10/03/2021 [leg muscles, leg dermatomes, disc prolapse, physiology of immnunity, rheumatic fever, sarcoidosis, inhaler use, uveitis, anatomy of the eye, Bechette's disease, Omdamzatron]

Question 1

Muscles int he anterior compartment of the leg?

Answer 1

Tibialis anterior, extensor digitorun longus, exntensor hallucis longus and fibularis tertius

Question 2

Collectively what do the anterior leg muscles do?

Answer 2

Dorsiflex and invert eh footy at the ankle joint

Question 3

Whihch muscles extend the toes

Answer 3

Extensor digitorum longus and extensor hallucis longus

Question 4

Innervation of the muscles

Answer 4

Deep fibular nerve [L4-S1]

Question 5

Blood supply anterior muscles leg

Answer 5

Anterior tibial artery

Question 6

Location, action, attachments, innervation of the tibilias anterio

Answer 6

The tibialis anterior muscle is located alongside the lateral surface of the tibia. Attachments: Originates from the lateral surface of the tibia, attaches to the medial cuneiform and the base of metatarsal I. Actions: Dorsiflexion and inversion of the foot. Innervation: Deep fibular nerve.

Question 7

Extensor digiroum longus

Answer 7

The extensor digitorum longus lies lateral and deep to the tibialis anterior. The tendons of the EDL can be palpated on the dorsal surface of the foot. Attachments: Originates from the lateral condyle of the tibia and the medial surface of the fibula. The fibres converge into a tendon, which travels to the dorsal surface of the foot. The tendon splits into four, each inserting onto a toe. Actions: Extension of the lateral four toes, and dorsiflexion of the foot. Innervation: Deep fibular nerve

Question 8

How can you test the power of the tibilias anteiror?

Answer 8

To test the power of the tibialis anterior, the patient can be asked to stand on their heels.

Question 9

Which is the strongest muscle santerior compartmetn?

Answer 9

Tibilias anterior

Question 10

Extnesor hallucis longus

Answer 10

The extensor hallucis longus is located deep to the EDL and TA. Attachments: Originates from the medial surface of the fibular shaft. The tendon crosses anterior to the ankle joint and attaches to the base of the distal phalanx of the great toe. Action: Extension of the great toe and dorsiflexion of the foot. Innervation: Deep fibular nerve

Question 11

Fibularis tertarius

Answer 11

The fibularis tertius muscles arises from the most inferior part of the EDL. It is not present in all individuals and is considered by some texts as a part of the extensor digitorum longus. Attachments: Originates with the extensor digitorum longus from the medial surface of the fibula. The tendon descends with the EDL, until they reach the dorsal surface of the foot. The fibularis tertius tendon then diverges and attaches to metatarsal V. Actions: Eversion and dorsiflexion of the foot. Innervation: Deep fibular nerve

Question 12

When does footdrop occur? Sx of it

Answer 12

Footdrop is a clinical sign indicating paralysis of the muscles in the anterior compartment of the leg. It typically occurs as a consequence of damage to the common fibular (peroneal) nerve – from which the deep fibular nerve arises. In footdrop, the muscles in the anterior compartment are paralysed. The unopposed pull of the muscles in the posterior leg produce permanent plantarflexion. This can interfere with walking – as the affected limb can drag along the ground. To circumvent this, the patient can flick the foot outwards while walking – known as an ‘eversion flick

Question 13

Which muscle porduces eversioin of the subtalar joint?

Answer 13

Fibularis tertaius

Question 14

Muscles in the lateral compartment of the leg

Answer 14

There are two muscles in the lateral compartment of the leg; the fibularis longus and brevis (also known as peroneal longus and brevis)

Question 15

Function of the muscles in the lateral compartment

Answer 15

The common function of the muscles is eversion – turning the sole of the foot outwards. They are both innervated by the superficial fibular nerve

Question 16

Attahcments, actions, innervation, location of the fibularis longus

Answer 16

The fibularis longus is the larger and more superficial muscle within the compartment. Attachments The fibularis longus originates from the superior and lateral surface of the fibula and the lateral tibial condyle. The fibres converge into a tendon, which descends into the foot, posterior to the lateral malleolus. The tendon crosses under the foot, and attaches to the bones on the medial side, namely the medial cuneiform and base of metatarsal I. Actions: Eversion and plantarflexion of the foot. Also supports the lateral and transverse arches of the foot. Innervation: Superficial fibular (peroneal) nerve, L4-S1

Question 17

Fibularis brevis

Answer 17

The fibularis brevis muscles is deeper and shorter than the fibularis longus. Attachments: Originates from the inferolateral surface of the fibular shaft. The muscle belly forms a tendon, which descends with the fibularis longus into the foot. It travels posteriorly to the lateral malleolus, passing over the calcaneus and the cuboidal bones. The tendon then attaches to a tubercle on metatarsal V. Actions: Eversion of the foot. Innervation: Superficial fibular (peroneal) nerve, L4-S1.

Question 18

How can the common fibular nerve be lcoated?

Answer 18

The common fibular nerve can be a difficult structure to identify. However, it can be located using the fibularis longus as an anatomical landmark. There is a small space between the parts of the fibularis longus that originate from the head of the fibula, and the neck of the fibula. The common fibular nerve passes through this gap, and is easily identified. After passing through the gap, the nerve terminates by bifurcating into two terminal branches; the deep and superficial fibular nerve

Question 19

Which nerve innervated lateral compartment leg?

Answer 19

Superficial fibular

Question 20

How is the posterior compartment leg seperated?

Answer 20

The posterior compartment of the leg contains seven muscles, organised into two layers – superficial and deep. The two layers are separated by a band of fascia

Question 21

Function of the posterior leg muscles? Innervation too.

Answer 21

The posterior leg is the largest of the three compartments. Collectively, the muscles in this area plantarflex and invert the foot. They are innervated by the tibial nerve, a terminal branch of the sciatic nerve

Question 22

Where do all the calf muscles insert?

Answer 22

The superficial muscles form the characteristic ‘calf’ shape of the posterior leg. They all insert into the calcaneus of the foot (the heel bone), via the calcaneal tendon.

Question 23

What does the calcaneal reflex test?

Answer 23

nerve roots S1-2

Question 24

To minimise friction duyring movement, what is located with the calcaneal tendon?

Answer 24

To minimise friction during movement, there are two bursae (fluid filled sacs) associated with the calcaneal tendon: Subcutaneous calcaneal bursa – lies between the skin and the calcaneal tendon. Deep bursa of the calcaneal tendon – lies between the tendon and the calcaneus

Question 25

Location, attahcments, actions, innervation of the gastrocnemius

Answer 25

The gastrocnemius is the most superficial of all the muscles in the posterior leg. It has two heads – medial and lateral, which converge to form a single muscle belly. Attachments: The lateral head originates from the lateral femoral condyle, and medial head from the medial femoral condyle. The fibres converge, and form a single muscle belly. In the lower part of the leg, the muscle belly combines with the soleus to from the calcaneal tendon, with inserts onto the calcaneus (the heel bone). Actions: It plantarflexes at the ankle joint, and because it crosses the knee, it is a flexor there. Innervation: Tibial nerve.

