis and neural loss, balloon neurones and tau positive pick bodies

50
Q

What’s the different tau isoforms?

A

Physiologically single genre 17q21 with 16 exons alternative splicing -> 6 isoforms with 4R or 3R microtubule sites

51
Q

How do the different isoforms of tau affect tauopathies?

A

Ad- has all 6 isoforms
Corticobasal degeneration and PSP - only 4R
PCIK’S DISEASE- ONLY 3r

52
Q

FTD is a heterogeneous presentation give an example of a pathology (gentic)

A 
Tau and progranulin mutations.
progranulin causes unilateral atrophy
TDP-43 (trafficking protein) mutation
FUS pathology
c9ORF72 mutations
53
Q

What are the risk factors for strokes?

A

Smoking, diabetes, HTN, PVD, OCP, dyslipidemia, ETOH++, sickle cell anaemia, polycythaemia vera

54
Q

What are the investigations for strokes and TIAs?

A

CT (MRI)
Bloods - Lipids, FBC, ESR, U&E, HBA1c.
CXR, ECG, BP, carotid doppler

55
Q

What is the management of an ischaemic stroke?

A 
Thrombolysis <4 hrs
Asprin +/- dipyridamole
\+/- carotid endarterectomy
Long term
- antihypertensives, anticoagulants, v lipids
56
Q

What are the S&S of ACA and PCA?

A

ACA- contralateral leg weakness (mainly)

PCA- Visual disturbance

57
Q

What are the causes of acute pancreatitis

A

I GET SMASHED
Duct obstruction - gall stones (1st), tumours (malignancy), trauma (eg ERCP)
Metabolic- alcohol(1/3), Drugs eg thiazides and steroids, hypercalcemia, hyperlipidemia, poisons
Poor blood supply- shock
Infection/ inflammation- mumps
AI
Idiopathic

58
Q

How can alcohol cause acute pancreatitis?

A

metabolic
spasm of sphincter of oddi ->
proteinous secretion causing obstruction

59
Q

What are the different patterns of injury in acute pancreatitis?

A

Periductal- necrosis of the acinar cells near ducts (2nd to infection) - obstruction
Perilobullar- necrosis at edges of lobules due to poor blood supply
Panlobular - combination of both

60
Q

What is the pathway of inflammation in pancreatitis

A

Blockage of duct, reflux of bile up pancreatic duct, damage to acini and enzyme release

61
Q

What are the complications of pancreatitus (6)

A

Complications: chronic pancreatitis, pseudocysts, pancreatic abscess, shock, hypoglycaemia, hypocalcemia (hence Ca may be normal at presentation)

62
Q

causes of chronic pancreatitis

A

metabolic - Alcohol (No1), haemochromatosis
duct obstruction - CF, ductal abnormality, tumours, gallstones (less common)
Idiopathic

63
Q

Describe a pancreatic pseudocyst

A

A pancreatic enzyme-rich/ necrotic fluid-filled pocket lined with fibrous tissue without epithelial lining, that connects to pancreatic duct

64
Q

What are the characteristics of IgG4 related disease

A

IgG4 positive plasma cells mediated inflammation of the pancreas and many other areas of the body (eg gall bladder)

65
Q

What are the different types of pancreatic tumours?

A 
Carcinomas:
Ductal adenoma (most common)
Acinar
Cystic neoplasm
Pancreatic neuroendocrine tumours
66
Q

What is PanIN?

A

Precancerous dysplasia

Pancreatic intraducatal neoplasia - K-Ras mutation causing mucin secretion

67
Q

Whats the histological appearance of pancreatic ductal carcinoma

A

Macro - grey and gritty, invades surrounding structures

Micro - mucin secretion in desmoplastic stroma

68
Q

What are the pathways of metastasis for ductal carcinoma (pancreatic)

A

Direct- bile ducts/ duodenum
Lymphatic
Haematological -> liver
Serosa -> peritoneum

69
Q

Where in the pancreas has a better prognosis (ductal cancer)

A

Head of the pancreas as likely to present sooner with obstructive symptoms

70
Q

What are the features of pancreatic neuroendocrine tumours?

A

Highly variable - in terms of malignancy
most are non-secretory.
Insulinoma are the most common secretory type
Commonly associated with MEN1

71
Q

What are the risk factors for gall stones

A

FFFF
^BMI, Female, OCP, ^age,
specific groups eg Native americans
Rapid weight loss

72
Q

What are the different types of gallstones

A

Cholesterol - most common, lipid-based, multiple, radiolucent commonly
Pigments - bilirubin, often multiple, radio-opaque contains calcium

73
Q

What are the complications of gallstones

A

Cholestasis, Cholecystitis, Ascending cholangitis, pancreatitis, cholangiocarcinoma, chronic cholecystitis - inflammation + fibrous diverticulae (Rokitansky-Achoff sinuses)

74
Q

Which cells of the pancreas are

a. source of enzymes
b. exocrine
c. endocrine

A

a. acinar
b. acinar and ducts
c. islet of langerhans

75
Q

What are the lipid soluble vitamins and their associated derangements

A

A- retinol - colourblindness
D- cholecalciferol- Rickets amd osteomalacia: vCa2+ - hypersensitivity of nerves, ^PTH and bone resoption
E- Tocopherol - antioxident > anaemia, neuropathy and malignancy and IHD
K- Phytomenadione: causes clotting issues with F2,7,9 and 10 - check PTT and give PO or IM replacement vit K

76
Q

What are the water soluble vitamins?

A 
B1 thiamine
B2 riboflavin
B3 niacin
B6 Pyridoxine
B9 Folate
B12 Hydroxycobalamin
C ascorbate
77
Q 
What are the deficiencies associated with
B1- thiamine
B2 Riboflavin
B3 Niacin
B6 Pyridoxine
B9 Folate
B12 Hydroxycobalamin
C Ascorbic acid
A

B1- beri beri, wernicke’s encephalopathy, Korsakoff’s psychosis
B2- glossitis
B3- pellagra- 4Ds
B6- dermatitis and anaemia
B9 - megaloblastic anaemia, neural tube defects
B12 - pernicious anaemia
C- scurvy - bleeding gums, fatigue, depression, athropathy

78
Q

What are the signs and symptoms of

a. beri beri
b. wernike’s
c. Korsakoff’s
d. pellagra

A

a. wet = CVS- oedma, HF, Dry= neurological
b. opthalmaplegia, ataxia and acute confusion
c. opthalmaplegia, ataxia, acute confusion, anterograde amnesia (confabulation), psychosis
d. diarrhoea, dermatitis, dementia, death

79
Q

What are the management options for obesity

A

Conservative - diet, exercise and education (some evidence for a very low calorie diet 800kCal undersupervision)
Medical - orlistat or GLP-1 analogues
Surgical - adjustable band, gastric sleeve, gastric bypass.

80
Q

What are the management options for obesity

A

Conservative - diet, exercise and education (some evidence for a very low calorie diet 800kCal under supervision)
Medical - orlistat or GLP-1 agonist
Surgical - adjustable band, gastric sleeve, gastric bypass.

81
Q

What are the different types of amino acids?

A

Dispensable- human body can synthesis
conditional -indispensible neonates are unable to synthesis
Indispensable - cannot synthesis - dietary requirement

82
Q

Which type of carbohydrates are associated with ^ Gut metabolism?

A

non-starch polysaccharides are fibre

83
Q

Which type of fats

a. ^LDL
b. ^HDL

A

a. saturated fats

b. Polyunsaturated fats, trans-monounsaturated fat

84
Q

Which type of fats

a. ^LDL
b. ^HDL

A

a. SATURATED FATS, trans-monounsaturated fat

b. Polyunsaturated fatty acids

85
Q

Pathology of atherosclerosis and how it causes IHD

A

Enodthelial damage> platelet damage > endothelial proliferation with lipidprotein depsotis (fatty streak)> monocytes>intima and become macrophages that ingest lipid> foam cell + plt aggregation and activation to form fibrous cap
Causes flow disruption most commonly carotids and coronary arteries

86
Q

Riskfactors for atherosclerosis?

A

Non-modifiable - age, male, post menopausal women, genetic eg FH familial hypercholesterolaemia

Modifiable- HTN, lipids- ^LDL and vHDL, DM, smoking, obesity, stress (^ inflmation- HSV, CMV, chlamydia and pneumonia)

87
Q

What are the different types of IHD?

A

MI
Angina - stable, vasospasm (Prinzmental), unstable
HF - LHF,RHF CHF
IDH with sudden death

88
Q

Describe the histology of HF?

A

Dilated heart, scarring, atrophic walls, fibrous replacement of the ventricular myocardium

89
Q

Describe the pathological process of an MI?

A

Artery occlusion due to sudden change in atherosclerotic plaque/ emboli
LAD>RCA>LCx Ischaemia > myocytes cell death > v contractility<60 sec
Ireverisble damage if >30 mins
0-6hrs- normal histology
6-24- loss of nuclei and homogeneous cytoplasm = necrosis
1-4 days =neutrophil infiltration then lymphocytes then macrophages
5-10 removal of necrotic debris
1-2 weeks - tissue granulation, vasogenesis, ^ fibrosis
weeks - scaring and decellurisation

90
Q

WHat are the compliations associated with an MI?

A

Death, arrythmis, Rupture (myocardial or papillary) Tamponade, HF, Valvular disease, aneurysms, Dressler syndrome (pericarditis), embolism/ extension or expansion, recurrence
DARTH VADER

91
Q

What are the different types of valvular disease?

A

Rheumatic - following group A strep
calcification - AS
Endocarditis - infection
AR - can be ridgid (rheum), destructive (endo) or dilatory - marfans, syphilis, ankylosis spondylitis

92
Q

What are the causes of

a. dilated cardiomyopathy
b. hypertrophic
c. restrictive

A

a. idopathic, myocarditis, alcohol, chemo, iron, thyroid disorders, MD, peri-partum, hemochromatosis,
b. congenital HOCM
c. idiopathic, amyloid, sarcoidosis

93
Q

Describe the histology of

a. pulmonary oedma
b. acute lung injury
c. asthma

A

a. Intralveolar fluid - looks like liver
b. Diffuse alveolar damage, hyaline deposition from leaky capillaries, plum firm airless lungs
c. eosinophilic infiltration, mast cells, mucus plugs, bronchial smooth muscle hypertrophy, vasodilation

94
Q

Describe the histology of
a. COPD

b. bronchiectasis

A

a. dilated airways, mucus gland hyperplasia, gobelet cell hyperplasia, mild inflammation
b. permanent dilation of bronchi with inflam and fibrosis (lower is often worse)

95
Q

What are the causes of bronchietasis? (4 types)

A

recurrent chest infections eg in CF, cilary dyskenisia, immunocomp
obstructive - asthma
Pulmonary fibrosis
Connective tissue disorder

96
Q

Describe the differences between bronchopulmonary and lobar pneumonia

A

Lobar is infection and inflation homogeneous throughout one lobe - widespread fibrous consolidation, congestion, red hepatisation and grey (CXR white out), due to highly virulent pathogens - less common now

Bronchopulmonary = peri-bronchial consolidation often lower lobe. CXR = patchy, low virulence CAP - Staph, strep, Hib

97
Q

Describe the presentation of PE (small and big)

A

small- SOB, may be sudden onset or progressive depending on the size and number of PEs. Can cause pulmonary HTN
Large- often presents as sudden death

98
Q

Describe the histology of fibrotic diseases (pulmonary)

A

^Fibrosis often in lower lobes and peripheries, loss of normal alveolar structure

99
Q

What is paraneoplastic syndrome?

A

Effects of a malignancy not directly due to its presence in a tissue
eg Immune response to tissue, seccretory functions
eg
Endo - Scc SIADH, cushing’s, ^PTH
Non endo- procoagulants,

100
Q

What are the signs of local invasion in pulmonary malignancy?

A 
Chest wall=Chest pain
Vessles= Haemoptysis
Nerves=Horners
Oesophagus= dysphagia
Large vessels =SVC syndrome
101
Q

What are the associations with

a. SCC (pulmonary)
b. adeno (pulmonary)
c. large cell
d. small cell

A

a. smoking!
b. KRAS=smokers, EGFR= non-smokers, ALK=young, extrathoracic mets
c. poor prognosis
d. smoking! paraneoplastic syndromes

102
Q

What are the molecular testing options for lung cancer?

A

ECFR (TK receptor) = TKis
ALK translocation - signet ring
ROS1 translocation -rostinib
KRAS - poor prognosis

Pathology (6 decks)

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