Conditions Flashcards
Alcoholic Liver Disease
Includes fatty liver, alcoholic hepatitis and cirrhosis.
Steatosis due to decreased NAD (less FA breakdown and more FA synthesis)
Chronic alcohol consumption results in the secretion of pro-inflammatory cytokines, oxidative stress, lipid peroxidation and acetaldehyde toxicity.
This causes inflammation, apoptosis and eventually fibrosis.
AST:ALT = 2:1 (elevated ratio)
Hepatic Steatosis
Fatty liver disease-
Large vacuoles of fat accumulate in hepatocytes.
It is reversible.
Often associated with alcohol or metabolic syndromes. Diagnosed by elevated liver enzymes (ALT > AST in nonalcoholic, 1:2 in alcoholic)
Hereditary Haemochromatosis (bronze diabetes)
Genetically inherited disorder (autosomal recessive) which results in increased intestinal absorption of dietary iron.
Iron is deposited in skin, liver, pancreas, heart and endocrine organs. It is associated with scarring of liver and pancreas.
Symptoms: liver damage, heart dysfunction, multiple endocrine failures (pancreas)
Diagnosis: elevated serum liver enzymes and transferrin saturation
Treatment: repeated bleeding
Carbon Monoxide Poisoning
Binds to Hb in the blood and prevents O2 release at tissues causing hypoxia. This results in decreased aerobic respiration and can cause reversible or irreversible hypoxic injury.
Paracetamol Overdose
Causes serious liver damage due to a build up of NAPQI which depletes the liver’s supply of the antioxidant glutathione. (NAPQI produced by phase 1 metabolism by cytochrome p450 enzyme system)
Diagnosis: raised ALT, AST and bilirubin
Treatment: N -acetylcysteine or liver transplant
Pancreatitis
Inflammation of the pancreas- acute or chronic.
Causes: GET SMASHED
Diagnosis: elevated serum amylase and lipase.
Increased serum lipase released from pancreatic acinar cells results in fat necrosis on pancreas and fat elsewhere in the abdominal cavity.
Testicular Torsion
Spermatic cord twists and cuts off blood supply to the testicle causing ischaemia. This results in testicular infarction.
Volvulus of the bowel
A loop of bowel is twisted around a focal point along the mesentery attached to the intestinal tract that may result in bowel obstruction. Results in ischaemia to the affected portion of the intestine.
Infective hepatitis
Infection of the liver by the hepatitis A virus.
Diagnosis: Elevated ALT
Rhabdomyolysis
Large amounts of myoglobin are released from damaged striated muscle. May cause kidney failure if kidney tubules become blocked.
Muscle tissue may be damaged by direct trauma or damage to blood supply (hypoxic/ischaemic injury)
Alpha 1 anti trypsin deficiency
Genetically inherited disorder.
Liver produces a version of the alpha1 trypsin protein that is incorrectly folded. The protein cannot be packaged by the ER and accumulates within the ER instead of being secreted by the liver and can cause liver disease.
The systemic deficiency of the enzyme (normally deactivates the enzymes in neutrophils) means that proteases in the lungs can act unchecked and patients develop emphysema as lung parenchymal tissue is broken down by neutrophil proteases.
Coal worker’s pneumoconiosis
Exogenous pigments - e.g. coal dust are inhaled and phagocytosed by macrophages in the lungs. Seen as blackened lung tissue (anthracosis) or blackened peribroncial lymph nodes with macrophages from the lungs. Usually harmless however coal workers or others with high exposure the lungs may become fibrotic or emphysematous.
Haemosiderosis
Haemosiderin (endogenous pigment) is deposited in many organs due to a systemic overload of iron. Haemosiderin is an iron storage molecule derived from Haemoglobin and is formed when there is a local or systemic excess of iron, e.g. Haemorrhage into tissues.
Seen in conditions such as haemolytic anaemias, blood transfusions and hereditary Haemochromatosis.
Lobar pneumonia
Pneumonia affecting a large area / one or more lobes of the lung.
Often caused by streptococcus pneumoniae and is a primary pneumonia (affects young healthy adults)
4 pathological stages - congestion, red hepatisation, grey hepatisation and resolution
Acute appendicitis
Sudden inflammation of the appendix resulting in the appendix becoming filled with mucus and swelling. The swelling causes occlusion of the small vessels and stasis of lymphatic flow. The appendix becomes ischaemic and necrotic. Bacteria leaks out through the dying walls and pus forms around and within the appendix.
More common in young adults.