Question 26

Plantaris

Answer 26

Plantaris The plantaris is a small muscle with a long tendon, which can be mistaken for a nerve as it descends down the leg. It is absent in 10% of people. Attachments: Originates from the lateral supracondylar line of the femur. The muscle descends medially, condensing into a tendon that runs down the leg, between the gastrocnemius and soleus. The tendon blends with the calcaneal tendon. Actions: It plantarflexes at the ankle joint, and because it crosses the knee, it is a flexor there. It is not a vital muscle for these movements. Innervation: Tibial nerve.

Question 27

Soleus

Answer 27

The soleus is located deep to the gastrocnemius. It is large and flat, named soleus due to its resemblance of a sole – a flat fish. Attachments: Originates from the soleal line of the tibia and proximal fibular area. The muscle narrows in the lower part of the leg, and joins the calcaneal tendon. Actions: Plantarflexes the foot at the ankle joint. Innervation: Tibial Nerve

Question 28

name all the superficial muscles calf

Answer 28

gastrocnemius, plantaris, soleus

Question 29

name all the depp muscles in the calf

Answer 29

popliteus, tibialis posterior, flexor digitorium longus, flexor hallucis longus

Question 30

Popliteus

Answer 30

The popliteus is located superiorly in the leg. It lies behind the knee joint, forming the base of the popliteal fossa. There is a bursa (fluid filled sac) that lies between the popliteal tendon and the posterior surface of the knee joint. It is called the popliteus bursa. Attachments: Originates from the lateral condyle of the femur and the posterior horn of the lateral meniscus. From there, it runs inferomedially towards the tibia and inserts above the origin of the soleus muscle. Actions: Laterally rotates the femur on the tibia – ‘unlocking’ the knee joint so that flexion can occur. Innervation: Tibial nerve.

Question 31

Tibialis posterior

Answer 31

The tibialis posterior is the deepest out of the four muscles. It lies between the flexor digitorum longus and the flexor hallucis longus. Attachments: Originates from the interosseous membrane between the tibia and fibula, and posterior surfaces of the two bones. The tendon enters the foot posterior to the medial malleolus, and attaches to the plantar surfaces of the medial tarsal bones. Actions: Inverts and plantarflexes the foot, maintains the medial arch of the foot. Innervation: Tibial nerve.

Question 32

Flexor digitorum longus

Answer 32

The FDL is (surprisingly) a smaller muscle than the flexor hallucis longus. It is located medially in the posterior leg. Attachments: Originates from the medial surface of the tibia, attaches to the plantar surfaces of the lateral four digits. Actions: Flexes the lateral four toes. Innervation: Tibial nerve

Question 33

Flexor hallucis longus

Answer 33

The flexor hallucis longus muscle is found on the lateral side of leg. This is slightly counter-intuitive, as it is opposite the great toe, which it acts on. Attachments: Originates from the posterior surface of the fibula, attaches to the plantar surface of the phalanx of the great toe. Actions: Flexes the great toe. Innervation: Tibial nerve.

Question 34

Which muscle in the deep calf acts on only one joint?

Answer 34

Popliteal on the knee

Question 35

Nerves C2-4

Answer 35

Skin of the neck

Question 36

Nerves C5-T1

Answer 36

Arms

Question 37

Nerves T2 to L2

Answer 37

Chest and abdomen

Question 38

Nerves L3-S1

Answer 38

skin of the legs

Question 39

Serves S1-S4

Answer 39

groin

Question 40

Cervical spial nerves

Answer 40

C2: lower jaw, back of the head C3: upper neck, back of the head C4: lower neck, upper shoulders C5: area of the collarbones, upper shoulders C6: shoulders, outside of arm, thumb C7: upper back, back of arm, pointer and middle finger C8: upper back, inside of arm, ring and little finger

Question 41

Thoracic spinal nerves

Answer 41

T1: upper chest and back, armpit, front of arm T2: upper chest and back T3: upper chest and back T4: upper chest (area of nipples) and back T5: mid-chest and back T6: mid-chest and back T7: mid-chest and back T8: upper abdomen and mid-back T9: upper abdomen and mid-back T10: abdomen (area of belly button) and mid-back T11: abdomen and mid-back T12: lower abdomen and mid-back

Question 42

Lumbircal spinal nerves

Answer 42

L1: lower back, hips, groin L2: lower back, front and inside of thigh L3: lower back, front and inside of thigh L4: lower back, front of thigh and calf, area of knee, inside of ankle L5: lower back, front and outside of calf, top and bottom of foot, first four toes

Question 43

Sacral spinal nerves

Answer 43

S1: lower back, back of thigh, back and inside of calf, last toe S2: buttocks, genitals, back of thigh and calf S3: buttocks, genitals S4: buttocks S5: buttocks

Question 44

Coccygeal spinal nerves

Answer 44

buttocks, area of tailbone

Question 45

What is a slipped disc?

Answer 45

When you have a ‘slipped’ (prolapsed) disc, a disc does not actually slip. What happens is that part of the inner softer part of the disc (the nucleus pulposus) bulges out (herniates) through a weakness in the outer part of the disc. A prolapsed disc is sometimes called a herniated disc. The bulging disc may press on nearby structures such as a nerve coming from the spinal cord. Some inflammation also develops around the prolapsed part of the disc. Inflammation may irritate a nerve and also causes swelling, which may put pressure on a nerve.

Question 46

Prognosis slipped disc?

Answer 46

In most cases, the symptoms tend to improve over a few weeks. Research studies of repeated magnetic resonance imaging (MRI) scans have shown that the bulging prolapsed portion of the disc tends to shrink (regress) over time in most cases. The symptoms then tend to ease and, in most cases, go away completely. About 50 out of every 100 people improve within 10 days, and 75 out of a 100 after four weeks. In only about 2 out of every 100 people with a ‘slipped’ (prolapsed) disc is the pain still bad enough after 12 weeks that they end up having to have surgery (see below

Question 47

What are chemokines?

Answer 47

Chemokines induce chemotaxis (chemical-induced migration) in local cells. Following the release of chemokines, local cells are attracted to these proteins and follow their concentration gradient to the source, where the concentration is highest. The source is where the chemokines were originally released and where the cells attracted are most needed. They are mainly produced by macrophages during infection, for example, Interleukin-8 (IL-8) recruits neutrophils to the site during the acute phase response. Cells need chemokine receptors to respond to these cytokines. Chemokine receptors are G protein-coupled receptors which activate phospholipase C, leading to the release of calcium from intracellular stores. This, subsequently, gives rise to several downstream effects including, cytoskeletal changes, pseudopod formation and enhanced cell adhesion through integrins

Question 48

Pro-inflammatory action of chemokines

Answer 48

Chemokines can have many actions within tissues. These can be: Pro-inflammatory – for instance, recruiting immune cells to the site of infection or injury. These chemokines are inducible. Cells produce or upregulate pro-inflammatory chemokines in response to infection or trauma. Chemokine secretion is stimulated by other pro-inflammatory cytokines (TNF α, IFN γ) or microbial products (lipopolysaccharide). Pro-inflammatory chemokines allow immune cells such as neutrophils and monocytes to exit the bone marrow and hone into affected tissues.

