Pathology Flashcards
Diaphragm innervation at this cervical vertebrae
C3
Two types of heart block
Type 1- PR interval same
Type 2- PR interval increasing
What antibody is measured in people with Strep infection and for RF?
ASOT
and AntiDNAseB
Diseases caused by Strep (GAS)
- Pharyngitis
- Septicaemia
- Cellulitis
- Scarlet fever
- Streptococcal shock syndrome
- Rheumatic fever
Acute rheumatic fever
Abnormal immune response to GAS infection
Features of ARF (Jones criteria)
JONES Joints- Polyarthritis O- Heart- Carditis (pancarditis) N- Subcutaneous nodules E- Erythema marginatum S- Chorea
Minor- Fever, arthralgia, acute phase reactants, prolonged PR interval
Treatment for RF
Benzathine Penicilin
**Glucocorticoids for severe RF
And symptom control
Three main epicardial coronary arteries
1) Left coronary artery (anterior 2/3 of IV septum, apex, anterior wall of LV)
2) Right coronary artery (posterior 1/3 of IV septum, inferior/posterior LV)
3) Left circumflex artery (lateral LV)
Structure of a valve
Endothelium
Dense collagenous core
Central loose CT core
Elastin fibres
Three forms of valvular heart disease
1) Valvular stenosis (narrowing with failure to open completely)
2) Valvular incompetence
3) Functional regurgitation
What does valvular insufficiency lead to?
Volume overload
Acquired valve disease
Mitral and aortic stenosis is 2/3 of all
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Aortic regurgitation
Mitral stenosis
Rheumatic fever is the major cause
Clinical features:
- Atrial fibrillation
- Haemoptysis
- Pulmonary congestion
- Right ventricular hypertrophy
Opening snap
Mitral valve incompetence
LA enlargement
Acute LV failure
Chordae rupture causing atrial fibrillation
Systolic murmur
Mitral valve prolapse
Ballooning/hooding of mitral valve leaflets
Aortic valve stenosis
Small pulse, LV hypertrophy
LV failure
Sudden death
Ejection systolic murmur
Streptococci in RHF
B haemolytic
Rheumatic fever
Connective tissue disorder characterised by fibrinoid necrosis, inflammation and fibrosis
Aschoff bodies
Nodules in the hearts of RF patients- granulomatous structure with fibrinoid change, lymphocytic infiltration
Anitschow cells
Enlarged macrophages within Achoff bodies
Pancarditis
Endocarditis
Pericarditis
Myocarditis
Three features of chronic rheumatic fever
Fusion of valve commissure
Thickening and fibrosis of valve cusps
Thickening of chordae tendineae
Infective endocarditis
Damage of heart valves by a microbe by formation of vegetations
Three complications of IE
Valve perforations
Myocardial abscess
Septic emboli
Cardiomyopathy
Abnormality in the myocardium- cardiac disease of unknown or unusual cause with pathological processes within myocardium or endocardium or both
Classification of cardiomopathy
1) Aetiological (primary or secondary)
2) Clinico-pathological (Dilated, hypertrophic, restrictive)
Primary cardiomyopathy three causes
Familial
Idiopathic
Endomyocardial fibrosis
Secondary cardiomyopathy three causes
Infective
Metabolic
Connective tissue disorders
Histological abnormalities of DCMP
Enlarged heart upto 3x
Dilated, flabby heart
Hypertrophied cells
Endocardial and interstitial fibrosis
Hypertrophic myopathy
Left ventricular hypertrophy of a non-dilated chamber without obvious cause
Marked hypertrophy of heart muscle without ventricualr dilation
Restrictive cardiomyopathy
Abnormal diastolic function due to rigid left ventricular wall
Clinical manifestations of cardiomyopathy
Angina
Dyspnoea
Fatigue
Syncope
Can lead to: Heart failure Sudden death Stroke Atrial fibrillation
What is a common complication of all cardiomyopathy?