Complication- the appendix may rupture causing peritonitis which can lead to sepsis and death
Bacterial meningitis
Inflammation of the meninges caused by various bacteria (streptococcus pneumoniae, Neisseria Meningitidis, E. Coli)
Astrocytes and microglia identify bacteria and release cytokines to recruit other immune cells.
The blood-brain barrier becomes more permeable leading to cerebral oedema.
Moreover, the inflammation caused by white blood cells leads to interstitial oedema (fluid between cells).
This oedema leads to increased intracranial pressure and can lead to cerebral ischaemia as it becomes increasingly difficult to perfuse the brain.
Ascending cholangitis and liver abscess
An infection of the bile duct (cholangitis) caused by bacteria that ascends from its junction with the duodenum. Tends to occur if the bile duct is already partially obstructed by gallstones.
This obstruction diminishes host antibacterial defences and causes immune dysfunction.
The infection ascends into the hepatic ducts causing serious liver infection and may result in a liver abscess.
Hereditary angio-oedema
Extremely rare, autosomal dominant condition.
Deficiency of C1-esterase inhibitor (prevents spontaneous activation of complement system)
The spontaneous activation of the complement system causes attacks of non-itchy cutaneous angio-oedema and recurrent abdominal pain due to intestinal oedema.
Often a family history of sudden death due to laryngeal involvement.
Chronic granulomatous disease
Phagocytes can’t generate the free radical superoxide (O2-).
This results in chronic infection in the first year of life, numerous granulomas and abscesses. Affects skin, lymph nodes, lung, liver and bone.
Due to phagocytes being unable to kill ingested bacteria due to no oxygen burst.
Gastritis
Inflammation of stomach lining.
Common causes- H. Pylori and NSAIDs.
H. Pylori burrows into the mucus lining of the stomach to avoid the acidic environment and produces toxic chemicals, e.g. Proteases.
Induces inflammation and locally high levels of TNF/interleukin-6.
NSAIDs- inhibit cyclooxygenase-1. Reduces prostaglandins that normally protects the stomach.
Tuberculosis
Caused by mycobacterium tuberculosis.
Attacks the lungs- 1) bacterium inhaled 2) reaches the pulmonary alveoli where it invades and replicates inside macrophages. Stored temporarily in a phagosome then in a phagolysosome. 3) Phagolysosome attempts to use reactive oxygen species to kill the bacterium, however, due to the thick waxy mycolic acid capsule this unsuccessful. 4) TB reproduces inside macrophage and kills it.
Primary site of infection = ghon focus
Classified as a granulomatous inflammatory disease as macrophages, lymphocytes and fibroblasts aggregate to form granulomas surrounding the infected macrophages. Langhans giant cells present. Caseous necrosis may occur in the centre of the granuloma.
Rheumatoid Arthritis
Chronic inflammatory disorder that often affects the small joints in the hands and feet. It affects the lining of the joints causing a painful swelling (caused by abundant proliferation of synovium) that can eventually result in bone erosion and joint deformity.
Central mediators = TNF-alpha, interleukin-1
Ulcerative Colitis
A form of inflammatory bowel disease that only attacks the large intestine.
Inflammation is limited to the mucosa and submucosa.
Crypt abscesses and disruption in crypt architecture are often common.
It is thought that hydrogen sulfide interrupts the pathway that produces N-butyrate (which supplies the colon epithelia with nutrients)
Crohn’s disease
A type of inflammatory bowel disease that may affect any part of the GI from the mouth to anus.
Shows a transmural pattern of inflammation (may span the entire depth of the intestinal wall). Often an abrupt transition from normal tissue to ulcerated tissue (skip lesion).
Often mucosal inflammation characterised by a focal infiltration of neutrophils into the epithelium. The neutrophils may infiltrate the crypts leading to inflammation or abscesses.
Granulomas of giant cells aggregate but do not show caseation unlike TB.
Often a “cobblestone appearance” of bowel mucosa seen.
Leprosy
Chronic infection caused by mycobacterium leprae. Primarily infects Schwann cells in the peripheral nerves leading to nerve damage due to demyelination.
Phagocytosis of M. Leprae by macrophages is mediated by complement receptors CR1/3/4 and is regulated by protein kinase.
Syphilis
STI caused by the spirochete bacterium Treponema pallidum.
Primary stage = a painless ulcer on the genitals.
Secondary stage = diffuse rash, latent syphilis with little to no symptoms
Tertiary stage = gummas (soft, tumour like balls of inflammation) typically affect skin, bone and liver.