Question 49

Homeostatic actions of chemokines

Answer 49

Homeostatic – for instance, attracting cells required for angiogenesis and allowing for the growth of new blood vessels. These chemokines are constitutively produced. In other words, the body maintains basal levels without the need for a specific stimulus. For example, stromal cells within the bone marrow secrete CXCL12 which binds to its receptor, CXCR4, and this helps to retain neutrophils in the bone marrow until they are mobilised into the circulation during infection. Chemokines are involved in immune surveillance and allow T cells and dendritic cells to migrate and circulate through secondary lymphoid organs in search of potential pathogens. Chemokines are also key to the development of lymph organs and positioning of cells within lymphoid tissues. for example, a specific subset of B cells- responsible for mounting T-independent responses and producing IgM against encapsulated bacteria – localise to the marginal zone in the spleen through CXCR7. Note: some chemokines have both pro-inflammatory and homeostatic roles

Question 50

What are the three main groups of interferons?

Answer 50

Interferons are a type of cytokine released by host cells in response to pathogens (e.g. viruses and bacteria) and tumour cells. They are grouped according to their complementary receptor. There are three main groups: type I (interferon-α and interferon-β); type II (interferon-γ) and type III (Interferon λ). Type III has similar actions to type I and type II

Question 51

Role of type 1 interferons

Answer 51

Type-I Interferons Almost any body cell can produce type-I interferons, including fibroblasts, endothelial cells and macrophages. Type I interferons such as Interferon-α and interferon-β interfere with viral replication and help the immune system fight viral infections. They are expressed in response to microbial products. Once secreted by the infected cell, they bind to the interferon receptors on the same cell and neighbouring cells. This autocrine and paracrine signalling causes changes in gene expression within the cell. As a result, this leads to the destruction of viral mRNA and prevents host and viral protein translation. They also upregulate NK cell ligands and MHC I on the cell surface. Therefore, NK cells and cytotoxic T cells are more likely to detect and attack virus-infected cells

Question 52

Role of type 2 interferons

Answer 52

Interferon-γ is a type-II interferon. NK cells, cytotoxic T cells and Th1 cells produce interferon-γ in response to IL-12 and IL-18. Interferon-γ activates macrophages and increases their ability to kill pathogens by enhancing pinocytosis and lysosome function. Type-II interferons also upregulate MHC II expression. This promotes antigen-presentation and effective phagocytosis. Note: there is overlap between interferon-I and interferon-II actions but they are both important for anti-viral and anti-tumour responses

Question 53

What produces interleukins?

Answer 53

Interleukins are another type of cytokine produced by T-lymphocytes, monocytes and macrophages

Question 54

Functions of interleukins

Answer 54

Promoting the production and differentiation of B and T lymphocytes – Specifically, IL-1α/β, IL-4, IL-7 and IL-21. Activating neutrophils and natural killer cells – for example, IL-2, IL-8 and IL-12. Producing detectable signs – interleukin-6 (IL-6) increases body temperature (fever) which inhibits microbial growth. IL-6, additionally, raises acute phase proteins such as C-reactive protein (CRP) which is associated with inflammation. Promoting vascular permeability which causes swelling and allows faster recruitment of cells involved in immunity

Question 55

When are TNF produced?

Answer 55

Tumour necrosis factor (TNF) is a cytokine mainly produced by macrophages when they encounter an endotoxin. However, it can also be produced by other cells of the immune system including, mast cells, B cells and T cells.

Question 56

Function of TNF

Answer 56

Local induction of apoptosis. Increasing local vascular permeability. Neutrophil chemotaxis. Stimulation of a pro-inflammatory state – for instance, by increasing CRP production in the liver and prostaglandin E2 production by macrophages. TNF also induces fever. Suppression of appetite

Question 57

What can high levels of TNF induce?

Answer 57

High concentrations of TNF can induce shock through the increase in vascular permeability and resulting drop in blood pressure. On the other hand, chronic exposure to low levels leads to the syndrome of cachexia which is often seen in chronic infection and cancer

Question 58

Il-a/B, IL-2, IL-4, IL-6, IL-8, IL-10, IL-10, IL-12, IL-17, interferon-alpha, interferon-beta, interferon gamma, TNF-alpha/beta sources and main actions

Answer 58

Important Cytokines and Their Roles Cytokine Main Source Main Actions IL-1 α/ β Macrophages Fever T cell activation Macrophage activation IL-2 T helper 1 cells T cell growth B cell growth NK cell growth IL-4 T helper 2 cells Activation and growth of B cells Induces differentiation of CD4 T cells into T helper 2 cells IL-6 Macrophages Fever Production of acute phase proteins Lymphocyte activation Stimulates antibody production IL-8 Macrophages Chemotaxis of neutrophils Activation of neutrophils IL-10 T helper 2 cells Macrophages Inhibits immune function IL-12 Macrophages Activation of NK cells Induces differentiation of CD4 T cells into T helper 1 cells IL-17 T helper 17 cells Induces inflammatory response Recruits neutrophils Interferon-α T cells B cells Monocytes/Macrophages Inhibits viral replication Interferon-β T cells B cells Monocytes/Macrophages Inhibits viral replication Interferon-γ T helper 1 cells NK cells Activation of macrophages Activation of NK cells Inhibits viral replication Increases expression of MHC class I and II Inhibits T helper 2 cells TNF-α/β T helper cells Macrophages Activation of macrophages Nitric oxide production Induces inflammatory response Fever Shock

Question 59

When are interferons, interleuekens, TNF use in therapy?