Mural thrombus
Myocarditis
Inflammation of the myocardium with lymphocytic infiltration
Can cause sudden cardiac death or cardiac failure
Three main causes of myocarditis
1) Infections
2) Immune mediated
3) Others (e.g. sarcoidosis, amyloidosis)
Tumours of the heart
Primary tumours- Myxomas, fibromas, lipomas
Secondary
Myxomas
Most common primary tumour of the heart in adults
Commonly located in the left atrium
Most common site is fossa ovalis in the atrial septum
Carney’s complex
10% of people with myxoma have this
Rhabdomyoma
Primary tumour of the heart in infants and children
Three classifications of pericarditis
Effusive
Constrictive
Adhesive
Obstructive disease
Increase in resistance to airflow due to partial/complete obstruction
Chronic bronchitis, emphysema, bronchiectasis, asthma
Restrictive disease
Reduced expansion of lung parenchyma and decreased total lung capacity
Fibrosis, pneumonia,
Chronic bronchitis
Clinical diagnosis
75 ml of sputum everyday
Caused by chronic irritation
**Goblet cell metaplasia and increased mucous production
Complications of chronic bronchitis
Infective exacerbation
Pneumonia
Right heart failure
Emphysema
Abnormal permanent enlargement of airspaces distal to terminal bronchiole ACCOMPANIED by destruction to their walls without fibrosis
*Just enlargement is not emphysema
Clinical features of emphysema
Barrel chest
Progressive dyspnoea
Wheezing
Decreased exercise tolerance
Types of emphysema
Centriacinar- involves the upper lobe (smokers) Panacinar- all zones (a-antitrypsin deficiency) Distal acinar (distal portion of acinus)
Protease-antiprotease theory of emphysema
Smoking causes accumulation of macrophages and neutrophils in respiratory bronchioles. Anti-protease (a1 antitrypsin) is found in the bronchial mucus. Smoking inhibits this.
*Constant protease- antiprotease imbalance leads to emphysema
Bronchiectasis
Permanent and abnormal dilatation of bronchi and bronchioles as a result of bronchial obstruction
Causes- tumour, foreign body obstruction
Clinical features of bronchiectasis
Constant infection in dilated bronchi
Persistent cough
Foul smelling sputum
Haemoptysis
Asthma
Hyperactive airways which go into a state of reversible bronchoconstriction due to increased responsiveness to various stimuli
Main cells in asthma and histological features
Focal necrosis of epithelium with eosinophilic infiltration
Hypertrophy of mucous glands
Hypertrophy of smooth muscle of bronchial wall
Eosinophils
Charcot-Leyden crystals
Curschmann spirals
Chronic interstitial disease
Heterogenous group of disorders characterised predominantly by inflammation and fibrosis of the pulmonary connective tissue
UIP
Usual interstitial pneumonia
Fibroblastic foci- patchy interstitial fibrosis and inflammation
Pneumoconiosis
Pulmonary fibrosis due to inhaled dust
“Coal workers”
“Asbestosis”
Asbestos
Localised pleural plaques
Pleural effusions
Asbestosis
Pressure versus volume overload
Pressure- increased systolic pressure- PARALLEL addition- CONCENTRIC hypertrophy
Volume- increased diastolic pressure- SERIES addition- ECCENTRIC hypertrophy
**In both pressure and volume overload there is increase in weight and size of the heart
Congestive heart failure
End stage chronic heart disease- failure of the pump
Forward failure- diminished cardiac output, reduced tissue perfusion
Backward failure- pooling of blood in the venous system, oedema
High pressure left to right shunt- what heart failure
Right heart failure
Five clinical manifestations of left heart failure
Dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Fatigue and weakness Cachexia
Five clinical manifestations of right heart failure
Peripheral oedema Splenomegaly Hepatomegaly Jaundice Abdominal symptoms
Hypertension- left vs right
Left sided- Systemic hypertension
Right sided- Pulmonary hypertension
Systemic hypertension
Concentric left ventricular hypertrophy
Eventually left heart backward failure, lung congestion, pulmonary oedema
Pulmonary hypertension
Elevation of pulmonary artery pressure due to pulmonary vascular disease
Can lead to right ventricle enlargement- cor pulmonale
Cor pulmonale
Cor pulmonale is defined as an alteration in the structure and function of the right ventricle (RV) caused by a primary disorder of the respiratory system. Pulmonary hypertension is often the common link between lung dysfunction and the heart in cor pulmonale
3 causes of pulmonary hypertension
Mitral regurgitation
LV diastolic dysfunction
Pulmonary arterial hypertension
