Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Histopathology Part 1- (p135-148- Cardio and Resp) > Flashcards

Histopathology Part 1- (p135-148- Cardio and Resp) Flashcards

1
Q

Which WBCs are responsible for acute inflammation?

A

Neutrophils and macrophages (late acute)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which WBCs are responsible for chronic inflammation?

A

Macrophages (including granulomas like sarcoidosis), lymphocytes and plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which WBC is involved in allergic reactions and parasitic infections?

A

Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Two types of carcinoma?

A

Squamous cell carcinoma

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histological features of squamous cell carcinoma?

A

Keratin production
Intracellular bridges
Don’t form glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sites of squamous cell carcinomas?

A 
Skin
H+N
Oesophagus
Anus
Cervix
Vagina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Histological features of adenocarcinoma?

A

Form glands -> secrete glandular fluid

Mucin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sites of adenocarcinoma?

A 
Lung
Breast
Stomach
Colon 
Pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the Congo Red stain used to detect?

A

Amyloidosis- +ve apple green birefringence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does a positive result for the Prussian Blue stain show?

A

Iron (haemochromatosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the definition of atherosclerosis?

A

Chronic inflammation in intima of large arteries characterised by intimal thickening and lipid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 7 steps of atherogenesis?

A
  1. Endothelial injury
  2. LDL enters intima and is trapped in subintimal space
  3. LDL converted into modified and oxidised LDL causing inflammation
  4. Macrophages take up oxLDL via scavenger receptors and become foam cells
  5. Apoptosis of foam cells causing inflammation and cholesterol core of plaque
  6. Increase in adhesion molecules on endothelium results in more macrophages and T cells entering the plaque
  7. VSMC form the fibrous cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3 principal components of atherosclerotic plaques?

A

Cells- including SMC, macrophages and other leukocytes
ECM including collagen
Intracellular and extracellular lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is atherosclerosis more common?

A

Areas of turbulent blood flow where there is low shear stress which is atherogenic e.g. ostia of major branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors for atherosclerosis (modifiable and non-modifiable)?

A

Modifiable- T2DM, HTN, Hypercholesterolaemia and Smoking

Non-modifiable- Gender (M>F), age, FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Complications of myocardial infarction?

A 
Mechanical- 
Contractile dysfunction due to loss of muscle -> cardiogenic shock
Congestive cardiac failure
LV infarct
Cardiac rupture
Ventricular aneurysm

Arrhythmias-
VF usually occurs in first 24h, cause of sudden death
90% develop arrhythmia following MI

Pericardial- pericarditis, tamponade, Dressler’s syndrome (months after)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the histological findings <6h post-MI?

A

Normal by histology (CK-MB also normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the histological findings 6-24h post-MI?

A

Loss of nuclei, homogenous cytoplasm, necrotic cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the histological findings 1-4d post-MI?

A

Infiltration of polymorphs then macrophages (clear up debris)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the histological findings 5-10d post-MI?

A

Removal of debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the histological findings 1-2w post-MI?

A

Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the histological findings wks-months post-MI?

A

Strengthening, decellularlising scar tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Common causes of HF?

A 
IHD
Valve disease
Myocarditis
HTN
DCM
Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Complications of HF?

A 
Sudden death
Emboli
Arrhythmias
DVT + PE
Pulmonary oedema
Hepatic cirrhosis- nutmeg liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pathophysiology of HF?

A

Damage -> reduced CO + SV
Compensatory mechanisms:
Low CO -> Activation of RAS -> Salt and water retention to maintain perfusion. Eventually -> fluid overload

Low SV -> Activation of SNS via baroreceptors -> maintains perfusion but increases TPR -> increased afterload -> LVH and increased EDV -> dilatation and poor contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Investigations in HF?

A

BNP
CXR
ECG
Echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of dilated cardiomyopathy?

A 
Idiopathic
Alcohol
Peripartum
Genetic
Sarcoidosis
Haemochromatosis
Myocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Causes of HCM?

A

Genetic

Storage diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of restrictive cardiomyopathy?

A

Sarcoidoisis
Amyloidosis
Radiation-induced fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is seen histologically in HCM?

A

Myocyte disarray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the inheritance pattern of HCM?

A

Autosomal dominant mutations in genes encoding sarcomeric proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which mutations are most common for HCM?

A

betaMHC gene, MYBP-C + Trop-T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is hypertrophic obstructive cardiomyopathy?

A

Septal hypertrophy resulting in outflow tract obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Myocyte loss with fibrofatty replacement typically affecting the RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the peak age of acute rheumatic fever?

A

5-15yrs

36
Q

What are the clinical features of Acute Rheumatic Fever and what is diagnosis based on?

