Section 1

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Increase in cell size.

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Last updated

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Date created

Mar 14, 2020

Cards (429)

Section 1

(50 cards)

Increase in cell size.

Front

Define hypertrophy.

Back

Overgrowth of granulation tissue.

Front

What is proud flesh?

Back

Nucleus disappears.

Front

Define karyorrhexis.

Back

When the wound splits open.

Front

What is wound dehiscence?

Back

Usually surgery required with correction of alignment, removing fibrous tissue, possible none grafting and reproducing the haematoma to start the healing process again.

Front

What can be done to heal fibrous union of bones.

Back

Gathering of cells e.g. neutrophils at the site of infections.

Front

Define cellular accumulations.

Back

Overgrowth of scar tissue. This is when there is an overgrowth of collagen.

Front

What is a keloid?

Back

Persistant inflammation without resolution.

Front

Define chronic inflammation.

Back

The tissue is returned to normal.

Front

What is regeneration?

Back

• Haematoma • Soft callous • Hard callous • Remodelling

Front

What are the 4 stages of bone healing?

Back

Cell growth and division (mitosis)

Front

Define proliferation.

Back

Leakage of protein rich fluid (esp. fibrinogen) into the extravascular space.

Front

What is the fluid exudate?

Back

Dermis forms scar. Surface epithelium regenerates.

Front

When skin heals which layer forms the scar tissue and which regenerates?

Back

• Movement (too much, too little) • Infection • Foreign body • Nutrition • Medication - corticosteroids • Other medical conditions - diabetes

Front

What things can cause failure of bone to heal?

Back

Congestion and stasis - loss of laminar flow enabling white cells to come into contact with the endothelial cells.

Front

What is the purpose of the fluid exudate?

Back

Cell/organ kills itself.

Front

Define suicide and apoptosis.

Back

• Nutrition - protein, vitamin C • Diabetes • Steroid medication - anti-inflammatory and slows collagen synthesis • Infection • Blood supply • Mechanical factors - movement • Foreign material

Front

What host factors influence repair in all tissues?

Back

A cell that produces ECM and collagen, important in healing.

Front

What is a fibroblast?

Back

Comorbidity associated with primary damage.

Front

Define collateral damage.

Back

Change of cell type e.g. epithelial cell types change

Front

Define metaplasia.

Back

Primary damage leads to secondary damage.

Front

Define sequential damage.

Back

• 24 hours - blood clots and a scab forms. Neutrophils flood to the site of inflammation. Mitosis of basal epithelium. • 1-2 days - epithelial cells grow along the exposed dermis. • 3 days - granulation tissue in dermis, fibroblast and macrophages at site of injury, neutrophils gone, new capillaries form. • 5 days - fibrous union (collagen fibrils bridge wound), epidermis at pre-incision thickness

Front

Describe the timeline of healing by primary intention.

Back

Progenitor cells from periosteum and bone marrow differentiate within the granulation tissue to produce cartilage.

Front

Describe soft callous.

Back

State of non-replication (important in genetic mistakes e.g. cancer)

Front

Define senescence.

Back

Swelling (from cellular accumulations or cellular release of contents)

Front

Define oedema.

Back

• Formation of new endothelial channels (angiogenesis) • Migration and proliferation of fibroblasts laying down collagen • Deposition of ECM • Maturation and organization of fibrous scar

Front

Outline the process of healing by scarring (granulation tissue)?

Back

Whole chunk of tissue dies due to loss of blood supply (ischemia).

Front

Define infarction.

Back

Well done

Front

Read this stuff

Back

Immediate host response to any form of tissue insult.

Front

Define acute inflammation.

Back

Intracellular degradation of cytoplasmic constituents in lysosomes (autophagosome + lysosome).

Front

Define autophagy.

Back

An innate response to any form of insult. To remove and injurious agent and any damaged tissue.

Front

What is acute inflammation and what is its purpose?

Back

Cell/organ killed.

Front

Define homicide and necrosis.

Back

Tissue comprised of: • New vessels • Fibroblasts laying down collagen • Extracellular matrix

Front

What is granulation tissue?

Back

Nucleus starts to disappear.

Front

Define karyolysis.

Back

Nucleus of cell gets smaller.

Front

Define pyknosis.

Back

With weight bearing the bone framework is orientated to give maximum strength and return the bone to the pre fractures state.

Front

Describe remodeling.

Back

• Non-union - bone ends too far apart • Fibrous union - the bone ends are joined by fibrous tissue, bone not formed.

Front

What are two possible results of failure of bone to heal?

Back

Blood clot forms at fracture. Infiltration by neutrophils and later macrophages (acute inflammation). Haematoma gradually removed and granulation tissue emerges.

Front

Describe haematoma.

Back

Decrease in cell size.

Front

Define atrophy.

Back

• Labile cells - constantly dying and being replaced - epithelial cells. • Stable cells - cells quiescent but can divide in response to stimuli - endothelium, liver, kidney, etc. • Permanent cells - have no capacity to divide - neurons, myocardium.

Front

What are the three types of cells (e.g. dividing capacities)? Give an example.

Back

Surgery; The immediate closure of a surgical field in a multitrauma patient after the major vascular injuries and other sources of life-threatening bleeding have been repaired.

Front

Define damage control.

Back

Formed as ossification of the cartilage occurs.

Front

Describe hard callous.

Back

Endothelial cells become sticky. White cells roll along the endothelial cells finally becoming adhered to the endothelium. The cells then escape through the endothelial wall by a process termed diapedesis. Cells migrate along a chemical gradient provided by C5a and bacterial products (if present).

Front

How is the cellular exudate formed?

Back

Cell replication in numbers to increase organ size

Front

Define hyperplasia.

Back

Tissue unable to return to normal (e.g. connective tissue framework is lost, or non-regenerating cells).

Front

What is scarring?

Back

Other side first

Front

This side first

Back

• Regeneration • Scarring

Front

What are the two outcomes of the acute inflammatory response?

Back

Same as above then: • 5 days - wound contraction (by myofibroblasts) followed by fibrous union.

Front

Describe the process of healing by secondary intention.

Back

• Heat • Pain • Swelling (tumor) • Redness (rubor) • Loss of function

Front

What are the 5 clinical signs of inflammation?

Back

• Primary intention - edges of wounds bought together by suturing. • Secondary intention - large deficit of tissue, wound edges can't be brought together.

Front

What are the two ways that skin heals?

Back

Section 2

(50 cards)

S = fibrous connective tissue (granulation tissue) T = woven bone

Front

This is a histological preparation of an area of non-union in bone healing. What are the tissues labeled S and T?

Back

An inflammatory arthritis developing in response to the deposition of irate crystals within the synovium of joints, ligaments, tendons and soft tissues.

Front

What is gout?

Back

A degenerative disease due most likely to the loss of homeostatic mechanisms within the cartilage.

Front

What is osteoarthritis?

Back

• Haematogenous dissemination from some other focus (fro tissue via blood) or a bacteraemia (in blood) • Spread of infection from an adjacent site to bone • Trauma • Iatrogenic - surgical

Front

How do organisms gain entry into the bone?

Back

Reparative response by remaining cartilage at the edges of a damaged joint. Most common in osteoarthritis by may be seen in other conditions that result in extensive joint damage.

Front

What is an osteophyte?

Back

Inflammation in the bone marrow

Front

What is osteomyelitis?

Back

• Increasing pressure in bone shaft, decreases blood flow → medullary bone dead af • Pus forced through aversion system, gathers subperiosteally → lifts periosteum, removes blood flow →cortical bone dead af (sequestrum) • Involucrum forming • Pus may ooze into soft tissue forming abscess which can reach skin surface → ruptures → sinus → sequesterm extrudes through sinus

Front

Describe chronic osteomyelitis.

Back

• Immune response → inflammation, proliferation of the synovium (=pannus) expands into joint space. • Enzymes related to the inflammation damage eventually erode the underlying cartilage • Underlying bone is exposed and damaged, so the bone surface pitted and irregular

Front

Describe joint changes in rheumatoid arthritis.

Back

Margination of neutrophils by adhesion molecules (selections and integrins)

Front

What process is occurring in this image? What cells and molecules are involved?

Back

A shock absorber during normal joint movement. Distributes weight and prevents bone crushing and crepitus.

Front

What is cartilage?

Back

Dead bone resulting from either pressure within the marrow cavity or due to loss of the blood supply because of lifting of the periosteum (white/pale).

Front

What is the sequestrum?

Back

• An acute phase protein produced in the liver in response to IL6 from macrophages, following tissue insult • Binds to phosphocholine on the surface of dead and dying cells, activates complement • Increases in proportion to the degree of inflammation • Peaks at 48 hours (t1/2 = 18 hours)

Front

What is C-reactive protein (CRP)?

Back

• Loss of proteoglycans (ground substance) - superficial chondrocytes die, deeper proliferate to form clusters. • Fibrillation - dehydration and superficial layer cracks. • Cartilage fragments break off • Cartilage lost in areas of greatest stress • Bone exposed → eburnation (bone polished)

Front

What changes in cartilage occur due to loss of cartilage maintenance?

Back

X = cartilage. Y = new bone. Z = granulation tissue. a = osteoblast. b = chondrocyte.

Front

Name the tissues X, Y and Z and the cells a and b.

Back

Aspirin interfere with uric acid excretion in urine.

Front

Why is aspirin not used as an NSAID in the treatment of gout?