Sequelae of right ventricular failure from lung disease
Chronic lung disease –> Reduction in pulmonary vascular bed –> Pulmonary hypertension –> Hypertrophy of right ventricle –> Right ventricular failure
Types of ischaemic heart disease
Angina pectoris
MI
Heart failure
Sudden cardiac death
Pathogenesis of MI
Atherosclerotic plaques –> Fissuring and ulcerations –> Adhesion, activation and aggregation of platelets –> Thrombus formation
Transmural
Full thickness necrosis in a territory supplied by a single coronary artery STEMI
Subendocardial
Circumferential necrosis around 1/3 to 1/2 of the ventricular wall and may extend beyond the territory supplied by a single coronary artery NSTEMI
Extent of infarction in MI
- Size of occlusion
- Site of occlusion
- Rate of development
- Duration
- Myocardial demand
Three clinical features
Troponin- I and T
Creatinine kinase
Lactate dehydrogenase
Complications of MI
Sudden death
Arrhythmias
Left ventricular congestive heart failure
Cardiogenic shock
Atherosclerosis
Hardening and thickening of arterial walls due to build up of fatty material
Response to injury hypothesis
Injury to endothelium due to oxidised LDL cholestrol
Surface adhesion molecules expressed for lymphocytes and other inflammatory cells to bind
Monocytes migrate and T lymphocytes release cytokines
Fibroproliferative response- smooth muscle cells migrate from media to intima to produce collagen
Three complications of atherosclerosis
1) Calcification
2) Ulceration of the atheroma
3) Rupture of the atheroma
Hypertensive vascular disease
Caused by hypertension
known causes- renal disease, drugs, pregnancy
Malignant hypertension
Hypertensive emergency- Severe rise in BP, renal failure, retinal haemorrhages, encephalopathy
Hyaline arteriosclerosis
Eosinophilic hyaline thickening of tunica media
Three consequences of hypertensive disease
1) LV hypertrophy
2) Heart failure
3) Arrhythmias
Vegetation
Platelet thrombus that develops and propagates
What is the most common site of vegetation
Aortic site
Mitral site
Complications of endocarditis
Septic emboli
Vasculitis
Severe regurgitation leading to HF
Clinical presentation of endocarditis
And common clinical signs
Presentation
- Chills
- Myalgia
- Rigors
Clinical signs
- Splinter haemorrhages
- Janeway lesions
- Clubbing
- Roth’s spots
- Splenomegaly
Duke’s criteria for endocarditis
1) Positive blood culture
2) Evidence of endocardial involvement
Relevance of segmental anatomy
Related to frequency of infection
10 segments
Defense mechanisms of the lung
Upper:
- Mucociliary epithelium (to trap particles)
- Cough reflex
Lower
- Alveolar macrophages
- Mucosal associated lymphoid tissue
- Bronchus associated lymphoid tissue
Samples for infection
Sputum Bronchoalveolar lavage Bronchial washings Fine needle aspirate Lung biopsy
Three classifications of pneumonia
1) Aetiology/agent
2) Clinical scenario (pneumonia syndromes)
3) Pathology/anatomical
Pneumonia syndromes:
- Community acquired
- Health-care associated
- Hospital acquired
- Pneumonia in the immunocompromised
Lobar pneumonia and bronchopneumonia
Parts of community acquired pneumonia
Lobar- affects the whole lobe
Broncho- affects pulmonary lobules
Four stages of morphology of acute bacterial pneumonia
1) Congestion- parenchyma heavy, congested, boggy, red
2) Red hepatisation- red exudate, red lung
3) Grey hepatisation- lung grey, disintegration of red cells
4) Resolution
Presentation of pneumonia
Fever Rigor Productive cough Haemoptysis Pleuritic chest pain
Complications of pneumonia
Organised pneumonia Fibrosis Pneumothorax Pleural effusion Pericarditis
Acintomycosis
Persistent chronic suppurative infection with abscess formation
Morphology of mycobacterium TB infection
Primary TB- Inhaled bacilli, sensitisation develops, Ghon focus)
Active involvement by caseating/noncaseating granulomas
Progression to either:
- Healing
- Latency
- Secondary TB
- Progressive pulmonary TB
- Miliary TB
Full oxygen carrying capacity of Hb
75-80 mmHg
Hypoxia versus hypoxaemia
Hypoxia- Low O2 in tissues
Hypoxaemia- Low O2 in blood
Causes of hypoxaemia
1) Low PiO2
2) Hypoventilation
3) Diffusion limitations
4) V/Q mismatch
5) Right to left shunt
Causes of hypoxia
Anaemia
Blood flow obstruction
Hypoxaemia
Peripheral and central respiratory drive
Peripheral
- Low O2
- High CO2
- High H+
Central
- High CO2
- HIgh H+
What can opioids do in terms of respiratory drive
Make people insensitive to CO2 concentrations
Chronic hypercapnia