Answer 59

Cytokines (literally “cell movement”) are a group of small proteins used in cell–signalling. They are produced by a wide range of cells, including macrophages, lymphocytes, mast cells, endothelial cells and fibroblasts. They are responsible for producing some of the cardinal signs of inflammation and influence both the innate and adaptive immune responses. There are different types of cytokines including chemokines, interferons, interleukins, lymphokines and tumour necrosis factors. In this article we will look at different classes of cytokine and their actions. Chemokines Chemokines induce chemotaxis (chemical-induced migration) in local cells. Following the release of chemokines, local cells are attracted to these proteins and follow their concentration gradient to the source, where the concentration is highest. The source is where the chemokines were originally released and where the cells attracted are most needed. They are mainly produced by macrophages during infection, for example, Interleukin-8 (IL-8) recruits neutrophils to the site during the acute phase response. Cells need chemokine receptors to respond to these cytokines. Chemokine receptors are G protein-coupled receptors which activate phospholipase C, leading to the release of calcium from intracellular stores. This, subsequently, gives rise to several downstream effects including, cytoskeletal changes, pseudopod formation and enhanced cell adhesion through integrins. Chemokine actions Chemokines can have many actions within tissues. These can be: Pro-inflammatory – for instance, recruiting immune cells to the site of infection or injury. These chemokines are inducible. Cells produce or upregulate pro-inflammatory chemokines in response to infection or trauma. Chemokine secretion is stimulated by other pro-inflammatory cytokines (TNF α, IFN γ) or microbial products (lipopolysaccharide). Pro-inflammatory chemokines allow immune cells such as neutrophils and monocytes to exit the bone marrow and hone into affected tissues. Homeostatic – for instance, attracting cells required for angiogenesis and allowing for the growth of new blood vessels. These chemokines are constitutively produced. In other words, the body maintains basal levels without the need for a specific stimulus. For example, stromal cells within the bone marrow secrete CXCL12 which binds to its receptor, CXCR4, and this helps to retain neutrophils in the bone marrow until they are mobilised into the circulation during infection. Chemokines are involved in immune surveillance and allow T cells and dendritic cells to migrate and circulate through secondary lymphoid organs in search of potential pathogens. Chemokines are also key to the development of lymph organs and positioning of cells within lymphoid tissues. for example, a specific subset of B cells- responsible for mounting T-independent responses and producing IgM against encapsulated bacteria – localise to the marginal zone in the spleen through CXCR7. Note: some chemokines have both pro-inflammatory and homeostatic roles. Pen1234567. Derivative of image by Kohidai, L. / CC BY-SA (https://creativecommons.org/licenses/by-sa/3.0) Fig 1 – Diagram demonstrating the process of chemotaxis. The cell moves along the concentration gradient of chemokine to reach the area of highest concentration. Interferons Interferons are a type of cytokine released by host cells in response to pathogens (e.g. viruses and bacteria) and tumour cells. They are grouped according to their complementary receptor. There are three main groups: type I (interferon-α and interferon-β); type II (interferon-γ) and type III (Interferon λ). Type III has similar actions to type I and type II. Interferon actions These cytokines have a number of roles : Type-I Interferons Almost any body cell can produce type-I interferons, including fibroblasts, endothelial cells and macrophages. Type I interferons such as Interferon-α and interferon-β interfere with viral replication and help the immune system fight viral infections. They are expressed in response to microbial products. Once secreted by the infected cell, they bind to the interferon receptors on the same cell and neighbouring cells. This autocrine and paracrine signalling causes changes in gene expression within the cell. As a result, this leads to the destruction of viral mRNA and prevents host and viral protein translation. They also upregulate NK cell ligands and MHC I on the cell surface. Therefore, NK cells and cytotoxic T cells are more likely to detect and attack virus-infected cells. Type-II interferons Interferon-γ is a type-II interferon. NK cells, cytotoxic T cells and Th1 cells produce interferon-γ in response to IL-12 and IL-18. Interferon-γ activates macrophages and increases their ability to kill pathogens by enhancing pinocytosis and lysosome function. Type-II interferons also upregulate MHC II expression. This promotes antigen-presentation and effective phagocytosis. Note: there is overlap between interferon-I and interferon-II actions but they are both important for anti-viral and anti-tumour responses. Interleukins Interleukins are another type of cytokine produced by T-lymphocytes, monocytes and macrophages. They have a wide range of functions, including: Promoting the production and differentiation of B and T lymphocytes – Specifically, IL-1α/β, IL-4, IL-7 and IL-21. Activating neutrophils and natural killer cells – for example, IL-2, IL-8 and IL-12. Producing detectable signs – interleukin-6 (IL-6) increases body temperature (fever) which inhibits microbial growth. IL-6, additionally, raises acute phase proteins such as C-reactive protein (CRP) which is associated with inflammation. Promoting vascular permeability which causes swelling and allows faster recruitment of cells involved in immunity. Tumour Necrosis Factor Tumour necrosis factor (TNF) is a cytokine mainly produced by macrophages when they encounter an endotoxin. However, it can also be produced by other cells of the immune system including, mast cells, B cells and T cells. TNF α and β have similar functions, including: Local induction of apoptosis. Increasing local vascular permeability. Neutrophil chemotaxis. Stimulation of a pro-inflammatory state – for instance, by increasing CRP production in the liver and prostaglandin E2 production by macrophages. TNF also induces fever. Suppression of appetite. High concentrations of TNF can induce shock through the increase in vascular permeability and resulting drop in blood pressure. On the other hand, chronic exposure to low levels leads to the syndrome of cachexia which is often seen in chronic infection and cancer. Important Cytokines and Their Roles Cytokine Main Source Main Actions IL-1 α/ β Macrophages Fever T cell activation Macrophage activation IL-2 T helper 1 cells T cell growth B cell growth NK cell growth IL-4 T helper 2 cells Activation and growth of B cells Induces differentiation of CD4 T cells into T helper 2 cells IL-6 Macrophages Fever Production of acute phase proteins Lymphocyte activation Stimulates antibody production IL-8 Macrophages Chemotaxis of neutrophils Activation of neutrophils IL-10 T helper 2 cells Macrophages Inhibits immune function IL-12 Macrophages Activation of NK cells Induces differentiation of CD4 T cells into T helper 1 cells IL-17 T helper 17 cells Induces inflammatory response Recruits neutrophils Interferon-α T cells B cells Monocytes/Macrophages Inhibits viral replication Interferon-β T cells B cells Monocytes/Macrophages Inhibits viral replication Interferon-γ T helper 1 cells NK cells Activation of macrophages Activation of NK cells Inhibits viral replication Increases expression of MHC class I and II Inhibits T helper 2 cells TNF-α/β T helper cells Macrophages Activation of macrophages Nitric oxide production Induces inflammatory response Fever Shock Clinical Relevance - Cytokine Therapy Cytokines are important for promoting and modifying immune responses. Therefore, they are therapeutically administered in some conditions. Interferons: Hepatitis B and C to reduce risk of hepatocellular carcinoma Chronic granulomatous disease to reduce risk of serious infection Hairy cell leukaemia Ovarian tumours Interleukins: Renal carcinoma Melanoma TNF: Ovarian tumours

Question 60

What is sarcoidosis?

Answer 60

Sarcoidosis is a rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin.

Question 61

Sx of sarcoidosis

Answer 61

The symptoms of sarcoidosis depend on which organs are affected, but typically include: tender, red bumps on the skin shortness of breath a persistent cough It’s impossible to predict how sarcoidosis will affect a person, as the condition can affect any organ and the symptoms vary widely depending on which organs are involved. Most people with sarcoidosis develop symptoms suddenly, but they usually clear within a few months or years and the condition does not come back. This is known as acute sarcoidosis. Some people do not have any symptoms at all, and the condition is diagnosed after an X-ray carried out for another reason. A few people find their symptoms develop gradually and get worse over time, to the point where they become severely affected. Lots of granulomas may form in an organ and prevent it from working properly. This is known as chronic sarcoidosis. Sarcoidosis most often affects the lungs, skin and/or lymph nodes (glands).

Question 62

How often are lung Sx in sarcoidosis? What are these?

Answer 62

The lungs are affected in about 90% of people with sarcoidosis. This is known as pulmonary sarcoidosis. The main symptoms are shortness of breath and a persistent dry cough. Some people with pulmonary sarcoidosis experience pain and discomfort in their chest, but this is uncommon

Question 63

Skin Sx in sarcoidosis

Answer 63

The skin is also affected in many people with sarcoidosis. This can cause tender, red bumps or patches to develop on the skin (particularly the shins), as well as rashes on the upper body

Question 64

causes of sarcoidosis?