Back

• Primary - cause unknown but usually due to enzyme deficiency with increased production and/or decreased excretion • Secondary - chronic renal disease. increased turnover of cells. Inborn errors of metabolism (Lesch-Nyhan syndrome).

Front

Describe the two classifications of gout.

Back

Hyperextension of the PIP and flexion at the DIP joint with stretching of the velar plate at the PIP and damage to the extensor tendon at the DIP.

Front

What is a swan neck deformity.

Back

Proliferation of the synovial lining cells, inflammatory cells, granulation tissue and fibrous connective tissue.

Front

What is the pannus?

Back

• Joint space occupied by pannus. The cortical bone becomes less dense. • Pannus release inflammatory cytokines that cause loss of articular cartilage and damage to the exposed bone. • Destruction of the adjacent joint capsule/tendons leads to instability and deformity, tendons may rupture • Radial (lateral) deviation of the wrists and ulnar (medial) deviation of fingers

Front

Describe joint pathology of RA.

Back

Painless lumps arising in the subcutaneous tissue of skin in areas which are subjected to pressure. In cases of severe disease. Nodules have a fibrinoid necrotic core which is surrounded by a palisade of macrophages lymphocytes and plasma cells. These nodules may also arise within the synovium.

Front

What is a subcutaneous rheumatoid nodule.

Back

• Infiltration by mononuclear cells (lymphocytes, monocytes, plasma cells) • Tissue damage continues • Attempts at repair

Front

Describe cellular features of chronic inflammation.

Back

• NSAIDs - naprogesic and diclofenac • Colchicine - inhibits neutrophil mobility and activity. • Low dose steroids (if NSAIDs unsuccessful) • Hydration • Medical assessment to reduce risk factors

Front

What treatments are available for gout.

Back

Deposits of urates surrounded by lymphocyte, macrophages and giant cells. Fibrous tissue surrounds the area.

Front

Describe the histology of a tophus.

Back

Secondary intention (may require skin graft).

Front

How will this wound heal?

Back

• Pain relief • Physiotherapy • Immunosuppression (steroids, TNF antagonists)

Front

Describe RA treatments available.

Back

• Normal blue/grey colour → pale blue-pink, due to changes in ground substance • Fibrillation

Front

Describe the changes that have occurred in this cartilage.

Back

By primary intention

Front

How will these lesions heal?

Back

Systemic, chronic inflammatory autoimmune disease. Affects mainly joints - proliferative synovitis with destruction of cartilage, ligaments, tendons and joint capsules leading to destruction and deformity of the joints.

Front

What is rheumatoid arthritis?

Back

- Vasodilation and congestion - Redness - Pus

Front

What are the common features of acute inflammation seen in these photographs?

Back

Persistent inflammation that has been present for a long time. Results from: • Acute inflammation - when inciting agent not removed • De novo - fleeting acute response is replaced by smoldering inflammation

Front

What is chronic inflammation?

Back

Flexion deformity of the proximal PIP joint due to rupture of the central slip of the extensor tendon so that the proximal phalanx pokes through the lateral slips of the tendon. Hyperextended distal joint.

Front

What is a boutinniere deformity?

Back

Acute episode less intense but continuous into chronic. Synovial cartilage thickened, inflamed and hyperplastic → pannus which results in damage to cartilage and subchondral bone → narrowing joint space. Perheral and bony tophi evident with bone remodeling.

Front

Describe chronic (advanced) gouty arthritis.

Back

• Anaemia of chronic disease • Fatigue • Loss of appetite • High CRP and acute phase proteins • Intermittent fever • Weight loss • Subcutaneous rheumatoid nodules

Front

Describe systemic pathology of RA.

Back

• Loss of the joint space due to loss of cartilage • Sclerosis of bone in the weight bearing areas (no bone cartilage) • Subchondral bone cysts • Osteophyte formation

Front

What changes occur to the overall joint in osteoarthritis.

Back

• Cartilage degenerates • Staining changes • Cartilage breaks down, exposed surface becomes frayed (fibrillated), eventually cartilage lost completely

Front

Describe fibrillation of cartilage.

Back

A deposit of crystalline uric acid and other substances at the surface of joints or in skin (e.g. pinna of ear) or cartilage. Urate crystals surrounded by neutrophils macrophages and giant cells.

Front

What is a tophus (pl. tophi)?

Back

New bone laid down beneath the periostem and may, if large enough, encase the dead bone.

Front

What is the involucrum?

Back

• 80-90% of cases caused by Staphylococcal aureus • Others include: - E. coli - Group B strep - Salmonella - M. tuberculosis

Front

Which bacteria usually cause osteomyelitis?

Back

• Broad spectrum treatment initially • Sensitivity test reveals correct antibiotic to use • Relieve pressure surgically and debride dead tissue and pus (if no clinical improvement after 24-48 hours)

Front

How do we treat osteomyelitis?

Back

Prevent instability of joints.

Front

What are the roles of supporting ligaments and joint capsules?

Back

- Swelling - Reddness - Pus

Front

What features of acute inflammation are seen in this photograph?

Back

Over time microtophi form in synovial membrane and cartilage, physical change in environment → solubility change of stored irate crystals → leak into synovial fluid → acute painful gout (typically in the hallux).

Front

Describe acute gouty arthritis.

Back

- Congested vessel (big red area in middle) - Background of stringy proteinaceous exudate - Neutrophils

Front

Describe abnormalities seen in this section of subarachnoid space with acute bacterial meningitis.

Back

Undiagnosed hyperuricaemia that may persist for years before the onset of symptomatic gout.

Front

Describe asymptomatic gout.

Back

Non-union. Fractured bone ends in both the tibia and fibula have not healed together.

Front

5 months after an operation this x-ray is taken, what has occurred?

Back

Small fractures occur in articulating bone. Joint fluid forced under pressure into subarticular space. The fluid incites a host response and become surrounded by a fibrous capsule.

Front

Describe cyst formation in osteoarthritis.

Back

• Neonates - metaphysis, epiphysis and joint space (growth and great blood flow here) • Children - ends of log bones (inc. metaphysis), blood vessels no longer penetrate to epiphysis • Adults - spinal column or elsewhere within the axial skeleton (most common in most vascular areas)

Front

How do the common sites of osteomyelitis change with age?

Back

Reoperate and debride the connective tissue and create a new soft callus.

Front

What must be done to ensure healing of a non-uninous fracture?

Back

Lines the non-articulating aspects of the joint. Secretes synovial fluid, which acts as a lubricant in the movement process.

Front

What is synovium?

Back

• Multifactorial: - Environment - Genetic - Immune system • CD4 +ve cells (TH1 and TH17) are a major source of cytokines inducing inflammation • Antibodies to citrullinated peptides result in immune complex deposition in joints. Diagnostic marker. • Genetic - HLA-DRB1 locus frequently in RA, non-HLA also important. • 80% of patients have rheumatoid factor which is an IgM antibody against the Fc portion of self IgG.

Front

Describe the pathogenesis of RA.

Back

Section 3

(50 cards)

• Neisseria meningitidis

Front

Which bacteria causes meningitis in adolescents?

Back

Originates from choroid plexus and circulates in the subarachnoid space.

Front

Where does CSF originate and in which space is it found?

Back

A lumbar puncture

Front

What is the diagnostic test for meningitis?

Back

Less dramatic: • Headache • Feeling unwell • Confusion • Vomiting

Front

What are the signs and symptoms of chronic meningitis?

Back

• Tuberculosis • Spirochetes • Fungi • Amoebe • Chemical

Front

What sort of infectious or other agents cause chronic meningitis?

Back

Fibrinous protein exudate and a cellular exudate comprising neutrophils and macrophages.

Front

This is fluid aspirated from an infected joint. What will this show when examined under a microscope?

Back

Varus deformity (bowed legs, toward the midline). Quadriceps muscle wasted.

Front

Describe the abnormality in these knees.

Back

• Bacteraemia • Trauma • Surgury

Front

How do organisms gain entry to a joint cavity?

Back

Supine patient with hip flexed 90 degrees will have rigidity and pain preventing full extension of the knee.

Front

What is Kerning's sign??

Back

• Bacterial (pyogenic) • Viral • Chemical

Front

What sort of infectious or other agents cause acute meningitis?

Back

Surgical drain and irrigate the joint and systemic antibiotic therapy. Failure to treat adequately will lead to serious joint damage.

Front

How do we treat septic arthritis?

Back

Articular cartilage on both is pitted with erosion of the cartilage exposing the underlying bone on the right femoral condyle.

Front

Describe this knee joint (patella above, femur bellow) from an osteoarthritis patient.

Back

Loss of typical bluish staining. Small islands of hyperplasia of the chondrocytes on the right. On the left the surface has become frayed which is termed fibrillation. Bits of cartilage may dislodge from here to form 'joint mice'.

Front

Describe the changes in this cartilage. Left is superficial cartilage and right is an area of cartilage adjacent to an area of bone.

Back

Nodules of uric acid crystals in soft tissues (found commonly in the ears).

Front

What is a soft tissue tophus in gout?

Back

• E coli • Group B Streptococci • Mycobacterium Tuberculosis

Front

Which bacterial species cause meningitis in neonates?

Back

• Organisms enter CSF • Release of cytokines from astrocytes and microglia • Changes to the blood/brain barrier result in increased permeability leading to vasogenic oedema and brain swelling (increased intracranial pressure, unconsciousness and vomiting) • Acute inflammatory exudate forms in the subarachnoid space

Front

Describe the pathophysiology of meningitis.

Back

Passive flexion of the neck causes flexion of both the hip and knee.

Front

What is Brudzinski's sign?