Desensitises central chemoreceptors to CO2 concentrations and hypoxia drives respiration
PCO2> 50mmHg
If given too much O2, respiratory rate will slow down and lethal CO2 concentrations will accumulate
Three pulmonary vascular diseases
1) Pulmonary thromboembolism
2) Pulmonary hypertension
3) Diffuse pulmonary haemorrhagic syndromes
Causes of pulmonary hypertension
Increased pulmonary blood flow
Increased pulmonary vascular resistance
Increased left heart resistance
Pulmonary hypertension
Mean pulmonary artery pressure >/ 25 mmHg at rest
>/30 mmHg exercise
Clinical presentation of pulmonary hypertension
Right heart failure (chest pain, abdominal discomfort)
Arrhythmia
What is genetic mechanism for pulmonary hypertension
Bone morphogenic protein receptor 2 (BMPR2)
Histological patterns of pulmonary hypertension
Plexogenic arteriopathy (changes in muscular arteries and arterioles) Thrombotic arteriopathy (acute thrombi) Hypoxic arteriopathy
Diffuse pulmonary haemorrhage
Patients will present with diffuse haemoptysis
Can be localised or diffuse
- Diffuse haemoptysis (with or without capillaries)
(e.g. Goodpasture’s syndrome)
Goodpasture’s syndrome
Autoimmune- antibodies around collagen
Primarily affects kidneys and lungs
Aneursym- definition and classification
Abnormal dilation in a vessel leading to weakness in tunica media of vessel/myocardium
Classification
- Cause (congenital, inflammatory, trauma)
- Morphology (saccular, fusiform)
- Anatomical site (aortic, AAA)
Clinical features of ruptured aneurysm
Seizures
Double vision
Vomitting
Headaches
Complications of aneurysm
1) Rupture
2) Occlusion
3) Mass effect
Morphology of aneurysms
- Saccular (berry)
- Fusiform
AAA
Fusiform aneurysm located in abdominal aorta below renal arteries and above bifurcation
Complications:
- Rupture
- Peripheral thromboembolism
Aortic dissection
Tear in intima due to weakness of tunica media
Blood enters here
Due to weakening of tunica media- chronic hypertension, Marfan’s syndrome
Complications
- Rupture, massive haemorrhage
- Occlusion of other branches
Clinical features
- Sudden onset excruciating pain
- Collapse, shock
What causes 90% of pharyngitis
Viral infections
- Influenza virus
- Rhinovirus
- Adenovirus
- Coronavirus
Causes of bacterial pharyngitis
- Streptococcal pyogenes
- H. influenzae
- Mycoplasma pneumoniae
Complications of Strep pharyngitis
Suppurative
- Otitis media
- Meningitis
- Sinusitis
- Peritonsillar abscess “Quinsy”
Non-suppurative
- Rheumatic fever
- Glomerulonephritis
Three tests for diagnosis of strep pharyngitis
Throat swab
ASOT
Blood culture
Epiglottitis
Acute inflammation of the epiglottis
Haemophilus influenza B (HIB)
Treatment- support the airway and Ceftriaxone and Amoxycillin
Diptheria
Diptherium bacteria produces toxin that adheres to mucosa to cause cell death and destruction
LeMierres disease
Jugular vein phlebitis
Croup
A clinical syndrome, not a diagnosis
Clinical features- Fever Hoarseness of voice Barking cough Inflammatory obstruction of subglottic area
Chronic sinusitis
> 3 weeks of facial pain, postnasal drip and nasal congestion
Gram -ve organisms and fungi
Otitis media
Follows a viral URTI
Congestion of the nasopharyngeal mucosa, inflamm
obstruction of the Eustacian tube, followed by fluid trapping and effusion formation in middle
ear, ear drum becomes inflamed and bulging
Mostly self-limiting, little evidence for other therapy
Tympanocentesis specimen collection
Otitis externa
Moisture driven ear infection (swimmer’s ear)
Pertussis
Bordatella pertussis
100 day cough
Attaches to nasopharynx, produces toxins and damages trachea/bronchi
Catarrhal phase –> Paroxysmal phase –> Convalescent phase
Complications of pertussis
Subconjuctival haemorrhage
Pneumothorax
Rib fractures
Hernia
Pathophysiology of bronchopneumonia
Microbes access lower respiratory tract —> Proliferate within alveoli —> get cleared by macrophages
If microbes overwhelm the capacity of the immune system –> inflammatory response initiated –> white cell migration –> leaky membranes –> decreased oxygenation
Typical and atypical causes of bacterial pneumonia
Typical- Strep pneum, H influenzae, Staph aureus
Atypical- mycoplasma pneum, legionella, chlamydophila psittaci
Pneumococcal pneumonia
Commonest form of pneumonia
Gram +ve diplococci
Typical and atypical clinical features of pneumonia
Typical
- Rigors
- Chills
- Productive cough
- Pleuritic chest pain
- Fever
Atypical
- Arthralgia
- Myalgia
- Headache
PSI
> 50 years (yes/no)
Any of these?
- Neoplasia
- Liver disease
- Renal disease
- Cerebrovascular disease
- Congestive HF
Any exam abnormalities (yes/no)
- BP <90 mmHg
- Resp rate >30
- Temp >40
- Pulse >125/min
- Altered mental state
Yes- II, II, IV or V
No- I
CURB-65
Confusion
Urea > 7mmol/L
Resp rate >30
BP <90
65- Age >65
SMART-COP
Age <50 or Age >50
Systolic BP <90 Multilobar CXR involvement Albumin <35 Resp rate >25 >30 Tachycardia >125
Confusion
Oxygen stat <93% <90%
PH <7.35
Total of 11 points
What antibiotic is added to cover atypical pneumonia organisms?
Clarithromycin
Three complications of pneumonia
- Respiratory failure
- Multi-organ failure
- Disseminated intravascular coagulation
Four organisms that can cause health-care associated pneumonia
1) ESBL
2) Acintobacter species
3) MRSA
4) Pseudomonas aeruginosa
**HAP particularly affects upper lobes
MAC pneumonia
Mycobacterium avium and M intracellular complex
Environmental, soil and water
*Chronic pneumonia in patients with pre-existing conditions
Transudate vs exudate
Transudate- imbalance in oncotic and hydrostatic pressures
Exudate- Inflammation of pleura or decreased lymphatic drainage
Light’s criteria to define an exudate
1) Ratio of pleural fluid protein to serum protein >0.5
2) Ratio of pleural fluid LDH to serum LDH >0.6
3) Pleural fluid LDH > 2/3 of upper limit of normal
*Transudate if all of the above are absent
Empyema
Frank pus in pleural space
**Need pre-existing pleural fluid for this to develop
Aspergillus infections
Allergic bronchopulmonary aspergillosis
Aspergilloma
Invasive aspergillosis
Probability of TB transmission
Infectiousness of host
Environment
Virulence
Host defences
Diagnosis of TB
1) Positive Mantoux test
2) Positive quantiferon
Treatment of TB
Isoniazif
Rifampicin
Clinical symptoms of TB
Prolonged cough Fever Weight loss Night sweats Pneumonia Haemoptysis
Conmonest benign tumour of the nasal cavity
Pleiomorphic adenoma
Squamous cell carcinoma
Non-keratinising has better prognosis than keratinising
Sinonasal adenocarcinoma
Wood dust exposure
Salivary gland poor prognosis
Olfactory neuroblastoma
Arise from specialised sensory neuroepithelial cells of olfactory membrane
Sinonasal undifferentiated carcinoma
Metastasises to brain, kidney etc
Lymphoepithelial carcinoma
EBV infection
Nasopharyngeal angiofibroma
Arise from fibrovascular stroma, wall of the roof
Nasopharyngeal carcinoma
Strongly associated with EBV
Papilloma
Benign tumour of the larynx
HPV associated
Clinical symptoms of lung cancer
Cough Sputum Haemoptysis Weight loss Chest pain SOB
Horner syndrome
Occurs in lung cancer
Sympathetic ganglia invasion
4 main types of lung cancer
1) Squamous cell carcinoma (Male)- commonest in smokers; central
2) Adenocarcinoma (Female)- commonest in non-smokers; peripheral
3) Small cell carcinoma
4) Large cell carcinoma
Carcinoid tumours
Neuroendocrine malignant tumours
Three histological types of mesothelioma
Epitheloid
Sarcamatoid
Biphasic