Answer 64

Causes of sarcoidosis The body’s immune system normally fights off infections by releasing white blood cells into the blood to isolate and destroy the germs. This results in inflammation (swelling and redness) of the body tissues in that area. The immune system responds like this to anything in the blood it does not recognise, and dies down when the infection has been cleared. It’s thought that sarcoidosis happens because the immune system has gone into “overdrive”, where the body starts to attack its own tissues and organs. The resulting inflammation then causes granulomas to develop in the organs. There are many similar conditions, such as rheumatoid arthritis and lupus, that are caused by the body attacking its own tissues. These are collectively known as autoimmune conditions. It’s not known why the immune system behaves like this. It’s possible that some environmental factor triggers the condition in people who are already genetically susceptible to it. Sarcoidosis can occasionally occur in more than one family member, but there’s no evidence that the condition is inherited. The condition is not infectious, so it cannot be passed from person to person

Question 65

Tx of sarcoidosis

Answer 65

How sarcoidosis is treated Most people with sarcoidosis do not need treatment as the condition often goes away on its own, usually within a few months or years. Simple lifestyle changes and over-the-counter painkillers (such as paracetamol or ibuprofen) are often all that’s needed to control the pain of any flare-ups. Doctors will monitor your condition to check if it’s getting any better or worse without treatment. This can be done with regular X-rays, breathing tests and blood tests. Medicines If treatment is recommended, steroid tablets are usually used. This helps relieve symptoms and prevent damage to affected organs by reducing inflammation and preventing scarring. However, steroid tablets can cause unpleasant side effects such as weight gain and mood swings if taken in high doses. Other side effects, such as weakening of the bones (osteoporosis), can also develop if steroids are taken for a long time. Therefore, they’re only used when necessary. You may initially be given a high dose of steroid medicine for a short period of time, before switching to a low dose for the months or years that follow. Your condition will be monitored during this time to see how well the treatment is working. In some cases, taking calcium or vitamin D supplements can help reduce the risk of osteoporosis caused by long-term use of steroid medicine. However, you should only take these if advised to by a doctor. Some people with sarcoidosis may have an increased risk of developing complications, including kidney stones, while taking steroid medicine. Other medicines may sometimes be used if steroids are not enough or there are concerns about side effects. In these cases, a medicine called an immunosuppressant might be recommended. This may help to improve your symptoms by reducing the activity of your immune system

Question 66

Prognosis of sarcoidosis

Answer 66

Symptoms of sarcoidosis may come and go, and can usually be managed with over-the-counter painkillers so they do not affect everyday life. Most people with the condition find their symptoms have disappeared within a few years of their diagnosis. For some people the condition slowly gets worse over time and they end up with organ damage. For example, their lungs may stop working properly, causing increasing breathlessness. Help is available for people with severe, persistent sarcoidosis – ask your doctor for advice and visit SarcoidosisUK (which has a list of support groups) or the British Lung Foundation.

Question 67

Reliever inhalers

Answer 67

Reliever inhalers - contain bronchodilator medicines You can take a reliever inhaler as required to ease symptoms when you are breathless, wheezy or tight-chested. The medicine in a reliever inhaler relaxes the muscle in the airways. This opens the airways wider, and symptoms usually quickly ease. These medicines are called bronchodilators as they widen (dilate) the airways (bronchi). The two main reliever medicines are salbutamol and terbutaline. These come in various brands made by different companies. There are different inhaler devices that deliver the same reliever medicine. Salbutamol brands include Airomir®, Asmasal®, Salamol®, Salbulin®, Pulvinal Salbutamol® and Ventolin®. Terbutaline often goes by the brand name Bricanyl®. These inhalers are often (but not always) blue in colour. Other inhalers containing different medicines can be blue too. Always read the label. If you only have symptoms every now and then, the occasional use of a reliever inhaler may be all that you need. If you need a reliever three times a week or more to ease symptoms, a preventer inhaler is usually advised.

Question 68

Preventer inhalers

Answer 68

Preventer inhalers - usually contain a steroid medicine These are taken every day to prevent symptoms from developing. The type of medicine commonly used in preventer inhalers is a steroid. Steroids work by reducing the inflammation in the airways. When the inflammation has gone, the airways are much less likely to become narrow and cause symptoms such as wheezing. Steroid inhalers are usually taken twice per day. If you have an exacerbation (flare-up) of your asthma symptoms, you may be advised to take the preventer inhaler more often. It takes 7-14 days for the steroid in a preventer inhaler to build up its effect. This means it will not give any immediate relief of symptoms (like a reliever does). After a week or so of treatment with a preventer, the symptoms have often gone, or are much reduced. It can, however, take up to six weeks for maximum benefit. If your asthma symptoms are well controlled with a regular preventer you may then not need to use a reliever inhaler very often, if at all. Inhalers that contain medicines called sodium cromoglicate (brand name Intal®) or nedocromil (brand name Tilade®) are sometimes used as preventers. However, they do not usually work as well as steroids. The main inhaled steroid preventer medications are: Beclometasone. Brands include Asmabec®, Clenil Modulite®, and Qvar®. These inhalers are usually brown and sometimes red in colour. Budesonide. Brands include Easyhaler Budesonide®, Novolizer Budesonide® and Pulmicort®. Ciclesonide. Brand name Alvesco®. Fluticasone. Brand name Flixotide®. This is a yellow-coloured or orange-coloured inhaler. Mometasone. Brand name Asmanex Twisthaler®. Bone strength (density) may be reduced following long-term use of high doses of inhaled corticosteroids. Therefore people who use steroid inhalers for asthma need to make sure they have a good supply of calcium in their diet. Milk is a good source of calcium but dairy products may need to be avoided for some people with asthma. Other good dietary sources of calcium include: Bread. Some vegetables (curly kale, okra, spinach and watercress). Some fruits (eg, dried apricots)

Question 69

LABA inhalers

Answer 69

Long-acting bronchodilator inhalers The medicines in these inhalers function in a similar way to relievers, but work for up to 12 hours after each dose has been taken. They include salmeterol (brand name Serevent® and Neovent®) and formoterol (brand names Atimos®, Foradil®, and Oxis®). A long-acting bronchodilator may be advised in addition to a steroid inhaler if symptoms are not fully controlled by the steroid inhaler alone. Some brands of inhaler contain a steroid plus a long-acting bronchodilator for people who need both to control their symptoms. Examples of combination inhalers are: Fostair® (formoterol and beclometasone). Seretide® (salmeterol and fluticasone). This is a purple-coloured inhaler. Symbicort® (formoterol and budesonide).

Question 70

The four main groups of inhaler devices

Answer 70

Pressurised metered dose inhalers (MDIs). Breath-activated inhalers - MDIs and dry powder inhalers. Inhalers with spacer devices. Nebulisers

Question 71

How to use th estandard inhaler

Answer 71

A standard MDI is shown above. The MDI has been used for over 40 years and is used to deliver various types and brands of medicines. It contains a pressurised inactive gas that propels a dose of medicine in each ‘puff’. Each dose is released by pressing the top of the inhaler. This type of inhaler is quick to use, small, and convenient to carry. It needs good co-ordination to press the canister and breathe in fully at the same time. Sometimes these are known as evohalers (depending upon the manufacturer). The standard MDI is the most widely used inhaler. However, many people do not use it to its best effect. Common errors include: Not shaking the inhaler before using it. Inhaling too sharply or at the wrong time. Not holding your breath long enough after breathing in the contents. Until recently, the propellant gas in MDI inhalers has been a chlorofluorocarbon (CFC). However, CFCs damage the Earth’s ozone layer and so are being phased out. The newer CFC-free inhalers work just as well, but they use a different propellant gas that does not damage the ozone layer.