Back

• Ziehl Nielsen staining • PCR/latex agglutination detect microbial antigens

Front

What are the main processes of identification in suspected unusual organisms in CSF specimens.

Back

When the CSF becomes contaminated by infective or irritating agents, inflaming the arachnoid, pia and cerebrospinal fluid within the subarachnoid space.

Front

What is meningitis?

Back

Material scraped out of a tissue for examination.

Front

What is curretted material?

Back

PCR and/or grown on special culture medium.

Front

How do you identify chronic bacterial tuberculosis.

Back

• Clear • Pressure: 6-18 cm H2O • Cells: 0-6 cells/ml. Usually mononuclear - 75% lymphocytes. • Protein: 0.2-0.4 g/L • Glucose: approximately 1/3 of serum glucose

Front

Describe the properties of normal CSF.

Back

Infection within the joint cavity leading to acute inflammation.

Front

What is septic arthritis?

Back

• Streptococcus pneumoniae • Listeria monocytogenes

Front

Which bacterial species cause meningitis in elderly?

Back

Several layers of hyper plastic synovium (top arrow). Chronic inflammatory infiltrate predominantly plasma cells (middle arrow). Fibrosis (bottom arrow).

Front

Describe the histology of this greater magnification image of the pannus.

Back

• Cloudy (not purulent) • Pressure: mild-moderate • Cells: increased, mainly mononuclear • Protein: mild increase • Glucose: mild-moderate decrease • Gram stain: negative

Front

Describe the properties of CSF in chronic bacterial tuberculosis.

Back

• Clear-cloudy • Pressure: mild-moderate • Cells: increased, mainly mononuclear • Protein: moderate increase • Glucose: normal range • Gram stain: negative (no bacteria)

Front

Describe the properties of CSF in acute aseptic meningitis.

Back

Chronic tophaceous gout (gout with formation of uric crystals). Bony erosions with loss of joint space and complete destruction of joints. Arrow indicates a tophi - a calcification formed as a result of new bone laid down but the periosteum.

Front

Describe the pathological process that have occurred in this image. What is indicated by the arrow?

Back

• Plasmodium

Front

What protozoan can cause meningitis?

Back

• Enteroviruses • Herpes simplex type 2 • Varicella zoster • Mumps

Front

What viruses can cause meningitis?

Back

• Gram stain • Culture • Protein and glucose assessment

Front

What are the main processes of identification in routine CSF specimens.

Back

• Cryptococci • Candida

Front

What types of fungi can cause meningitis?

Back

• Headache • Stiff neck • Kernig's sign - straight leg raising stretches meninges and causes pain • Fever • Anorexia -> nausea and vomiting • Late - confusion and loss of consciousness (intracranial pressure)

Front

What are the signs and symptoms of acute meningitis?

Back

CSF inoculated by viruses. Aseptic as not found on gram stain. CSF contains mononuclear cells (lymphocytes (T cells, B cells, NK cells) and monocytes)

Front

Describe aseptic meningitis.

Back

Red material is residual pannus which is inflamed. The cartilage has eroded and damage to the underlying bone due to the overlying pannus.

Front

What is the red material in this image? What has happened to the cartilage?

Back

• Acute inflammatory exudate within the subarachnoid space. • Neutrophils predominate. • Stringy background is fibrin (converted from fibrinogen which is the major protein in the fluid exudate) • Vessels are dilated and congested

Front

Describe the histology of the subarachnoid space in bacterial meningitis.

Back

• Haemotogenous • Direct (trauma) • Local extension (sinusitis, osteomyelitis) • Iatrogenic • Along nerves (rabies, herpes zoster)

Front

What are the 5 routes of CNS infection??

Back

Ligament of head of femur remains. Loss of cartilage and polishing of the exposed bone = eburnation. Lumpy osteophytes seen around base of head.

Front

Describe this femoral head from and osteoarthritic patient.

Back

• Creamy colour (turbidity) • Increased pressure • Increase cell count (almost 100% neutrophils in bacterial meningitis) • Increased inflammatory proteins • Descreased glucose as inflammatory cells consume it • Gram stain: positive (bacteria present)

Front

Describe the properties of CSF in acute bacterial meningitis.

Back

Fleshy projections of synovium with the darkly staining areas representing chronic inflammatory cells (mostly plasma cells).

Front

Describe the histology of this pannus.

Back

• Pia mater • Arachnoid mater • Dura mater

Front

What are the three layers of the meninges?

Back

• Haemophilus influenzae

Front

Which bacteria causes meningitis in infants?

Back

• Septic • Aseptic • Chemical or non-infectious

Front

What are the three types of meningitis?

Back

Osteoarthritis: - loss of joint space medially - Sclerosis of the adjacent bone - Osteophytes

Front

What abnormalities are seen on this x-ray?

Back

• Swollen • Marked vasocongestion and dilation of the vessels • Pus in the subarachnoid space especially around the brain stem and cerebellum

Front

Describe the gross appearance of the brain in meningitis.

Back

The bone at the top is dead, the cellular tissue bellow is an acute inflammatory exudate of pus due to the infection present.

Front

Describe the pathology of the bone in this image.

Back

Subarachnoid infection is caused by bacteria in the CSF.

Front

Describe septic meningitis.

Back

Staphlococcus aureus

Front

Which bacteria most commonly causes septic arthritis?

Back

• Haemophilus influenzae • Streptococcus pneumoniae • Niesseria meningitidis

Front

What causes of bacterial meningitis can be dramatically reduced with vaccination?

Back

A = cartilage. B = cysts with fibrous wall. C = sclerotic bone. D = eburnated surface.

Front

Identify the structures A, B, C and D.

Back

Section 4

(50 cards)

• Removal of the underlying cause (e.g. gram negative bacteria - antibiotics) • Replace the coagulation products - Antibiotics - Fresh frozen plasma - Coagulation products - Packed red cells

Front

How is DIC treated?

Back

- Small nodules - Granulomata - Features of tuberculous meningitis

Front

Describe the abnormalities seen in this image.

Back

• Recovery • No significant changes occur to the brain

Front

Describe the outcome of viral meningitis.

Back

• Unclear but thought to be related to the adrenal vessels sustain endothelial injury due to endotoxins • Proposed that an increased in adrenal venous pressure may result in hemorrhage • ACTH is released as part of the shock response leading to increased blood flow and platelet aggregation in adrenal veins.

Front

Describe the Cause of WF Syndrome.

Back

A rash of purple spots on the skin caused by internal bleeding from small blood vessels.

Front

What is purpura?

Back

• Acute adrenal insufficiency due to massive hemorrhage into the adrenal glands • Part of the spectrum of shock esp. that associated with N. meningitides but also pneuococcus and H. influenza

Front

What is Waterhouse-Friederichsen Syndrome?

Back

Disseminated intravascular coagulation: • Scattered, diffuse, exaggerated thrombosis in microcirculation due to: - Exposure of sub-endothelial collagen - Release of tissue thromboplastin (tissue damage) • Activates both clotting cascade and fibrinolytic system at same time

Front

Define DIC.

Back

• Non-propagating organisms in blood • Minimal/no mediators, toxins • Minimal/no endothelial or tissue damage and coagulation • DIC not possible

Front

Define bacteremia.

Back

• Prostacylin • Nitrous oxide • ADPase

Front

What three substances prevent platelets adhesion and activation (antiplatelet)?

Back

Giant cell within a granuloma. Surrounding epithelioid cells. T- lymphocytes further out.

Front

Describe the histology of this section of granulation tissue taken from the subarachnoid space in chronic tuberculosis meningitis.

Back

Inactivates thrombin.

Front

Describe the anticoagulation mechanisms of anti-thrombin.

Back

Prevents initiation of tissue factor pathway.

Front

Describe the anticoagulation mechanisms of tissue factor pathway inhibitor.

Back

Cellular and tissue damage has occurred.

Front

What is the irreversible stage of shock?

Back

• Newborn/infant - 20-30% • Children 2% • Adults 19-37%

Front

Describe the percentages of mortality due to meningitis in newborns/infants, children's and adults.

Back

Bilateral haemorrhagic necrosis of the adrenal glands in child with N. meningitides septicaemia.

Front

Describe this image.

Back

Turn off coagulation.

Front

Describe the anticoagulation mechanisms of thrombomodulin, protein C and protein S.

Back

Compensatory mechanisms maintain organ function.

Front

What is the non-progressive stage of shock?

Back

• Tissue factor pathway inhibitor (TFPI) - Tissue factor and FactorVIIa inhibitor • Protein C system - Factor IXa, VIIIa, Xa and Va inhibitor • Antithrombin III - Factor Xa, Va and IIa (thrombin) inhibitor

Front

What are the three anticoagulation pathways?

Back

• Inflammation - vascular constriction • Platelets - adhere via vWF an exposed collagen - aggregate into bulky plug • Tissue factor - pro-coagulation effects • Antiplasmins and plasminogen activator (t-PA) inhibitors - antifibrinolytic effects.

Front

Describe how endothelial injury or activation promotes thrombosis.

Back

• 150-400x10^9/L

Front

What is the normal range of platelets in blood?

Back

• Non-progressive • Progressive • Irreversible

Front

What are the three stages of shock?

Back

Waterhouse-Friederichsen syndrome. Several fulminating intra adrenal haemorrhage. A complication of severe shock

Front

Describe this image.

Back

A substance secreted by endothelial cells which binds to the sub endothelium. Loss of endothelial cells during trauma exposes vWF bound to collagen and platelets bind via glycoprotein receptors (Gp1b).

