week 11 n 12 Flashcards
what is Streptococcal pharyngitis?
- respiratory disease
- Strep throat
– Back of throat and tonsils
-Caused by type A strep;
-Fever, Sore throat, red tonsils, enlarged lymph, Headache, nausea, vomiting.
what is Acute Glomerulonephritis
- Complication of Streptococcal Pharyngitis (Strep Throat)
- cause: This condition occurs when antigen-antibody (Ag-Ab) complexes become trapped in the glomerular basement membrane of the kidneys after a streptococcal infection.
This leads to reduced glomerular blood flow and damage to the basement membrane. - symptoms: It typically manifests as hematuria (blood in the urine), hypertension, and edema.
- can heal by itself
what is Rheumatic Fever?
- This autoimmune condition develops 2 weeks after an upper respiratory tract infection (URTI), specifically strep throat.
- antibodies produced in response to the strep infection cross-react with antigens in the connective tissues of the heart, joints, skin, and brain.
what is Pancarditis
inflammation of the entire heart)
what is Endocarditis
Inflammation of the heart’s inner lining, including the heart valves, potentially leading to valve damage and rheumatic heart disease.
Myocarditis?
Inflammation of the heart muscle.
Pericarditis?
Inflammation of the pericardium (the sac surrounding the heart).
Rheumatic Fever also causes
Arthritis and Joint Inflammation due to Deposits of inflammatory material on the heart valves.
Aschoff Bodies: Inflammatory nodules found in the myocardium, characteristic of rheumatic heart disease.
untreated streptococcal infections=
acute kidney damage or autoimmune complications, like rheumatic fever, which primarily affects the heart and joints and serious cardiac complications due to the immune cross-reactivity between streptococcal antigens and heart tissue.
Lower respiratory tract infection =
Pneumonia
Inflammation of the lung
* Bronchopneumonia
– mainly involves bronchi & bronchioles
– more common in elderly, very young, or the
debilitated
* Lobar pneumonia
– lobar more common in otherwise healthy
adults
- antibiotics &
physiotherapy
Stages of Lobar Pneumonia Pathology:
Stage 1: Congestion (0-24 hours):
During the early phase of pneumonia, protein-rich exudate enters the alveoli, leading to venous congestion in the affected lung tissue.
The histological image shows congested capillaries with red blood cells and early exudation into the alveolar spaces.
Stage 2: Red Hepatisation (1-4 days):
In this phase, inflammatory cells, particularly neutrophils, and red blood cells (RBCs) enter the alveoli.
The exudate becomes more fibrinous, and the affected lung tissue resembles liver tissue (hence, the term “hepatization”).
The histology reflects alveoli filled with red blood cells and fibrin.
Stage 3: Grey Hepatisation (4-7 days):
In this stage, white blood cells (WBCs) and RBCs die, and the exudate becomes dominated by fibrin, giving the affected tissue a solid, grey-brown appearance.
Histologically, there are fewer RBCs and more necrotic debris and fibrin filling the alveolar spaces.
Stage 4: Resolution (8-10 days):
The body begins to resorb the exudate, digesting the inflammatory debris, and alveolar structure is preserved.
Histologically, this stage shows the restoration of the alveoli, with macrophages clearing out the debris.
what are these slides showing?
Histological Comparison to Normal Liver Tissue. The slides also provide a comparison between the histology of lobar pneumonia (red and grey hepatization) and the normal liver tissue, emphasizing how the affected lung tissue resembles the liver due to the accumulation of cells and exudate.
whats this?
This slide illustrates the pathophysiology of an embolism infarction in the lung:
An embolus (likely a thrombus) blocks a pulmonary artery, leading to necrosis of lung tissue downstream.
Red blood cells leak into the alveoli, and necrosis occurs in the alveolar walls.
Hemosiderin-laden macrophages are present as part of the chronic response to hemorrhage.