Question 72

How are breath activate dinhalers used?

Answer 72

Breath-activated inhalers These are alternatives to the standard MDI. Some are still pressurised MDIs, but don’t require you to press a canister on top. The autohaler shown above is an example. Another example of a breath-activated MDI is the easi-breathe inhaler. Other breath-activated inhalers are also called dry powder inhalers. These inhalers do not contain the pressurised inactive gas to propel the medicine. You don’t have to push the canister to release a dose. Instead, you trigger a dose by breathing in at the mouthpiece. Accuhalers, clickhalers, easyhalers, novolizers, turbohalers and twisthalers are all breath-activated dry powder inhalers. You need to breathe in fairly hard to get the powder into your lungs. Some types are shown below. accuhaler turbohaler The individual devices all have some differences in how they are operated but, generally, they require less co-ordination than the standard MDI. They tend to be slightly bigger than the standard MDI.

Question 73

How are spacer devices used?

Answer 73

Spacer devices spacer device Spacer devices are used with pressurised MDIs. There are various types - an example is shown above. The spacer between the inhaler and the mouth holds the medicine like a reservoir when the inhaler is pressed. A valve at the mouth end ensures that the medicine is kept within the spacer until you breathe in. When you breathe out, the valve closes. You don’t need to have good co-ordination to use a spacer device. A face mask can be fitted on to some types of spacers, instead of a mouthpiece. This is sometimes done for young children and babies who can then use the inhaler simply by breathing in and out normally through the mask. There are several different types of spacer. Examples are Able Spacer®, Aerochamber Plus®, Nebuchamber®, Optichamber®, Pocket Chamber®, Volumatic® and Vortex®. Some spacer devices fit all MDIs; others are only compatible with specific brands of inhalers. Tips on using a spacer device. The following are tips if you are prescribed a holding spacer. These have a valve at the mouth end - the spacer in the picture above is an example: If your dose is more than one puff then do one puff at a time. Shake the inhaler before firing each puff. Start breathing in from the mouthpiece as soon as possible after firing the puff. Try to hold your breath for a few moments when you have breathed in. Breathe in and out a few times before firing the next puff. Try to hold your breath for a few moments each time you breathe in. Check that the valve opens and closes with each breath. A face mask can be put on to the valve end for babies and young children. They just breathe normally with their face against the mask. The valve opens and closes with each breath in and out. Hold the spacer slightly tilted with the inhaler end uppermost to help the valve open and close easily. Static charge can build up on the inside of the plastic chamber. This can attract particles of medicine, and reduce the output when the spacer is used. To prevent this, wash the plastic spacer as directed by the maker’s instructions. This is usually before first use, and then about once a month with washing up liquid and water. Let it dry in air without rinsing or wiping

Question 74

How are nebulisers used?

Answer 74

Nebulisers Nebulisers are machines that turn the liquid form of your short-acting bronchodilator medicines into a fine mist, like an aerosol. You breathe this in with a face mask or a mouthpiece. Nebulisers are no more effective than normal inhalers. However, they are extremely useful in people who are very tired (fatigued) with their breathing, or in people who are very breathless. Nebulisers are used mainly in hospital for severe attacks of asthma when large doses of inhaled medicines are needed. They are used less commonly than in the past, as modern spacer devices are usually just as good as nebulisers for giving large doses of inhaled medicines. You do not need any co-ordination to use a nebuliser - you just breathe in and out, and you will breathe in the medicine.

Question 75

Do you get SE from inhalers?

Answer 75

Do you get side-effects from inhalers? At standard inhaled doses, the amount of medicine is small compared with tablets or liquid medicines. Therefore, side-effects tend to be much less of a problem than with tablets or liquid medicines. This is one of their main advantages. However, some side-effects do occur in some people. Read the leaflet that comes with the inhaler for details of possible side-effects. The following just highlights the more common and important ones to be aware of. One problem that might occur when using a steroid inhaler (especially if you are taking a high dose) is that the back of your throat may get sore. Thrush infection in the mouth may develop. This can usually be treated easily with a course of pastilles to suck or liquid that you hold in your mouth. You might also notice that your voice becomes more hoarse. If you rinse your mouth with water and brush your teeth after using a steroid inhaler you are less likely to develop a sore throat or thrush. Also, some inhaler devices (such as spacers) are less likely to cause throat problems. A change to a different device may help if mouth problems or thrush occur. Note: a persistent hoarse voice that does not settle, needs further investigation as it can be due to other causes. If you have this symptom you should tell your GP. If you use a high dose of inhaled steroid over a long time it may be a risk factor for developing osteoporosis. You can help to prevent osteoporosis by taking regular exercise, not smoking, and eating a diet with enough calcium. Children who use an inhaled steroid over a long time should have their growth monitored. There is a small risk that enough steroid may get from the lungs and into the body (via the bloodstream), to delay growth. This risk has to be balanced against the risk of a child with asthma not having a steroid preventer. Long-term ill-health (such as with conditions like severe asthma) could also affect a child’s growth. Steroid medicines may aggravate depression and other mental health problems, and may occasionally cause mental health problems. This is more a concern with steroid tablets but, rarely, can be caused by steroid inhalers. Even a severe form of mental health problem called psychosis may, rarely, be triggered by a steroid inhaler. Seek medical advice if worrying mood or behavioural changes occur

Question 76

Which is the best inhaler device to use?

Answer 76

Which is the best inhaler device to use? This depends on various factors such as: Convenience. Some inhalers are small, can go easily in a pocket, and are quick to use. For example, the standard MDI inhaler. Your age. Children under the age of 6 years generally cannot use dry powder inhalers. This is because such a strong breath is needed to inhale the medicine within the inhaler. Children aged under 12 years generally cannot use standard MDI inhalers without a spacer. Some elderly people find the MDI inhalers difficult to use. Your co-ordination. Some devices need more co-ordination than others. Side-effects. Some of the inhaler medicine hits the back of the throat. Sometimes this can cause problems such as thrush in the mouth. This tends to be more of a problem with higher doses of steroid inhalers. Less medicine hits the throat when using a spacer device. Therefore, a spacer device may be advised if you get throat problems, or need a high dose of inhaled steroid. Often the choice of inhaler is just personal preference. Most GPs and practice nurses have a range of devices to demonstrate, and let you get a feel for them. If you are unhappy with the one you are using then ask your GP or practice nurse if you can try a different type

Question 77

how and when to use steroid inhaler

Answer 77

How and when to use a steroid inhaler There are several types of steroid inhaler, which are used in slightly different ways. A doctor or nurse will show you how to use your inhaler. Make sure you use it exactly as advised. The Asthma UK website has videos explaining how to use the different types of inhaler. You’ll usually need to take 1 or 2 puffs from your inhaler in the morning and 1 or 2 puffs in the evening. It’s important to keep using your inhaler, even if you feel better. It will only stop your symptoms if it’s used every day.

Question 78

If take too much or miss dose, or want ot stop with steroid inhalers

Answer 78

If you miss a dose or take too much If you forget to take a dose, take it as soon as you remember. If it’s nearly time for your next dose, skip the one you missed. Do not take a double dose to make up for a forgotten dose. Accidentally taking too many puffs from a steroid inhaler is unlikely to be harmful if it’s a one-off. Speak to a doctor, nurse or a pharmacist if you’re worried. Using a steroid inhaler too much over a long period can increase your chances of getting side effects. Stopping treatment Do not stop using your inhaler unless you’re advised to by a doctor. When you stop your treatment, you usually need to reduce your dose gradually. This can help avoid unpleasant side effects (withdrawal symptoms), such as severe tiredness, joint pain, being sick and dizziness.

Question 79

SE steroid inhalers, coping with SE, and using with food and alcohol

Answer 79

Side effects of steroid inhalers Steroid inhalers usually cause few or no side effects if used correctly and at normal doses. Some people get: a sore mouth or throat a hoarse or croaky voice a cough oral thrush – a fungal infection that causes white patches, redness and soreness in the mouth nosebleeds If you’re taking a high dose for a long time, there’s also a small chance you could get some of the side effects of steroid tablets, such as an increased appetite, mood changes and difficulty sleeping. You can report any suspected side effect to the Yellow Card scheme. Coping with side effects of steroid inhalers The following tips may help reduce the side effects of steroid inhalers: use your inhaler exactly as you’ve been shown – speak to a doctor or nurse if you’re not sure how to use your inhaler correctly use your inhaler with a spacer, a hollow plastic tube or container with a mouthpiece at one end and a hole for the inhaler at the other rinse your mouth out with water and spit it out or brush your teeth after using your inhaler If you’re taking a high dose for a long period of time, you may be given a steroid treatment card that explains how you can reduce the risk of side effects. Using steroid inhalers with other medicines, food or alcohol Some medicines can interfere with the way steroid inhalers work, but this is uncommon if you’re only taking low doses for a short period. Tell a doctor if you take any other medicines, including herbal remedies and supplements, before starting to use a steroid inhaler. If you’re already using an inhaler, ask a doctor or pharmacist for advice before taking any other medicines, remedies or supplements. You can usually drink alcohol while using a steroid inhaler and you should be able to eat most foods. Do not smoke though, as this can make your medicine less effective and make your symptoms worse

Question 80

Anatomically how is the eyeball split up?

Answer 80

Fibrous, vascular and inner layers

Question 81

What does the fibrous layer consist of? Function of it.

Answer 81

Fibrous Layer The fibrous layer of the eye is the outermost layer. It consists of the sclera and cornea, which are continuous with each other. Their main functions are to provide shape to the eye and support the deeper structures. The sclera comprises the majority of the fibrous layer (approximately 85%). It provides attachment to the extraocular muscles – these muscles are responsible for the movement of the eye. It is visible as the white part of the eye. The cornea is transparent and positioned centrally at the front of the eye. Light entering the eye is refracted by the cornea

Question 82

Whats in the vascular layer of the eye? Describe the parts

Answer 82

Vascular Layer The vascular layer of the eye lies underneath the fibrous layer. It consists of the choroid, ciliary body and iris: Choroid – layer of connective tissue and blood vessels. It provides nourishment to the outer layers of the retina. Ciliary body – comprised of two parts – the ciliary muscle and ciliary processes. The ciliary muscle consists of a collection of smooth muscles fibres. These are attached to the lens of the eye by the ciliary processes. The ciliary body controls the shape of the lens, and contributes to the formation of aqueous humor Iris – circular structure, with an aperture in the centre (the pupil). The diameter of the pupil is altered by smooth muscle fibres within the iris, which are innervated by the autonomic nervous system. It is situated between the lens and the cornea.

Question 83

What’s in the inner layer of the eye?

Answer 83

Inner Layer The inner layer of the eye is formed by the retina; its light detecting component. The retina is composed of two layers: Pigmented (outer) layer – formed by a single layer of cells. It is attached to the choroid, and supports the choroid in absorbing light (preventing scattering of light within the eyeball). It continues around the whole inner surface of the eye. Neural (inner) layer – consists of photoreceptors, the light detecting cells of the retina. It is located posteriorly and laterally in the eye. Anteriorly, the pigmented layer continues but the neural layer does not – this is part is known as the non-visual retina. Posteriorly and laterally, both layers of the retina are present. This is the optic part of the retina. The optic part of the retina can be viewed during ophthalmoscopy. The centre of the retina is marked by an area known as the macula. It is yellowish in colour, and highly pigmented. The macula contains a depression called the fovea centralis, which has a high concentration of light detecting cells. It is the area responsible for high acuity vision. The area that the optic nerve enters the retina is known as the optic disc – it contains no light detecting cells

Question 84

Describe the lens of the eye

Answer 84

The lens of the eye is located anteriorly, between the vitreous humor and the pupil. The shape of the lens is altered by the ciliary body, altering its refractive power. In old age, the lens can become opaque – a condition known as a cataract

Question 85

Describe the anterior and posterior chambers of the eye [bonus: if drainage of aqeuous humor obstructed what is this?]

Answer 85

Anterior and Posterior Chambers There are two fluid filled areas in the eye – known as the anterior and posterior chambers. The anterior chamber is located between the cornea and the iris, and the posterior chamber between the iris and ciliary processes. The chambers are filled with aqueous humor – a clear plasma-like fluid that nourishes and protects the eye. The aqueous humor is produced constantly, and drains via the trabecular meshwork, an area of tissue at the base of the cornea, near the anterior chamber. If the drainage of aqueous humor is obstructed, a condition known as glaucoma can result

Question 86

Eyeball arterail blood supply primarily

Answer 86

Vasculature The eyeball receives arterial blood primarily via the ophthalmic artery. This is a branch of the internal carotid artery, arising immediately distal to the cavernous sinus. The ophthalmic artery gives rise to many branches, which supply different components of the eye. The central artery of the retina is the most important branch – supplying the internal surface of the retina. Occlusion of this artery will quickly result in blindness.

Question 87

Venous drainage eye

Answer 87

Venous drainage of the eyeball is carried out by the superior and inferior ophthalmic veins. These drain into the cavernous sinus, a dural venous sinus in close proximity to the eye

Question 88

Two mian classifications of glaucoma

Answer 88

Glaucoma refers to a group of eye diseases that result in damage to the optic nerve. There are two main clinical classifications of glaucoma: Open angle – where the outflow of aqueous humor through the trabecular meshwork is reduced. It causes a gradual reduction of the peripheral vision, until the end stages of the disease. Closed angle – where the iris is forced against the trabecular meshwork, preventing any drainage of aqueous humor. It is an ophthalmic emergency, which can rapidly lead to blindness

Question 89

What is papilloedema and common causes of it

Answer 89

Papilloedema refers to swelling of the optic disc that occurs secondary to raised intracranial pressure. The optic disc is the area of the retina where the optic nerve enters and can be visualised using an ophthalmoscope. Common causes include: Intracerebral mass lesions Cerebral haemorrhage Meningitis Hydrocephalus In papilloedema, the high pressure within the cranium resists venous return from the eye. This causes fluid to extravasate from blood vessels and collect in the retina, producing a swollen optic disc

Question 90

What is uveitis?

Answer 90

Uveitis is the inflammation of the uvea, the pigmented layer that lies between the inner retina and the outer fibrous layer composed of the sclera and cornea. The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is an ophthalmic emergency and requires a thorough examination by an ophthalmologist or optometrist and urgent treatment to control the inflammation. It is often associated with other ocular problems

Question 91

Sx of uveitis

Answer 91

Anterior uveitis (iritis) Burning of the eye Redness of the eye Blurred vision Photophobia Irregular pupil Signs of anterior uveitis include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates (“KP”) on the posterior surface of the cornea. In severe inflammation there may be evidence of a hypopyon. Old episodes of uveitis are identified by pigment deposits on lens, KPs, and festooned pupil on dilation of pupil. Busacca nodules, inflammatory nodules located on the surface of the iris in granulomatous forms of anterior uveitis such as Fuchs heterochromic iridocyclitis (FHI).[1] Synechia Intermediate uveitis Most common: Floaters, which are dark spots that float in the visual field Blurred vision Intermediate uveitis usually affects one eye. Less common is the presence of pain and photophobia.[2] Posterior uveitis Inflammation in the back of the eye is commonly characterized by: Floaters Blurred visio

Question 92

Causes uveitis

Answer 92

Uveitis is usually an isolated illness, but can be associated with many other medical conditions. In anterior uveitis, no associated condition or syndrome is found in approximately one-half of cases. However, anterior uveitis is often one of the syndromes associated with HLA-B27. Presence of this type of HLA allele has a relative risk of evolving this disease by approximately 15%.[3] The most common form of uveitis is acute anterior uveitis (AAU). It is most commonly associated with HLA-B27, which has important features: HLA-B27 AAU can be associated with ocular inflammation alone or in association with systemic disease. HLA-B27 AAU has characteristic clinical features including male preponderance, unilateral alternating acute onset, a non-granulomatous appearance, and frequent recurrences, whereas HLA-B27 negative AAU has an equivalent male to female onset, bilateral chronic course, and more frequent granulomatous appearance.[4] Rheumatoid arthritis is not uncommon in Asian countries as a significant association of uveitis.[5] Noninfectious or autoimmune causes Behçet disease Crohn’s disease Fuchs heterochromic iridocyclitis Granulomatosis with polyangiitis HLA-B27 related uveitis Juvenile idiopathic arthritis Sarcoidosis Spondyloarthritis (especially seen in ankylosing spondylitis) Sympathetic ophthalmia Tubulointerstitial nephritis and uveitis syndrome Infectious causes Uveitis may be an immune response to fight an infection inside the eye. While representing the minority of patients with uveitis, such possible infections include: brucellosis herpesviruses (herpes zoster ophthalmicus - shingles of the eye) leptospirosis Lyme disease presumed ocular histoplasmosis syndrome syphilis toxocariasis toxoplasmic chorioretinitis tuberculosis Zika fever[6] Associated with systemic diseases Systemic disorders that can be associated with uveitis include:[7][8] ankylosing spondylitis Behçet’s disease chronic granulomatous disease enthesitis inflammatory bowel disease juvenile rheumatoid arthritis Kawasaki’s disease multiple sclerosis polyarteritis nodosa psoriatic arthritis reactive arthritis sarcoidosis systemic lupus erythematosus Vogt–Koyanagi–Harada disease Whipple’s disease Drug related side effects Rifabutin, a derivative of Rifampin, has been shown to cause uveitis.[9] Several reports suggest the use of quinolones, especially Moxifloxacin, may lead to uveitis.[10] White Dot syndromes Occasionally, uveitis is not associated with a systemic condition: the inflammation is confined to the eye and has unknown cause. In some of these cases, the presentation in the eye is characteristic of a described syndrome, which are called white dot syndromes, and include the following diagnoses: acute posterior multifocal placoid pigment epitheliopathy birdshot chorioretinopathy multifocal choroiditis and panuveitis multiple evanescent white dot syndrome punctate inner choroiditis serpiginous choroiditis acute zonal occult outer retinopathy Masquerade syndromes Masquerade syndromes are those conditions that include the presence of intraocular cells but are not due to immune-mediated uveitis entities. These may be divided into neoplastic and non-neoplastic conditions. Non-neoplastic: retinitis pigmentosa intraocular foreign body juvenile xanthogranuloma retinal detachment Neoplastic: retinoblastoma lymphoma malignant melanoma leukemia reticulum cell sarcoma ] THINK JIA MAINLY ANTEIOR UVEITIS

Question 93

What is Behcet’s disease? Sx and Cx, and usual onset

Answer 93

Behçet’s disease (BD) is a type of inflammatory disorder which affects multiple parts of the body.[1] The most common symptoms include painful mouth sores, genital sores, inflammation of parts of the eye, and arthritis.[2][1] The sores typically last a few days.[1] Less commonly there may be inflammation of the brain or spinal cord, blood clots, aneurysms, or blindness.[2][1] Often, the symptoms come and go Sx = Mouth sores, genital sores, inflammation of the eye, arthritis,[2] chronic fatigue Cx = blindness, joint inflammation, blood clots, aneurysms onset = 20 to 40s usually

Question 94

Cause of Behcets, Dx as well.

Answer 94

The cause is unknown.[2] It is believed to be partly genetic.[1] Behçet’s is not contagious.[2] Diagnosis is based on at least three episodes of mouth sores in a year together with at least two of the following: genital sores, eye inflammation, skin sores, a positive skin prick test

Question 95

What is not considered a common potential trigger autoinflammatory conditions?

Answer 95

Cold, immunisations, infections, stress yes. Allergies no!

Question 96

systemic effects of IL-1B

Answer 96

skin rash, vasdilation, hypotension, haematological abnomraities, elevated acute phase reactants [CRP/SAA], fever, fatigue, loss appeitie, pain, portduction of cortisol

Question 97

Common characteristic of autoinflammatory disorders

Answer 97

Question 98

Clinical features of FMF

Answer 98

Question 99

Clinical Sx and Sx of FMF

Answer 99

Question 100

Additional clinical preserntations in FMF

Answer 100

Question 101

CAP syndreom overview

Answer 101

Question 102

Clinical features CAP

Answer 102

Question 103

Amyloidosis dsecribe

Answer 103

Question 104

When should autoinflammatory disroders be suspected?

Answer 104

Question 105

DDX of autoinflammatory disorders

Answer 105

Question 106

Testing for autoinflammatory disorders

Answer 106

Question 107

Tx for FMF/CAPS in the UK

Answer 107

Question 108

Anakinra mode of action and administration

Answer 108

Question 109

Pro-ILB is activated by what as a central mediator?

Answer 109

IInflammasomes

Question 110

FMF onften presents how

Answer 110

abdominla pain

Question 111

how many levels of severity in CAPS?

Answer 111

3 and as get more severe = CNS involvement, [often presents with urticcarial rash firsh]

Question 112

why anakinra potential good Tx for CAPS/FMF?

Answer 112

good efficacy and safety profile