Front

What is von Willebrand Factor (vWF)?

Back

Renal glomerulus contains fibrin thrombi. This is the result of DIC with fibrin thrombi forming in the capillary network throughout the body. As a result the GFR would be compromised and she would go into renal failure.

Front

This is a renal glomerulus with a trichrom stain which shows protein as bright red. What protein is this? Describe the pathogenesis.

Back

• Vasodilation leading to low peripheral resistance, decreased blood pressure • Decreased myocardial contractility and decreased blood pressure • Endothelial damage, due to endotoxins, cytokines or decreased perfusion leakage. decreased volume and blood pressure • DIC especially in microcirculation - get micro thrombi, decreased perfusion (blood delivery to capillary bed)

Front

Describe the physiological effects of septic shock.

Back

Shed from megakaryocyte in bone marrow.

Front

How are platelets produced?

Back

Granulomas within the subarachnoid space. Arrow points to caseous necrosis (cheese like). Chronic inflammatory infiltrates and fibrosis.

Front

Describe the histology of this section of subarachnoid space in chronic tuberculosis meningitis.

Back

Dermal haemorrhaging due to vascular damage. Damaged endothelium leads to thrombus and necrosis of the skin.

Front

Describe the appearance of the skin in this image.

Back

Tissue type plasminogen activator (t-PA) (activates plasminogen to plasmin which breaks down fibrin).

Front

What substance breaks down fibrin (fibrinolytic)?

Back

• Disc-shaped • Granular • Anuclear

Front

Describe the structure of a platelet.

Back

• Exotoxins on bacterial surface released (mainly Staph. aureus and Strep, progenies) = super antigen • Binds to MHCII on antigen presenting cells and T cells (up to 10% T cells activated) • Causes release of massive quantities of cytokines (cytokine storm), causes septic shock

Front

Describe septic shock from gram positive bacteria.

Back

• Exhaustion of clotting factors, platelets, fibrinogen and protein C with production of D-dimers from fibrin breakdown. • Bleeding from drip sites, areas of trauma and areas of necrosis.

Front

Describe the outcome of DIC.

Back

• Propagating bacteria releasing toxins (sepsis) • Maximal mediators, toxins • Maximal endothelial and tissue damage and coagulation • DIC possible.

Front

Define septicaemia.

Back

• Cardiogenic • Hypovolemic • Neurogenic • Anaphylactic • Septic - especially due to gram positive bacteria

Front

What are the five types of shock?

Back

Binds to and stabilises FVIII, preventing it's proteolytic degradation.

Front

What is the function of circulating vWF?

Back

Autosomal dominant.

Front

Describe the inheritance of vW disease.

Back

• Adhesion, activation and shape change • Secretion (release reaction) • Aggregation - forming the primary platelet plug

Front

Describe the changes that occur to platelets when they come into contact with collagen or vWF.

Back

• Vasoconstriction • Platelets • Coagulation

Front

What are the three components of haemostasis after hemorrhage?

Back

Prevent bleeding when it is expected e.g. surgery give vWF, heavy menstrual bleeding use contraceptive pill.

Front

How is vW disease treated?

Back

• Lipopolysaccharides which are part of the bacterial wall • Act as endotoxins • These bind and activate neutrophils and macrophages with releases of cytokines (IL-1, 6, 8 and TNF-alpha plus nitrous oxide and platelet activating factor) • Severity of condition relates to amount of cytokines released

Front

Describe septic shock from gram negative bacteria.

Back

• Anti-thrombin • Thrombomodulin • Protein C • Protein S • Tissue factor pathway inhibtor

Front

What substances have anticoagulation effects?

Back

- Brain is swollen - Vessels are dilated and congested - There is pus in the subarachnoid space - The features are of acute inflammation

Front

Describe the abnormalities in this image.

Back

Tissue hypoperfusion with worsening circulation and metabolic functions.

Front

What is the progressive stage of shock?

Back

Clotting disease caused by vWF disorder. 1 - quantitative (low vWG concentration), most common. 2 - qualitative (poor vWF function) 3 - quantitative (homozygous, complete absence of vWF), most rare, but most severe. Platelet type - vWF normal but platelets have defective receptors.

Front

What is von Willebrand disease and what are the four types?

Back

Treating the endothelial-coagulation-multiorgan dysfunction: • Replace protein C, helps stop the action of FVa and FVIIIa and maintains fibrinolytic breakdown of intravascular fibrin • Protein C also provides signals to tissue cells that help to reverse the mutliorgan dysfunction • In fatal cases protein C may be well bellow 10% of normal.

Front

Describe the newer approach to treating DIC.

Back

Neutrophil on the right. Many gram negative diplococci - this is neisseria meningitis.

Front

Describe what is seen in this gram stain taken from a blood sample of a patient with DIC.

Back

Large gene with many possible mutations instead test bleeding times of 1st degree relatives.

Front

Why is genetic testing not done for vWD?

Back

Purple structure is a disrupted neutrophil, with smaller diplococci bacteria seen. Background is RBCs with a lack of platelets.

Front

Describe what is seen in this image taken from a blood sample of a patient with DIC.

Back

Exudate may become organized leading to fibrosis within the subarachnoid space • Fibrous bands around cranial nerves leading to palsies (paralysis and tremors) • Blockage of CSF flow leasing to hydrocephalus • Vasculitis of vessel supplying outer surface of cortex leading to cortical infarction • Epilepsy

Front

Describe what occurs in meningitis if treatment is delayed.

Back

Thrombosis of the dermal vessels and vascular collapse with a combination of necrosis and bleeding.

Front

How does meningococcus sepsis in children cause purpura and DIC?

Back

Section 5

(50 cards)

Platelets when activated. Increases aggregation via GPIIb-IIa

Front

What other cell secretes vWF and when?

Back

• Generation of thrombin which converts fibrinogen to fibrin • Fibrin polymerises to form a clot and is stabilized by FXIII

Front

Describe the common pathway where the two pathways meet up.

Back

A systemic illness due to immune mediated (autoimmune) damage to connective tissue.

Front

How is acute rheumatic fever caused?

Back

1 - platelet receptor activated by; collagen, vWF, ADP, TXA2, thrombin, serotonin or adrenaline 2 - platelet secretes granules: • Dense granules - ADP (for activating platelets) and serotonin (for platelet activation and vessel constriction) • Alpha granules - contain vWF, fibrinogen, factor V, platelet factor 4, and more 3 - Cyclooxygenase pathway activated, amplifies aggregation, activates more platelets and constricts vessels 4 - GPIIb and GPIIIa activated, fibrinogen or vWF binds and platelets aggregate.

Front

Describe platelet secretion (release reaction).

Back

Same as for atherosclerosis: - High cholesterol - Hypertension - Smoking - Diabetes - Low exercise - etc

Front

What are the risk factor of calcific aortic sclerosis?

Back

Platelet aggregometry.

Front

What is a third test possible to measure platelet function?

Back

A disorder characterized by rapid, uncoordinated jerking movements primarily affecting the face, hands and feet

Front

What is Sydenham chorea?

Back

- Calcific aortic sclerosis - Or calcification of the mitral valve annular ring

Front

Give an example of aging/wear and tear valve disease.

Back

Coagulation factros II, VII, IX and X. Coagulation inhibitor proteins C and S.

Front

What clotting factors and coagulation inhibitor proteins does vitamin K carboxylate (activate)?

Back

Production of coagulation factors (and carboxylation of vit. K dependent factors), platelet production.

Front

What is the role of the liver in haemostasis?

Back

Mitral valve prolapse with myxomatous degeneration.

Front

Give an example of valve disease of unknown pathogenesis.

Back

A systolic murmur +/- a diastolic murmur and eventually left ventricular myocardial hypertrophy.

Front

What clinical signs are produced by the calcific aortic sclerosis?

Back

International Normalized Ratio, used to standardise bleeding time by the sensitivity of the tissue factor in a bleeding analysis test.

Front

What is the INR and how is it used?

Back

Group A β haemolytic Streptococcal pharyngitis.

Front

Acute rheumatic fever follows 2-3 weeks after which infection?

Back

Tells us why we are getting poor APTT or PT. Patients blood is mixed with normal blood. If patients poor bleeding time is due to inhibitor of coagulation in blood clotting will not be or only be slightly improved. If patients poor bleeding time is due to lack of factor(s) in blood factors from normal blood will correct clotting time to normal.

Front

What is a mixing study for APTT and PT?

Back

A valve does not open properly and obstructs the forward flow of blood.

Front

What is valve stenosis?

Back

Tissue factor pathway. Most important, triggered by tissue injury.

Front

Describe the extrinsic pathway of coagulation.

Back

In plasma. Activated by shearing stresses and binding to foreign surfaces.

Front

Where is vWF found in an inactive form and how is it activated?

Back

• Blood pumped through capillary coated with platelet activators (collagen-adrenaline, collagen-ADP) • The time required to occlude (block) the capillary is a measure of platelet function

Front

How does a platelet function analyser (PFA-100) measure platelet function?

Back

If the spleen is enlarged (i.e. infection) it will pool more platelets reducing the blood concentration.

Front

What role can the spleen play in thrombocytopenia?

Back

- Congenital - Aging/wear and tear - Aquired - Unknown

Front

What are the 4 pathogenesises of valve disease?

Back

Length of extrinsic pathway to clot formation - 8-11 seconds.

Front

What is the Prothrombin Time (PT) and what is the normal range?

Back

Generally clinically silent but may cause stenosis, regurgitation and arrhythmias.