The presence of anthracosis pigment indicates environmental exposure to pollutants, which can further contribute to lung pathology.
Pulmonary embolism cause
multiple or repeated emboli can lead to pulmonary
hypertension
– raised pulmonary pressures
– increased workload on right heart
– right heart failure
* Symptoms:
– Dyspnea and tachycardia
– Pleuritic chest pain
– Deep vein thrombosis
– Sudden death
Obstructive airways diseases
asthma
* chronic bronchitis
* emphysema
what is asthma?
Chronic inflammatory disease of the
airways.
* Airflow reduction
– Bronchospasm
– Oedema
– Aggravation of airway
whats this?
In asthma, the airways undergo chronic inflammation, leading to structural changes such as thickening of the airway walls, smooth muscle hypertrophy, and increased mucus production. These changes result in narrowing of the airways, causing the typical symptoms of asthma, such as wheezing, shortness of breath, and coughing.Thickened Basement Membrane (Bm): One of the hallmarks of asthma is the thickening of the basement membrane, which is labeled in the image. This is caused by chronic inflammation and fibrosis (scarring).
disease? cause? Manifestations?Management?
Chronic Bronchitis - chronic inflammation of bronchial
mucosa leading to scarring, fibrosis,
and thickening. Causes
* environmental conditions
* pollutants
* cigarettes. Manifestations
* persistent cough - particularly mornings
* dyspnoea
* frequent respiratory infections Management
* bronchodilators
* cough suppressants
* oxygen
* antibiotics
whats this?
Histopathology Lung–Emphysema. Characterised by irreversible destruction
of terminal airspaces (without fibrosis)
* Loss of elastin and collagen. it differes to normal lung as its less complex, paler, more spaces and red filled bits. more white circles, they have ruptured.
Describe the protective
processes in the GIT.
Protective Processes:
The mucosal barrier: Mucus secretion helps protect the stomach lining from its own acid.
Bicarbonate secretion: Neutralizes stomach acid in the duodenum.
Prostaglandins: Promote mucus and bicarbonate secretion and maintain blood flow to the mucosa.
Describe the destructive
processes in the GIT.
Destructive Processes:
Helicobacter pylori (H. pylori) infection, which leads to chronic inflammation and ulcers.
Use of NSAIDs, which inhibit prostaglandins and reduce the protective mucus lining, making the stomach more susceptible to damage
Major Causes of Peptic Ulceration:
H. pylori infection: Responsible for the majority of peptic ulcers by causing chronic inflammation and mucosal damage.
NSAIDs: These medications reduce prostaglandin production, lowering mucus secretion and bicarbonate, thus promoting ulcers.
Other factors: Excessive alcohol consumption and smoking contribute to peptic ulcer formation
whats this?
histological sections of the gastrointestinal mucosa, possibly from the stomach or small intestine, under different stains. left= Inflammatory cell infiltration: A significant number of inflammatory cells, particularly lymphocytes and plasma cells, are present in the lamina propria.
Edema or congestion: There is some edema and congestion, with red blood cells visible within the blood vessels.
Crypt architecture: The crypts and villi seem distorted or inflamed, which may indicate a chronic inflammatory condition such as Helicobacter pylori gastritis or inflammatory bowel disease (IBD) like Crohn’s disease or ulcerative colitis.
right= The staining helps identify the location of specific proteins or cellular components, which can be crucial in diagnosing certain GIT disorders like coeliac disease, gastritis, or assessing mucosal damage and repair.
The left image shows inflammation, while the right image highlights specific cell populations or structures affected by the inflammatory process.
Bilirubin Metabolism
Bilirubin is produced from the breakdown of hemoglobin in red blood cells.
It is unconjugated in the blood and becomes conjugated in the liver, making it water-soluble for excretion via bile into the intestines.
In the intestines, bilirubin is further processed into urobilinogen, some of which is reabsorbed or excreted in urine or feces