A

Develops 2-4w after strep throat infection

Diagnosis is based on group A strep infection + 2 major criteria or 1 major and 2 minor criteria

Jones' Major Criteria (CASES)-
Carditis
Arthritis
Sydenham's chorea
Erythema marginatum
Subcutaneous nodules
Minor criteria:
Fever
Raised ESR or CRP
Migratory arthralgia
Prolonged PR interval
Previous rheumatic fever
Malaise
Tachycardia
37
Q

Main pathogen in acute rheumatic fever?

A

Lancefield group A strep

38
Q

Histology of acute rheumatic fever?

A 
Beady fibrous vegetations (verrucae)
Aschoff bodies (small giant cell granulomas) 
Anitschkov myocytes (regenerating myocytes)
39
Q

Treatment of acute rheumatic fever?

A

Benzylpenicillin

40
Q

What is the pathology of rheumatic heart disease?

A

Antigenic mimicry- cross reaction of anti-streptococcal antibodies with heart tissue

41
Q

What increases the risk of bacteraemia?

A 
Poor dental hygiene
IVDU
Soft tissue infection
Dental treatment
Cannulae/lines
Cardiac surgery
42
Q

Causative organisms in acute infective endocarditis?

A

Staph aureus and strep pyogenes

43
Q

Causative organisms in subacute infective endocarditis?

A

Strep viridans, staph epidermis, GACEK, coxiella, mycoplasma

44
Q

Clinic features of infective endocarditis?

A

Constitutional- fever, malaise, rigors and anaemia
Cardiac- new murmur (MR/AR usually)
Immune phenomena- Roth spots, Osler’s nodes + haematuria due to glomerulonephritis
Thromboembolic phenomena- Janeway lesions, septic abscesses in lungs/brain/spleen/kidney, microemboli, splinter haemorrhages, splenomegaly

45
Q

Criteria used for diagnosing infective endocarditis?

A

Duke criteria:
Major-
Positive blood culture growing typical organisms or 2 positive cultures >12h apart
Evidence of vegetation/abscess on echo or new murmur

Minor-
RF
Fever>38
Thromboembolic phenomena
Immune phenomena
Positive blood cultures not meeting major criteria

Need 2 major, 1 major + 3 minor or 5 minor

46
Q

How do you treat infective endocarditis?

A

Broad spectrum Abx once cultures taken, then treat according to sensitivies
Subacute- benzylpenicillin + gentamicin or vancomycin for 4wks
Acute- Flucloxacillin for MSSA, rifampicin + vancomycin + gentamicin for MRSA

47
Q

Causes of pericarditis?

A 
Fibrinous (MI, uraemia)
Purulent (staph)
Granulomatous (TB)
Hemorrhagic (tumour, TB, uraemia)
Fibrous (constrictive)
48
Q

Common cause of pericardial effusion?

A

Chronic heart failure

49
Q

Histological features of chronic bronchitis?

A

Dilatation of airways
Goblet cell hyperplasia
Hypertrophy of mucous glands

50
Q

Histology of bronchiectasis?

A

Permanant dilatation of bronchi and scarring

51
Q

Histology of asthma?

A

Whirls of shed epithelium (Curschmann spirals), eosinophils, Charcot-Leyden crystals

52
Q

Histology of emphysema?

A

Loss of alveolar parenchyma distal to terminal bronchiole

53
Q

Causes of bronchiectasis?

A 
Inflammatory-
Post-infectious 
Abnormal host defence (hypogammaglobulinaemia or chemotherapy)
Obstruction
Post-inflammatory
Secondary to bronchiolar disease or interstitial fibrosis
Systemic disease
Asthma
Congenital-
CF
PCD
Hypogammaglobulinaemia
Yellow nail syndrome
Young's syndrome- rhinosinusistis, azoospermia and bronchiectasis
54
Q

What is interstitial lung disease?

A

Group of >200 diseases characterised by inflammation and fibrosis of the pulmonary connective tissue, particularly the most peripheral and delicate interstitium of the alveolar wall

55
Q

What do you see on spirometry for interstitial lung disease?

A

Features of restrictive lung disease:
Decreased CO diffusion capacity
Decreased lung volume
Decreased compliance

56
Q

How does interstitial lung disease present?

A

SOB
End-inspiratory crackles
Cyanosis, pulmonary HTN and cor pulmonale
Honeycomb lung

57
Q

How is interstitial lung disease categorised?

A
  1. Fibrosing e.g. cryptogenic fibrosing alveolitis, pneumoconiosis, CTD
  2. Granulomatous e.g. sarcoid, EAA
  3. Eosinophilic
  4. Smoking-related
58
Q

What is the histological pattern of fibrosis in cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis?

A

Usual interstitial pneumonia (required for diagnosis):

Progressive patchy interstitial fibrosis with loss of normal lung architecture and honeycomb change, beginning at periphery of lobule, usually sub-pleural
Hyperplasia of type II pneumocytes causing cyst formation- honeycomb fibrosis

59
Q

Clinical presentation of cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis?