Front

What clinical signs are produced mitral valve calcification (calcification of the mitral valve annular ring)?

Back

A characteristic but uncommon non itchy rash.

Front

What is erythema marginatum of the skin?

Back

Where the valve cusps come together.

Front

What is a commissure?

Back

Time for conversion of fibrinogen to fibrin once thrombin is produced (common pathway) - 12-18 seconds.

Front

What does Thrombin Clotting Time (TCT) measure and what is the normal range?

Back

The valve does not close properly resulting in back flow of blood into the chamber of origin.

Front

What is a regurgitant/incompetent valve?

Back

Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.

Front

Why are subcutaneous nodules produced in acute rheumatic fever?

Back

- Acute rheumatic fever - Chronic rheumatic heart/valve disease

Front

What are the two types of rheumatic heart disease?

Back

Antibodies to Streptococcal M protein produced in approx. 3% individuals, cross react with connective tissue and other antigens systemically (esp. heart, joints and CNS). Additionally CD4+ T cells specific to Streptococcal peptides react with self antigens in the heart producing cytokines and activating macrophages. Causes inflammatory response.

Front

How does group A β haemolytic Streptococcal pharyngitis cause rheumatic fever?

Back

- Rheumatic heart disease - Or bacterial endocaridits

Front

Give an example of acquired valve disease.

Back

Length of intrinsic pathway to clot formation - 22-34 seconds.

Front

What does Activated Partial Thromboplastin Time (APTT) measure and what is the normal range?

Back

Degeneration of connective tissue.

Front

What is myxomatous degeneration?

Back

Contact activation pathway. Role in inflammation and infections.

Front

Describe the intrinsic pathway.

Back

Increased work load to the left atrium leading to left atrial hypertrophy and dilation.

Front

What changes are related to an abnormal mitral valve?

Back

70-100

Front

At what age is calcific aortic sclerosis most common?

Back

Bicuspid aortic valve

Front

Give an example of congenital valve disease.

Back

Standardisation issues.

Front

Why is bleeding time not often performed anymore?

Back

Well done :)

Front

Look at this diagram summarizing coagulation.

Back

Mitral and aortic.

Front

What are the two most commonly affected valves?

Back

Pancarditis (infection of whole heart): - Endocarditis (endocardium) - Myocarditis (myocardium) - Pericarditis (pericardium)

Front

What effects does acute rheumatic fever have on the heart?

Back

Production of bone matrix proteins which become calcified. Calcified martial fills and protrudes from the sinuses of valsalva (aortic sinus). Valve becomes rigid, results in stenosis and some regurgitation. Commissures not involved.

Front

Describe the pathogenesis of calcific aortic sclerosis?

Back

Transport across placenta limited. Stores depleted 2-4 days after birth. Breastmilk has low levels. Lack of bowel microflora to make vitamin K.

Front

Why are babies at risk of vitamin K deficiency?

Back

- Pancarditis - Migratory polyarthritis of large joints - Subcutaneous nodules - Erythema marginatum of the skin - Sydenham chorea

Front

What clinical signs are seen in acute rheumatic fever?

Back

- Inflammation and fibrinoid necrosis occurs in the CT beneath the endocardium. Results in swelling. As valves move, endothelium of valve cusps and chord tendineae are damaged. - Verrucae form; small 1-2mm sterile platelet thrombi in the areas of damage along the lines of closure of the valve and chordeae tenineae.

Front

Describe the effects of endocarditis in acute rheumatic fever.

Back

• Substance produced by the cyclic-oxygenase pathway in activated platelets • Amplifies aggregation • Activates more platelets • Constricts vessels

Front

What is thromboxane A2 (TXA2)?

Back

- 5-14 years old (mostly 9-11) - Associated with lower socioeconomic status - Associated with Māori and Polynesian populations

Front

Describe the demographic epidemiology of rheumatic heart disease incidence.

Back

• Activated Partial Throboplastin Time (APTT) • Prothrombin Time (PT) • Thrombin Clotting Time (TCT)

Front

What tests are available to test coagulation.

Back

Aggregation receptor (GpIIb/IIIa) binds to vWF and fibrinogen - released from platelets and circulating in plasma.

Front

Describe platelet aggregation.

Back

Increased work load to the left ventricle leading to myocardial hypertrophy.

Front

What ventricular changes are related to an abnormal aortic valve?

Back

Section 6

(50 cards)

Vascular cell adhesion molecule-1.

Front

What does VCAM-1 stand for?

Back

- Aortic valve - Commissures are normal - There are calcified nodules within the sinus of valsalva - This would lead to a stiff valve and the presence of a murmur = Calcific aortic sclerosis

Front

Describe the pathology of this image.

Back

- Tunica intima - Tunica media - Tunica adventitia

Front

What are the three layers of a blood vessel?

Back

Bacteraemia of virulent organisms. Bacteria bind to endocardium → inflammation and formation or large friable vegetations. Rapid growth with valvular damage, spread to adjacent myocardium, possible access formation in the systemic emboli.

Front

Describe the pathogenesis of acute bacterial endocarditis.

Back

Mitral valve deformity known as fish mouth or button whole. The commussures are fixed and the valve edges distorted such that the valve cannot close. Small thrombi are present on the upper surface.

Front

Describe this image.

Back

The result of deposition of fatty material within the intima of muscular and elastic arteries. Athero = gruel, sclerosis = hardening.

Front

What is atherosclerosis?

Back

- Hyperlipidaemia - Hypertension - Diabetes - Cigarette smoking - C reactive protein

Front

What are the controllable risk factors for atherosclerosis?

Back

Infection of the endocardium and particularly of valves of the heart.

Front

What is infective endocarditis?

Back

Infection of a normal valve or abnormal/scarred valve.

Front

What is acute endocarditis?

Back

Soft often necrotic centre (cell debris, cholesterol crystals, foam cells, calcium) with overlying fibrous cap (smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularisation)

Front

Describe the structure of a mature atherosclerotic plaque.

Back

Subacute: - Insidious onset - Low virulence organisms - Damaged valve - Low grande chronic infection Acute: - Sudden onset - High virulence organisms - Normal/abnormal valve - Destructive rampant infection

Front

Sort the descriptors into subacute or acute bacterial endocarditis: - Insidious onset or sudden onset - Low or high virulence organisms - Normal/abnormal valve or abnormal valve - Destructive rampant infection or low grade chronic infection

Back

Pale areas of infarction in the kidney. Darker areas of reddy/brown granulation tissue. Associated with abscess formation as a result of septic emboli.

Front

What pathology is evident in this photograph?

Back

- Aneurysm and rupture - Occlusion by thrombus - Critical stenosis (occlusion by plaque)

Front

What are the three possible outcomes of atheroscleosis?

Back

- Valve cusps are thickened - Annular calcification with nodules as indicated by the arrows = Mitral annular calcification

Front

What is wrong with this mitral valve?

Back

Inflammation of the CT leads to sterile fibrinosus exudate -> pericardial effusion.

Front

Describe the effects of pericarditis in acute rheumatic fever.

Back

- Fever - Malaise - Tiredness - Loss of appetite (super general! :/)

Front

What are the clinical signs of acute bacterial endocarditis?

Back

- Staplococcus aureus - Streptococcus pyogenes

Front

Which virulent organisms cause acute bacterial endocarditis?

Back

- Mainly oral commensal organisms (infection due to dental or surgical procedure) - Infection elsewhere

Front

What are the major sources of the bacteraemia leading to acute bacterial endocarditis?

Back

Weakened due to a decrease in oxygen supply and migrating SM cells.

Front

What affect does an atherosclerotic plaque have on the underlying media?

Back

- Activation of recruited monocytes and macrophages, ingesting lipids and become foam cells - Cytokine production - T cells and macrophages stimulate a chronic inflammatory state - Results in growth factor release with ECM production and smooth muscle proliferation - Smooth muscle cells may migrate from media or develop from progenitor cells recruited from the blood

Front

Order these events chronologically in the pathogenesis of atherosclerosis: - Results in growth factor release with ECM production and smooth muscle proliferation - T cells and macrophages stimulate a chronic inflammatory state - Smooth muscle cells may migrate from media or develop from progenitor cells recruited from the blood - Activation of recruited monocytes and macrophages, ingesting lipids and become foam cells - Cytokine production

Back

- Increases acute phase proteins - Increased leucocytes - Increased ESR

Front

What blood tests are indicative of acute bacterial endocarditis?

Back

Intercellular adhesion molecule-1.

Front

What does ICAM-1 stand for?

Back

- Vasodilator - Antinflammatory properties - Limits expression of VCAM-1 (vascular cell adhesion molecule-1).

Front

What are three functions of NO in blood vessels?

Back

There is marked left ventricular hypertrophy as a consequence of a stenotic and regurgitant valve.

Front

This heart would have had a stenotic aortic valve, what is the pathology?

Back

- Chronic aortic valve damage - Distortion of valve cusp - Fusion of commissures

Front

Describe this image.

Back

Intima. Will encroach on the lumen with time as apposed to deeper into the wall.

Front

What layer(s) of a blood vessel are mature plaques found in?

Back

Mitral valve is normal. There is one very large and several small vegetations present on the mitral aspect of the valve cusps. This is an acute bacterial endocarditis. Having formed on a normal valve the infecting organism must be high virulent e.g. S. aureus.

Front

Heart of a previously healthy adult. What is the pathogenesis?

Back

The valve cusps are thickened and distorted. There is a fusion of at least one commissure. The valve would be stenotic and regurgitant.

Front

What is wrong with this aortic valve?

Back

A - valve leaflet. This is thickened and boggy at the edges. B - cordae tendinae C - papillary muscle D - verrucae along lines of closure

Front

The heart is opened showing the mitral valve, what do the letters indicate?

Back

- Age - Male gender - Family history - Genetic inheritance

Front

What are the uncontrollable risk factors for atherosclerosis?

Back

Mitral valve with: - Thickened shortened cordae tedineae - Fibrotic thickened distorted valve cusp - Valve will be stenotic and regurgitant

Front

Describe this image.

Back

Left atrium volume is enlarged. The muscle mass will be increased. Left atrial hypertrophy but with dilation this the walls appear thin.

Front

Describe the pathology of this heart from a patient with mitral valve disease.

Back

Small blood vessels that supply the smooth muscle of larger blood vessels.

Front

What are vaso vasorum?

Back

- Vascular endothelial cells - Lymphocytes - Monocytes/macrophages - Smooth muscle cells

Front

What cells are involved in the pathogenesis of atherosclerosis?

Back

- Embolism of fragments of the vegetations - Rupture of the valve and adjacent myocardial abscess (usually in acute endocarditis)

Front

What complications can occur as a result of acute bacterial endocarditis?

Back

Valves stenotic and regurgitant: - Blood flow damages endothelium on top of (up stream) of valve - Small platelet fibrin form and low virulence organisms from bacteraemia infect them. Inflammatory response follows resulting in large friable vegetations comprising thrombotic material, inflammatory cells and bacteria.

Front

Describe the pathological effects of acute bacterial endocarditis.

Back

Haemorrhage into the plaque: - From the neovascularisation at the shoulders of the plaque - From rupture of the fibrous cap

Front

Along with occlusion by the plaque or by thrombus what is the third way that an occlusion may occur?

Back

Infection of a previously damaged valve or congenital valve.

Front

What is subacute endocarditis?

Back

Ischaemia: - Myocardial infarction - Cerebral infarction - Peripheral vascular disease - Gangrene of extremities

Front

What affect does partial or total occlusion of a vessel have on distal tissues in the heart, brain, vessels and distal tissues?

Back

Layers of elastic tissue in muscular arteries. - Internal elastic lamina between intima and media - External elastic lamina between media and adventitia

Front

What are the two elastic lamina and where are they found?

Back

Collections of T lymphocytes, plasma cells and activated macrophages called Antischkow cells. These are also known as caterpillar cells due to the characteristic clumping of the nuclear chromatin.

Front

What are Ashcoff bodies?

Back

- Risk factors - Endothelial cell damage - Expression of VCAM-1 and ICAM-1 - Binding of T lymphocytes and monocytes - T lymphocytes and monocytes enter intima - Influx of LDL - LDL oxidation - Activation of macrophages within the intima

Front

Order these events chronologically in the pathogenesis of atherosclerosis: - Binding of T lymphocytes and monocytes - Expression of VCAM-1 and ICAM-1 - Influx of LDL - T lymphocytes and monocytes enter intima - Endothelial cell damage - Activation of macrophages within the intima - LDL oxidation - Risk factors

Back

Scarring of the endocardium leads to: - thickened/distorted valve cusps (particularly closing edge) - Fusion of commissures - Thickening, fushion and shortening of chordae tendineae - All affect valve function (stenosis and regurgitation -> ongoing valve wear and tear)

Front

Describe the pathological effects of chronic rheumatic valvular disease.

Back

Chordae tendinae are markedly shortened and thickened as is the edge of the valve cusp. The effect would be to prevent adequate closure of the valve leading to incompetence. The thickening of the leaflet leads to stenosis.

Front

This image shows the chordae tedninae of the mitral valve. What is the pathology? What effect will this have on valve function?

Back

Areas of inflammation, Aschoff bodies and muscle necrosis. Decreases muscle contractility (greatest cause of ARF death).

Front

Describe the effects of myocarditis in acute rheumatic fever.

Back

When inflammation subsides the lesions from autoimmune reactions heal. The connective issue is unable to regenerate so healing is by fibrosis. Scarring will occur in the all layers of the heart. Endocardial scarring changes valve shape and therefore valve function.

Front

Describe healing of acute rheumatic fever.

Back

Blood vessel formation stimulated by cytokines at the shoulders of the cap of the plaque.

Front

What is neovascularisation?

Back

Haemorrhagic infarct in the MCA territory of the brain. Associated with abscess formation as a result of septic emboli (emboli → stroke → ischaemic necrosis)

Front

What is the pathology evident in this photograph?

Back

Mitral valves cusps thickened and shortened with a fish mouth/button hole deformity. The commissures are fused. Small thrombi are present on the upper surface of the valve. A small thrombus is present in the atrial appendage of the left atrium.

Front

What is the pathology of the valve indicated. What are the lesions indicated at a and b?

Back

A - thickened chordae tendinae B - thickening and distortion of the valve cusp as well as fusion of the commisure C - myocardial hypertrophy D - a large friabel vegetation representing subacute blood flow through a damaged valve. As a result of the rheumatic valve disease abnormal blood flow would result in further damage. Turbulent back flow of blood leads to superficial endothelial damage with the formation of platelet/fibrin thrombi. Bacteria colonize the thrombi and a vegetation develops.

Front

Heart of 59 year old man with history of rheumatic valve disease, resulting in a lifetime of ongoing damage. What is the pathology seen in this photograph and the structures seen at A, B, C and D.

Back

Section 7

(50 cards)

Same as atheroslcerosis: - Smoking, diabetes, hyperlipidaemia and hypertension - Age, male, family history, sedentary life style, obesity, use of oral contraceptives.

Front

What are the risk factors of ischaemic heart disease?

Back

Narrowing of lumens and thickened walls of small arteries and arterioles with aging and in hypertension.

Front

What is arteriosclerosis?

Back

Patients present with symptoms and signs of myocardial infarction without ECG changes. Troponin however elevated. Often falsely diagnosed as unstable angina.

Front

What is non-ST elevation myocardial infarction (non-STEMI)?

Back

Blood within the abdominal cavity. Large bulge in the middle is an aortic aneurysm.

Front

Describe what can be seen in this image.

Back

Mural thrombus at top - will be filling the aneurysm. Atherosclerotic debris bellow this. Medial bellow black elastic later will loss of elastin and fibrosis. Bottom is connective tissue of adventitia.

Front

Describe the pathological features of this section of aorta from an aortic aneurysm.

Back

<12 hours: oedema, hemorrhage 12-24 hours: nuclear pyknosis, myocyte hypereosinophilia 1-3 days: loss of nuclei and striations, increased nutrophils 3-7 days: disintegration of myofibres, dying neutrophils, some macrophages 7-10 days: phagocytosis, early granulation tissue 10-14 days: granulation tissue with early collagen formation 2-8 weeks: increasing collagen, decreasing cellularity

Front

Describe the microscopic changes in MI with time.

Back

Rupture of the fibrous cap of an atherosclerotic plaque. There has been formation of an occlusive thrombus due to the exposure of collagen

Front

Describe what has occurred at the arrow.

Back

Greater than 75% obstruction.

Front

At what percentage of obstruction is maximal blood flow impaired?

Back

<12 hours: none 12-24 hours: some mottling - dark/pale patchiness 1-3 days: pallor of infarct area 3-7 days: hyperemic border to pale infarct 7-10 days: pale and soft with clear redden margin 10-14 days: soft and shrinking infarct 2-8 weeks: grey-white scar

Front

Describe the macroscopic (gross) changes in MI with time.

Back

- Pink amorphous tissue referred to as hyaline - Hyperplastic smooth muscle with an onion ring appearance seen mainly in hypertension

Front

What is the wall thickened by in arteriosclerosis?

Back

In the sub endothelial area and extends towards the pericardium over 3-6 hours. Subendothlial area is the furthest away from the supply vessels and subject to intralumnial pressure.

Front

Where does necrosis begin and why?

Back

Pooling of blood in the lungs (pulmonary oedema)

Front

What is the result of left ventricular heart failure?

Back

Block beta1 and beta2 receptors from adrenaline and noradrenaline. Decreases heart rate and dilates vessels reducing the heart rate. E.g. Atenalol, Metoprolol.

Front

Why are Beta-blockers used? Give two drug examples.

Back

20 minutes.

Front

How long must myocardium be ischaemic for necrosis to occur?

Back

Media is thinned with loss of staining underlying an atherosclerotic plaque. The plaque has a necrotic centre containing cholesterol clefts and calcification. There is an overlying fibrous cap.

Front

Describe the pathological features of this section of aorta.

Back

Ulcerated plaques are present along aorta. A small aneurysm in the lower aorta with a thrombus present within it. A similar finding is noted in the right and left iliac arteries.

Front

Describe the pathological features of this section of aorta.

Back

- Beta-blockers - ACEi/ARBs/Aldosterone inhibitors - Diuretics

Front

What is the pharmacological treatment of heart failure?

Back

Damaged muscle will leak enzymes, the rise in the blood proportional to the amount of damage. Traditionally measured: - Creatine kinase - Lactate dehydrogenase - Aspartate transaminase Currently measured: - Creatine kinase (begins to rise after 6-9 hours and rapidly cleared) - Troponin - T & I (cTnT and cTnTI)

Front

Describe the cardiac enzyme changes characteristic of myocardial infarction.

Back

Rupture of the fibrous cap with bleeding into the plaque narrowing the lumen which is occluded by an overlying thrombus.

Front

Describe the pathology in this image.

Back

Inhibit the angiotensin II receptor. Results in perivascular muscle relaxation and a drop in blood pressure. E.g. Losartan, Valsartin.

Front

Why are angiotensin receptor blockers used? Give two drug examples.

Back

Above the bifurcation bellow the renal arteries.

Front

Where are aortic aneurysm usually found?

Back

Takes years to develop as the scar tissue slowly weakens and allows the involved area to dilate.

Front

How does myocardial infarction result in ventricular aneurysm?

Back

Loss of elastin and the thinning of the media. Residual atherosclerotic debris represents the intima and thrombus is above this. Grossly thrombus would fill the cavity of aneurysm.

Front

Describe the histology of this section from the base wall of an aortic aneurysm (elastin stained black, fibrous tissue is red).

Back

Transverse section through abdomen and aortic aneurysm, aorta very enlarged with wall calcification, large darker mural thrombus within this with a small lumen containing flowing blood.

Front

What is seen in this image?

Back

3-7 days post-MI. - Septal, free wall → cardiac tamponade - Papillary muscle → acute valve dysfunction

Front

How long after a MI is myocardial rupture likely to happen and what are the two types?

Back

Peripheral oedema, raised JVP and liver congestion.

Front

What are the consequences of increased pressure on the right ventricle?

Back

Well done :D :D

Front

This image is a helpful diagram of the last flashcard :D

Back

Transmural

Front

In which distribution of myocardial infarction is development of pericarditis most common?

Back

- Rise rapidly in 2-3 hours - Remain raised for 4-10 days - Very specific and sensitive - Raised in many other conditions affecting the heart

Front

Select the correct properties of troponin enzyme testing: - Rise rapidly in 2-3 hours or rise slowly in 10-12 hours - Cleared quickly in 24 hours or remain raised for 4-10 days - Not very specific and sensitive or very specific and sensitive - Raised in many other conditions affecting the heart or raised only in MI

Back

Compression of the heart by an accumulation of fluid in the pericardial sac.

Front

What is cardiac tamponade?

Back

Inhibits angiotensin converting enzyme. Causes relaxation of blood vessels and decreases blood volume this decreasing blood pressure. E.g. Enalapril, Captopril.

Front

Why are ACE inhibitors used? Give two drug examples.

Back

Due to left ventricular failure (>20% damage to LV mass) or cardiogenic shock (>40% damage to LV mass).

Front

How does myocardial infarction result in heart failure?

Back

Discrete area of coagulative necrosis in myocardium. Due to ischaemia as the result of significant obstruction or total occlusion of a coronary artery.

Front

What is myocardial infarction?

Back

Uncomplicated atherosclerotic plaque at top. Dilation of the lower aspect of the aorta bellow the renal arteries forming an aneurysm. Aneurysm contains a large thrombus (red/brown area). Haemorrhage in periaortic fat (left) indicates aortic rupture.

Front

Describe the pathological features of this section taken from an aortic aneurysm.

Back

Increased pressure (right ventricle pumps blood into pulmonary circuit).

Front

What affect does pulmonary oedema have on the right ventricle?

Back

Coughing, frothy sputum, shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea and crepitations

Front

What are the consequences of pulmonary oedema?

Back

- Lumen narrowed by 70% - Intima eccentrically thickened - Atherosclerotic plaque

Front

Describe the pathological features of this section of artery.

Back

Cardiac function decreased due to loss of functioning muscle.

Front

What is heart failure?

Back

- Subendothelial: inner area of myocardium does not receive adequate oxygen - Mural: deep within the muscle but not full thickness - Transmural: full thickness except for a small rim of viable tissue in the sub endothelial and supercardial areas

Front

What are the three distributions a MI can have?

Back

- Arrhythmias - Heart failure - Mural thrombus - Pericarditis - Myocardial rupture - Ventricular aneurysm

Front

What are 6 possible complications of myocardial infarction?

Back

Right side of vessel is large atherosclerotic plaque into which there has been a hemorrhage. Cholesterol clefts and calcification are seen. The fibrous cap shows a rupture and the lumen has been significantly narrowed by an occlusive thrombus. Vessel can be seen in the shoulder of the fibrous cap on the left.

Front

Describe the pathology of this section of atherosclerotic artery.

Back

Thinning of muscular media and loss of elastic fibres of the internal and external laminae. Intima eccentrically thickened by atherosclerotis plaques. Plaque is necrotic and contain cholesterol clefts. Overlying fibrous cap present. Small bleed inferiorly from the vessels of the shoulder of the fibrous cap.

Front

Describe the pathological features of this section of artery.

Back

Due to enhanced sympathetic activity as a result of increased levels of local or circulating catecholamines.

Front

How do myocardial infarction result in arrhythmias?

Back

A - mild atherosclerosis with fibrous plaques as indicated by the arrow B - Severe atherosclerosis with complicated plaques which are ulcerated with overlying thrombi. These may be a source of emboli.

Front

Describe the pathology seen in these images of separate aorta.

Back

VGE stain - elastic tissue is black and collagen red. Atherosclerotic plaque seen on top. Media with some disruption of elastin (black area).

Front

Describe the pathological features of this aortic section not involved with the aneurysm.

Back

- Large overlying plaque impedes O2 from nourishing the inner aspect of the media - Weakening of the media with loss of smooth muscle - Wall bulges forming a dip on the lumen aspect - Turbulent blood flow through dip results in thrombus formation - Further thinning and weakening and further thrombus formation establish the aneurysm

Front

Order these events chronologically in the pathogenesis of atherosclerotic aneurysm: - Weakening of the media with loss of smooth muscle - Further thinning and weakening and further thrombus formation established the aneurysm - Turbulent blood flow through dip results in thrombus formation - Large overlying plaque impedes O2 from nourishing the inner aspect of the media - Wall bulges forming a dip on the lumen aspect

Back

- Presentation as an abdominal mass - Source of distal emboli - Rupture into the abdominal cavity - Occlusion of branch vessels of the aorta

Front

What complications can result from aortic aneurysms?

Back

- Onset of intense crushing chest pain - May radiate to the jaw and left arm - Sweating, nausea and vomiting

Front

Describe the clinical symptoms of myocardial infarction.

Back

Well done :D :D

Front

This image is a helpful diagram of the last flashcard :D

Back

- Dead muscle does not conduct electrical impulses and this can be detected with the ECG - Typically ST elevation in leads associated with the area of myocardial damage is seen

Front

Describe the ECG changes characteristic of myocardial infarction.

Back

Section 8

(50 cards)

• Results from a cycle of obstruction/infection → damage to airways → healing by fibrosis → dilation →accumulation of mucus → obstruction/infection. • With continual inflammation and fibrosis, the small airways may become obstructed by fibrosis.

Front

What causes bronchiectasis and what does it lead to?

Back

Focus of inflammation in lung is around airways.

Front

What is meant by bronchocentric inflammation?

Back

The permanent dilation of bronchi and bronchioles.

Front

What is bronchiectasis?

Back

• Metaplasia of the normal respiratory epithelium to squamous epithelium • Hyperbolas of the mucus components of the bronchial glands with loss of serous glands • Basement membrane thickened • Smooth muscle is hypertrophied due to constant coughing.

Front

Describe the histology of the chronic bronchitis in this section of bronchi wall.

Back

Viable fibres at the top of the image. Dead fibers at the bottom, have no nuclei, loss of striations, decreased in size and surrounded by neutrophils.

Front

Describe the histology of this image:

Back

• Local/diffuse • External compression

Front

What are the two types of airway obstruction?

Back

• Goblet cell hyperplasia • Infiltrates of neutrophils, macrophages and T and B cells • Thickening of bronchiole walls due to peribronchiolar fibrosis and muscle hypertrophy

Front

Describe the inflammatory effects of smoking in young people.

Back

Centrilubular (acinar)

Front

What type of emphysema is shown in this image?

Back

• Hairs • Turbinates • Mucosal lysosomes and immunoglobulins (IgA)

Front

What immunological defences are found in the nose?

Back

Common, noncancerous, teardrop-shaped growths that form in the nose or sinuses.

Front

What are nasal polyps?

Back

• The dilated airways contain mucus plugs (white regular circular outline). • Irregular pink areas surrounding the airways are foci of pneumonia - the infection has spread to the parenchyma from the airway.

Front

Describe this image of lungs with bronchiectasis from a patient with cystic fibrosis.

Back

Mural thrombus.

Front

What pathological process is featured in this image?

Back

Spiral shaped mucus plugs that may contain desquamated epithelium that may be seen in the airways of some asthmatics.

Front

What is a Curschmann's spiral?

Back

• Obstruction of the lumen (foreign body, intraluminal tumour, mucus, increased thickness of the wall) • Fibrosis of the bronchial wall (result of damage to the wall followed by healing)

Front

Describe local/diffusion obstruction.

Back

Protect from aspiration.

Front

What is the purpose of the glottic and cough reflexes?

Back

Green - goblet cell hyperplasia Blue - thickened basement membrane Yellow - eosinophil infiltration Red - muscle hypertrophy

Front

Describe the points indicated by shapes in this bronchiole of an asthmatic.

Back

Inflammatory mediators from epithelial cells, alveolar macrophage and migrated leucocytes, especially, proteases (elastase) and oxidative species.

Front

What is the cause of alveolar wall destruction in emphysema?

Back

Act as a diuretic but have the benefit of sparing potassium loss. E.g. Spironolactone.

Front

Why are aldosterone antagonists used? Give a drug example.

Back

Panacinar

Front

What type of emphysema is shown in this image?

Back

Increase urine output decreasing blood volume. E.g. thiazide family of diuretics are the most commonly used.

Front

Why are diuretics used? Give a drug example.

Back

• Childhood onset • May be preceded by eczema • Commonly associated with rhinitis • Generally responds well to treatment • Specific IgE testing positive • Most common allergens indoor

Front

What is allergic asthma?

Back

An inherited autosomal recessive monogenic disorder presenting as a multisystem disease.

Front

What is cystic fibrosis?

Back

• Centrilobular (acinar) • Panacinar

Front

What are the two types of emphysema?

Back

• Early phase response - Type I hypersensitivity - IgE antibody with mast cells • Late phase response - Type IV hypersensitivity - T cell mediated response activates eosinophils, B cells, others

Front

Describe the early and late phase response of airway inflammation.

Back

• Goblet cell hyperplasia • Macrophage accumulation with destruction of elastic tissue • Fibrosis around bronchioles • May result in obliteration of the bronchiole

Front

Describe the histology of the chronic bronchitis in this section of small airway wall.

Back

1. Airway inflammation 2. Bronchial hyper-responsiveness 3. Bronchoconstriction 4. Bronchial wall oedema 5. Excess mucus secretion 6. Epithelial shedding 7. Airway remodelling

Front

Describe the pathophysiology of asthma.

Back

Mucociliary stream - removes particles from inhaled air and moves them up to the pharynx to be swallowed.

Front

What immunological defences are found in the major airways?

Back

Macrophages phagocytose foreign particles and microorganisms.

Front

What immunological defences are found in the alveolar?

Back

Obstruction of the airway as a result of tumour.

Front

Describe external compression obstruction?

Back

• Mucus hyper secretion • Airway oedema • Fibrosis of the bronchiolar walls • Bronchoconstriction

Front

How does persistent inflammation from smoke exposure lead to small airways disease in chronic bronchitis?

Back

Leads to loss of elastic recoil with collapse of the airways during expiration (pursed lip breathing).

Front

What effect does alveolar wall break down have during expiration?

Back

A condition of reversible airways obstruction.

Front

What is asthma?

Back

Rupture of free wall of ventricle

Front

What pathological process is featured in this image?

Back

The destruction of the alveolar walls distal to the terminal bronchiole resulting in irreversible enlargement of the airspaces. Fibrosis is not obvious. Smaller airways fibrosis contributes to obstruction.

Front

What is emphysema?

Back

Chest is hyper-inflated: • Diaphragms are flat • Lung markings reduced • Expansion of lung tissue in the apices • Ribs are parallel in orientation • Heart shadow is narrowed

Front

Describe the appearance of this emphysema chest x-ray.

Back

Unable to move chloride ions out of a cell causing sticky mucus to build up on the outside of the cell.

Front

Describe the effect of the cystic fibrosis mutation on the CFTR channel.

Back

Cough productive of sputum on most days for 3 months of at least 2 successive years. An epidemiological definition. Does not imply airway inflammation.

Front

What is chronic bronchitis?

Back

Often bilateral basal patchy opacification, relating to the focal nature of the consolidation.

Front

Describe the common pattern observed for bronchopneumonia on a CXR.

Back

Ventricular aneurysm, formed due to stretching and expansion of an old area of scarring in the myocardium. It may rupture.

Front

Describe the pathology of this image.

Back

• Mucus plugging lumen • Hyperplasia of smooth muscle • Thickened basement membrane

Front

Describe the pathology of this section of bronchus from asthma death.

Back

Ruptured papillary muscle

Front

What pathological process is featured in this image?

Back

Centrilobular affects the respiratory bronchioles, while panacinar emphysema affects the alveoli and alveolar ducts.

Front

What is the difference between centrilobular (acinar) and panacinar emphysema?

Back

• Late onset (adulthood) • Allergy tests negative • Commonly associated with sinusitis and nasal polyps • Responds less well to treatment • Needs higher doses of steroids to control

Front

What is intrinsic asthma?

Back

Sammich.

Front

Diffuse obstructive airway disease has something to do with small airway disease e.g. emphysema, chronic bronchitis, asthma.

Back

Acinus (respiratory bronchiole, alveolar ducts and alveoli): • Loss of elastic recoil • Gas exchange becomes difficult → air becomes trapped

Front

Describe the effects of emphysema?

Back

Yay :)

Front

Look a model of everything you just read!

Back

• Loss of airflow and collapse of dependent lung as gases reabsorbed into circulation • Mucus drainage ceases and macrophages ingest 'this material' and remain in local area resulting in lipoid pneumonia • If the obstruction is chronic infection may follow eventually leading to bronchiectasis.

Front

Describe the effects of localised obstruction.

Back

• Allergy • Infection • Cold • Exertion • Irritation • Drugs • Occupation exposure • Exercise

Front

Give some examples of asthma triggers.

Back

• Smoking • Atmospheric pollution • Genetic factors

Front

What are the risk factors of COPD?

Back

• Chemokines and cytokines maintain myofibroblasts in an activated state • Activated myofibroblasts produce increased levels of matrix protein leading to airway wall thickening • Activated myofibroblasts are also involved in increasing smooth muscle mass leading to lumen reduction

Front

Describe the causes of airway remodelling.

Back

Section 9

(29 cards)

Mycoplasma: a bacteria that lacks a cell wall. Common cause in children.

Front

What is mycoplasma atypical pneumonia?

Back

Mycoplasma, viruses, chlamoydophila (chlamydia) pneumoniae.

Front

What are the causative organisms of atypical pneumonia.

Back

Pneumonia where the clinical symptoms appear worse than the clinical findings. Severe upper respiratory tract infection with fever, headache and muscle aches.

Front

What is atypical pneumonia?

Back

• Fever • Dry cough • Dyspnoea

Front

How do patients with pneumocystis present?

Back

The alveoli walls are extended by the dense lymphocytic infiltrate. Alveolar spaces are clear.

Front

Describe the histology of this image taken from a case of mycoplasma pneumonia.

Back

Inflammation of the interstitial of the septa and the alveolar walls - oedema and infiltration by mononuclear cells predominantly lymphocytes and macrophages. Alveolar exudate is minimal except in severe infections.

Front

Describe the histological appearance of atypical pneumonia.

Back

Kills type one pneumocytes, leading to asphyxiation.

Front

How does pneumocystis cause death?

Back

Enzymatic digestion of the exudate with expectoration, phagocytosis by macrophages.

Front

Describe the resolution stage of lobar pneumonia.

Back

Elimination of causative organism where possible.

Front

What is the treatment for atypical pneumonia?

Back

• Congestion • Red hepatization • Grey hepatization • Resolution

Front

What are the four stages of lobar pneumonia?

Back

Grats.

Front

Lookie here!

Back

Bilateral perihilar and basal infiltrates.

Front

How does pneumocystis appear on a chest x-ray?

Back

Alveolar spaces filled with proteinaceous (fibrin) exudate, abundant neutrophils and red cells.

Front

Describe the red hepatization stage of lobar pneumonia.

Back

• Gram -ve bacilli • Gram +ve cocci

Front

What types of bacteria are common in nosocomial pneumonia?

Back

Disintegration of red cells with haemosiderin containing macrophages. There is persistence of the fibrosuppurative exudate.

Front

Describe the grey hepatization stage of lobar pneumonia.

Back

• Alveoli contain a frothy pink exudate - dead type I pneumocytes • Organism stains silver and cup shaped • Thickened, oedematous alveoli walls which contain scant mononuclear infiltrate

Front

Describe the histological effects of pneumocystis.

Back

Patchy interstitial thickening in the periportal and basal areas.

Front

Describe the x-ray findings for atypical pneumonia.

Back

IgM binds to I antigen on RBC in cooler periphery and C3 binds to IgM. When blood is warmed centrally IgM is released but C3 remains bound. This C3 acts as an opsonin and RBCs are phagocytosed.

Front

How does cold agglutinin cause RBC phagocytosis?

Back

Low grade bacterial pathogens: • CMV • Pneumocystis carinii And fungi and yeasts

Front

Which organisms cause opportunistic pneumonia?

Back

Expulsion of matter, as phlegm, from the throat or lungs.

Front

What is expectoration?

Back

Caused by Pneumocystis jiroveci fungus. Part of microflora of some people. Causes opportunistic infection (common in AIDS).

Front

What is pneumocystis?

Back

Streptococcus pneumoniae (90-95% cases).

Front

What is the most common microbe that causes lobar pneumonia?

Back

• Influenze • Respiratory Syncytial Virus • Measles • Adenoviruses • Others

Front

Which viruses can cause viral pneumonia?

Back

An autoimmune disease characterized by the presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells.

Front

What is cold agglutinin?

Back

• Abrupt onset • Fever • Shaking chills • Productive cough • Pleuritic chest pain • Dyspnea, tachypnea, hypoxia

Front

Describe the clinical features of pneumococcal pneumonia in adults.

Back

Involves usually a single lobe of the lung.

Front

What is the common distribution of lobar pneumonia.

Back

Hospital acquired pneumonia, developing 2-3 days after admission.

Front

What is nosocomial pneumonia?

Back

• Vomiting • Oesophageal lesions • Obstetric anaesthesia • Neuromuscular disorders • Sedation

Front

Give five ways in which aspiration pneumonia is commonly caused.

Back

Vascular dilation, intraalveolar fluid with a few neutrophils and bacteria.

Front

Describe the congestion stage of lobar pneumonia.

Back