A

Increasing exertional dyspnoea and non-productive cough

40-70y at presentation with hypoxemia -> cyanosis and pulmonary HTN

60
Q

Treatment for cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis?

A

Steroids
Cyclophosphamide
Azathioprine

61
Q

What is pneumoconiosis?

A

Typically occupational lung disease- a non-neoplastic lung reaction to the inhalation of mineral dusts or inorganic particles (majority affect upper lobe e.g. coal worker’s pneumoconiosis, silicosis, asbestosis)

62
Q

What is a granuloma?

A

A collection of histiocytes, macrophages +/- multi-nucleate giant cells

63
Q

Name some granulomatous infections

A

TB
Fungal- histoplasma, cryptococcus, coccidioides, aspergillus, mucor
Pneumocystitis
Parasites

64
Q

Name some non-infectious granulomatous conditions?

A

Sarcoid
Foreign body (aspiration or IVDU)
Drugs
Occupational lung disease

65
Q

What is extrinsic allergic alveolitis?

A

Group of immune-mediated lung disorders caused by intense/prolonged exposure to inhaled organic antigens -> widespread ALVEOLAR inflammation. Typically an occupational lung disease

66
Q

What do you see histologically in extrinsic allergic alveolitis?

A

Presence of polypoid plugs of loose connective tissue within alveoli/bronchioles- granuloma formation and organising pneumonia

67
Q

How does acute EAA present?

A

Inhalation of antigenic dust in sensitised individual -> systemic symptoms (fever, chills, chest pain, SOB, cough) within hours of exposure, usually settle by following day. Progresses to chronic EAA

68
Q

How does chronic EAA present?

A

Progressive persistent productive cough and SOB, finger clubbing and severe weight loss

69
Q

Name some common chronic EAA conditions and what causes them?

A 
Farmer's lung- mouldy hay/grain/silage
Pigeon fanciers lung- proteins in excreta/feathers
Humidifiers lung- heated water reserves
Malt workers lung- germinating barley
Cheese washer's lung- mouldy cheese
70
Q

What are the four common forms of lung cancer and who do they commonly occur in?

A

Squamous cell carcinoma (30-50%)- M>F, smokers
Adenocarcinoma (20-30%)- women and non-smokers
Small cell carcinoma (20-25%)- smokers
Large cell carcinoma (10-15%)

71
Q

What mutations most commonly cause squamous cell carcinoma?

A

p53/c-myc mutations

72
Q

Where does squamous cell carcinoma most commonly occur?

A

Proximal bronchi, late mestastasis

73
Q

Histology of squamous cell carcinoma?

A 
Keratinisation
Intracellular prickles (Desmosomes)
74
Q

What is adenocarcinoma?

A

Malignant epithelial tumour with glandular differentiation or mucin production

75
Q

Where does adenocarcinoma most commonly occur?

A

Peripherally and metastasises early

76
Q

Histology of adenocarcinoma?

A

Glandular differentiation (gland formation and mucin production)

77
Q

Where does small cell carcinoma usually occur?

A

Centrally in proximal bronchi, early metastasis to bone, adrenal, liver and brain

78
Q

What sort of cells does small cell carcinoma arise from?

A

Neuroendocrine- associated with ectopic ACTH, Lambert-Eaton, cerebellar degeneration

79
Q

What is a large cell carcinoma?

A

Poorly differentiated malignant epithelial tumour- large cells, large nuclei, prominent nucleoli

80
Q

Histology of large cell carcinoma?

A

No evidence of glandular or squamous differentiation

81
Q

What percentage of PEs derive from DVTs?

A

95%

82
Q

RF for PE?

A 
Female
Immobility
Cardiac disease
Cancer
Primary and secondary hypercoaguable
83
Q

Virchow’s triad?

A

Blood stasis
Damage to endothelium
Hypercoagulability

84
Q

What is the clinical definition of pulmonary HTN?

A

Mean pulmonary arterial pressure >25mmHg at rest

85
Q

How is pulmonary HTN classified?

A

According to aetiology
Class 1- PAH (idiopathic, hereditary, drugs/toxins)
Class 2- Pulmonary HTN associated with left heart disease (systolic/diastolic dysfunction, valve disease)
Class 3- Pulmonary HTN due to lung disease
Class 4- Chronic thromboembolic pulmonary HTN
Class 5- Pulmonary HTN with unclear multifactorial mechanisms (metabolic disorders, systemic disorders, haematological disorders)

86
Q

What is the pathophysiology of pulmonary oedema?

A

Intra-alveolar fluid accumulation leads to poor gas exchange

87
Q

Main aetiology of pulmonary oedema?

A

LHF

Pathology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions