Micrometer

My friend has shown me a very useful link to understand how to use Micrometer and here I am sharing with people who need it :)

http://www.stefanelli.eng.br/webpage/en-aka-micrometer-caliper-outside-millimetre-hundredth.html

Hope it helps :) x

Viral Hepatitis Worksheet

1. 

1. There are 5 types of hepatitis: A, B, C, D and E.
   
2. Acute VH is observed with all types and lasting less than 6 months. But chronic VH is viremia (virus enters the blood steam) and hepatic inflammation lasting longer than 6 months following infection. They are usually associated with Hepatitis B, C and D and it may lead to cirrhosis and end stage of liver disease, which leads to complication such as ascites, oedema, jaundice , hepatic encephalopathy, bleeding oesophageal varices, etc.
   
3. A, B, C, D and E
4. B, C, D
   
5. 
   

Parkinson's Disease

Mechanism of Cell death

- Neurones die undergo nercosis, cell swelling , vuculosis and lysis, which are associated with Ca++ overload of cells and membrane damage.

- they are not replaced in adult CNS

- progenitor (stem) cells may occur in some parts of the brain.

Excitotoxicity
- is the pathological process by which nerve cells are damaged and killed by excessive stimulation of neurotransmitters

Glutamate activates by NMDA, AMPA and metabotropic receptors.
Motor system
Eidemiology
Dopaminergic pathways
Metabolism of dopamine
Symptoms
Other symptoms and problems

Treatment of PD

Dompaminergic drugs ( 5 classes)

1. Dopamine precursors (e.g. Levodopa)
   
2. Dopamine receptor agonists (e.g. Apomorphine)
   
3. Monoamine oxidase B inhibitors
   
4. Catechol- O- methyltransferase inhibitors
5. Amantadine

Dopamine precursors
- Levodopa
- Dopa decarboxylase inhibitors

• Benserazide
  
• Carbidopa

SF:

• Dyskinesia
  
• Motor fluctuation ( develop after 5 years onset of the disease)
  

Dopamine receptor agonists
-Pramipexole
- Apomorphine ( expensive)

Monoamine oxidase B inhibitors
-Selegilence
- Rasagilene


Catechol- O- methyltransferase inhibitors (COMT inhibitor)
- Entacapone
-Tolcapone

Amantadine

Antimuscarinic drugs


Treatment strategies

Live disease

Liver Anatomy

• Hepatocytes - hexagonal units called lobules and each lobule centred around central vein that drains blood into hepatic vein
  
• Hepatic portal vein and artery are branched from the lobules .
• Sinusoids are formed by the vessels branch among the hepatocytes
• 70% of SA of hepatocytes to max exchange between blood and cells
  
• 15% faces the bile canaliculi

Function

• Metabolism ( Vitamine D, fat protein, carbo, hormones, drug and toxins )
  
• Clearance
  
• synthesis
  
• storage
  
• excretion
  
• secretion
  
• homeostasis ( glucose)
  
• Defence ( Kupffer cells- hepatic macrophages)
  

Type of live injury

1. hepatocellular - alcohol,toxins or drugs or viruses
   
2. cholestatic - blockage of bile duct
   
3. Infiltrative - cancer

Liver disease classification

1. acute LD
   
2. Acute LF/ fulminant hepatic F
   
3. Chronic LF
   

Causes - Autoimmune, alcohol, drugs, chronic viral hepatitis Wilson's disease

Autoimmune

• auto-antibodies in the serum
  
• usually presents as chronic progressive disease
  
• affects the biliary tree
  

Wilson's disease

• Inherited metabolic disease
  
• characterised by copper overload
  
• excessive absorption and deposition of dietary
  copper in liver, brain, kidneys and other tissues
  

Gilbert syndrome - Benign condition - no active treatment

• Hyperbilirubinemia- >50umol/L
  
• symptoms: Hyperpyrexia, fatigue, nausea, abdominal discomfort.
  

Sign and symptoms of liver Disease

• spider naevi
  
• finger clubbing
  
• Gynaecomastia
  
• Loss of body hair
  
• jaundice
  
• Enlarged Liver
  
• Alopecia- hair loss
  
• White nails
  
• Ascities - abnormal accumulation of fluid in the abdomen
  
• Portal Hypertension
  
• Pruritis - itch

Chronic complication of liver disease

Jaundice

• can be both an acute and a chronic sign of liver disease.
  
• it occurs when serum bilirubin levels are high. ( Bilirubin is metabolised by the liver) Therefore, it will accumulate if the liver is not functioning to its full capacity.
  
• it is clinically detectable when plasma bilirubin is 35umol/L.
  
• Jaundice presents as yellowing of the skin, mucous membrane and iris

Portal Hypertension (PH)

• Usual portal venous pressure is 2-5mmHg. If this becomes chronically high, collateral veins can form. ( This can form throughout the body) but are found mainly in the GI tract.
  
• The presence of these veins allows portal blood to enter the systemic circulation directly bypassing the liver.
  
• if the portal venous pressure remains high, this may lead to bleeding varices ( bleeding of dilated veins caused by liver disease) and it is potentially life-threatening. The damage can cause disruption of blood flow and liver function- processes that take place in the liver. metabolism, protein synthesis, etc. Raise in Bilirubin levels.
  
• PH also contributes to hepatic encephalopathy and ascites.

Cirrhosis- Progressive replacement of normal hepatic cells by fibrous tissue.
* associated with high level of aldosterone.

Ascites
- is the accumulation of fluid in the abdominal cavity. In liver disease, there are 3 main causes of ascities.

• PH : altering capillary pressure and permeability, leading to the accumulation of fluid in the peritoneal cavity.
  
• low blood albumin following reduced synthesis in the liver leads to fluid seepage from blood vessels.
  
• Aldosterone : the hormone responsible for fluid retention) . Accumulation when the damaged liver cannot metabolise it adequately.
  

Hepatic Encephalopathy

• occurs in profound liver dysfunction.
  
• Neurotoxic substances enter directly into the brain, bypassing the damaged liver.
• Ammonia is one such substance and it alters the permeability of the blood-brain barrier.
  
• the patient presents with an altered mental state, euphoria and confusion.
  
• In severe cases, coma can be the end-result.
  

Gynaecomastia

• The damaged liver is unable to metabolise oestrogen which can lead to feminisation in males.
  
• in Women, it presents as irregular menstrual cycle and reduce fertility.

Investigations

Liver function test (LFTs)

• Bilirubin is raised in hepatocellular damage, cholestasis and haemolysis
  
• Transaminases :aspartate transaminase (AST) and Alanine transaminase ( ALT) released from the liver in hepatocellular damage.
  
• Alkaline phosphatase (ALP) is released in cholestasis ( damage of bile duct)
  
• Albumin is synthesised in the liver. Serum albumin indicates the extent of chronic liver disease as it has a long half life ( approx 20 days)
  
• Prothrombin time: Clotting factors synthesised in the liver. Good indicator of acute liver disease due to short half life ( 6 hours) .

Liver biopsy- diagnostic

Management

Ascites- is the excess fluid in between the tissue lining the abdomen and the abdominal organd ( the peritoneal cavity.

• Sodium intake should be restricted to 60-90mEq per day (hyperkalemia)
  
• Spironolactone( aldosterone antagonist) is the drug of choice. SF: hyperkalemia and gyneacomastia. ( 100mg daily increasing to 400mg daily)
  
• Paracentesis is a procedure involving a needle of drainage of fluid from the peritoneal cavity. It can relieve the abdominal pressure from ascites.
  
• TIPSS- is placed to provide portosystemic shunting to reduce portal pressure.
  
• Liver transplant
  
• Desired weight loss: 0.5-1kg per day. Water in versus Water out should be monitored.
  

Portal Hypertension

• Propranolol : the only beta-blocker licenised for portal hypertension. it is given to reduce portal venous pressure and prevent recurrent variceal bleeds. ( 10mg BD-TDS)
  
• SF: vivid dreams, bradycardia, coldness of extremities, fatigue and bronchospasm.
  
• should not stop taking unless advised by a doctor
  

Hepatic Encephalopathy

• dietary protein intake should be reduced to 20g per day
  
• Lactulous : an osmotic laxative. It can reduce the pH of colonic content thus reducing colonic ammonia absorption. The GI transit time will be decreased, so patient are monitored for 2 to 3 bowel motions a day.
• Metronidazole reduces ammonia production from GI bacteria
  
• Interaction with alcohol: a disulfiram type reaction ( like dizziness and vomiting) occurs if metronidazole is taken with alcohol.
• Alternative: Neomycin - reduces plasma ammonia. Max of 7 days 1g QDS ( ototoxicity & nephrotoxicity)

Pruitis

• Antihistamines are not very effective but if given, non-sedating antihistamines would be preferable ( e.g. Loratidine) , as sedating could mask the effect of hepatic encephalopathy
  
• Anion exchange resins ( Colestyramine) bind to the bile acids that cause itching and it is 1st line treatment. it can redice the absorption of other drugs taken at the same time. - taken 1 hour before or 4 hours after taking a dose of anion exchange resins.
• Topical preparations such as calamine lotion can be used.
  

Oesophageal varices

• Vasopressin: reduce portal blood flow and portal pressure; it is given IV to stop bleeding. ( 20units IV over 15-20mins)
  
• SF: angina, myocardial infarction and arrhythmia
• Should not be given to patients with ishaemic heart disease. GTN ( glyceryl trinitrate) can be given to overcome the cardiac SF ( vasoconstriction)
  
• Terlipressin : given IV, is the drug of choice ; it releases vasopressin over several hours without the cardiac effects ( 2mg then 1 -2mg ever 4-6hours until bleeding is controlled for upto 72 hours)
  
• Octreotide: A somatostatin, given IV, stops variceal bleeding and reduce portal venous pressure. it inhibits release of vasodilating hormones (e.g. glucogon)
  

Haemostasis and Thrombosis

- a dynamic process of maintaining fluidity of the blood, repairing vascular injury and limiting blood loss while avoiding vessel occlusion ( Thrombosis) and inadequate perfusion of vital organs.

• formation of platelets which adhere to injured tissue
  
• Blood clotting factors : the protein circulating in the plasma.
  
• Results in formation of insoluble fibrin clot that reinforces the initial platelet plug.
  
• Fibrinolysis : happens when healing and tissues repair are under way.

3 systems

1. intrinsic pathway
   
2. extrinsic pathway
   
3. common pathway
   

Here's a very good website to explain these 3 pathways.

http://www.hopkinsmedicine.org/hematology/Coagulation.swf

Intrinsic pathway

Basic :

Blood on -ve charged surface
|
XII --- Kininogen + Prekallikrein
_________________________
|
|
Kallikrein
|
|
XIIa + XI
_______
|
|
IX (IXa) + VIIIa (cofactor) -----> convert X to Xa---> ( initiation of common pathway)

• initiated when blood comes into contact with -ve charged surface
  
• Factor XII interacts with high molecular weight - kininogon and prekallikrei. ---> to produce Kallikrein which activates factor XII ( XIIa)
  
• The activated factor XIIa then activates factor XI which activates factor IX
  
• the factor IXa together with activated factor VIIIa ---> as a cofactor which converts factor X to factor Xa.
  

Extrinsic Pathway

basic :

Tissue factor from damaged tissue
|
|
VII bind to it and form VIIa
|
|
Activates X to form Xa

• when tissue factor is exposed to the blood on the damaged tissue, The factor VII binds to it to form factor VIIa
  
• which activates factor X to to form factor Xa, leading to the initiation of common pathway.
  

Common pathway

Xa ( activation) +V
|
|
Prothrombin------- Thrombin
|
|
formation of fibrin ( stablised by XIIIa)

• the activation of Factor Xa is the point that intrinsic and extrinsic pathway converge to form a common pathway of coagulation cascade.
  
• Factor Xa together with activated V as cofactor, converts prothrombin to thrombin with a subsequent formation of fibrin which is stabilised by factor XIIIa and form a stable clot.
  

Fibrinolysis

Plasmin (fibrinolysin)
|
digests fibrin clots and II, V, VII, XII

• Clot dissolution
  
• mediated by plasminogen which circulates in plasma as an inactive form, which converts to its active form plasmin ( fibrinolysin) .
  
• This occurs when plasminogen binds to fibrin in the presence of plasminogen activator.
  
• Fibrinolysin digests fibrin clots and hydrolyses factors II, V, VIII and XII.

Thrombosis

- the development of thrombus in the arterial or venous circulation
- if venous thrombus breaks off and enter:

• Right circulation and lodge in the pulmonary arterial circulation->pulmonary emoblism (PE)
  
• Left circulation and lodge peripheral arterial --> cause stroke

Venous Thromboembolism

1. Deep vein thrombosis (DVT)
   
2. Pulmonary Embolism (PE)
   

Risk factor

• Age
  
• immobility
  
• major surgery in recent weeks
  
• pregnancy
  
• malignancy - cancer
  
• oestrogens
  
• inherited coagulation disorders. Previous venous thrombosis

Diagnosis

DVT

-clinical symptoms
- RF

• D-dimer : is a small protein fragment present in the blood after blood clotting generated by fibrinolysis
• the concention of D-dimer can be determined by a blood test.
  

• Duplux ultrasonography scan :

PE

• Pulmonary arteriography
  
• ventilation perfusion scanning
  

Treatment

Nonpharmacologic prevention - external pneumatic compressio, graduated compression socking or venous foot pumps. ( these devices increase venous outflow and reduce stasis within the leg veins.
pharmacologic prevention - Venous thromboembolism

• unfractionated heparin
• oral anticoagulants - warfain
  
• low molecular weight heparin

Unfractionated heparin (UFH)

Mechanism of action

• the major mechanism by which heparin blocks coagulation is by catalysing the inhibition of thrombin. UFH acts as an anticoagulant by catalysing the inactivation of thrombin (factor IIa) , activated factor X ( factor Xa) , and activated factor IX (IXa) by antithrombin
  

- used to prevent thrombosis ( venous , unstable angina)
- prevent blood clotting

Caution

• HIT
  
• Hyperkalaemia -
  

- short duration of action

Low molecular weight heparin

- longer duration of action compared to UFH

Oral anticoagulant - Warfarin

Mechanism of action

• is a vitamin K antagonist and interferes with the synthesis of coagulation factors.
  
• Because vitamin K is essential for production of prothrombin and factor VII, IX and X ( vitamin K is important for postranslational carboxylation of glutamic acid residues of these proteins)
  
• Warfarin blocks vitamin K reductase, needed for vitamin K to act as a cofactor in the synthesis of coagulation faction.
  

SF

• many drug interactions
  
• may lead to increased bleeding
  

Heparin-induced thrombocytopenia (HIT)
- is the development of a low blood count (thrombocytopenia) due to the administration of various forms of heparin.

- stop treatment and use heparinoid or hirudin

Heparinoid ( e.g. Danaparoid)
- a mixture of low molecular weight sulphated glycosaminoglycuronans

Mechanism of action

• inhibits factor Xa resulting inhibition of thrombus generation and thrombus formation
  

Hirudin ( Lepirudin and Bivaluridin)

- a direct thrombin inhibitor
- action independent of antithrombin.

Lepriudin

- a recomninant hirudin
caution
- risk of bleeding

Bivaluridin
Caution
- an exposure to lepirudin

Fondaparinux - a synthetic pentasaccharide

• bind to antithrombin thus inhiits activated factor X
  

SF : haemorrhage.

Pharmacological prevention - Arterial thromboembolism

- if affecting the cerebral circulation results TIAs ( transient ischaemic attacks or cerebral infarction ( a form of stroke)

Antiplatelets

1. Aspirin
   
2. clipidogrel
   
3. Glycoprotein IIb/IIIa inhibitors
   
4. Dipyridamole
   
5. Clopidogrel
   

Cardiac Arrhythmia

ECG ( electrocardiography)
- consist of 12 conventional electrode systems - 6 limb leads and 6 chest leads
- is a trace showing variations in potential over time arising from the heart


Normal ECG

• P-wave =
  
• PR segment
  
• QRS complex
  
• ST segment
  
• T wave

• TP interval

Arrhythmia

-Refer to any change in the normal rate or rhythm of the heart.

Sinus trachycardia
Sinus bradycardias

The skin

There is 2 types of acne:

1. Acne Vulgaris
   
2. Acne Rosacae

Acne Vulgaris

Symptoms

• Seborrhoea ( too much oil on the skin)
  
• Comedones ( blackheads)
  
• inflammation
  
• papules. ( small inflamed elevation of skin) . pustules or nodules
  
• Tenderness
• scaring
  

Cause

• at puberty: pilsoebaceoous gland increase sebum in response to testosterone ( males and female do produce testosterone but males produce more - so it effects more in men)
  
• flow of shedding.
  

- increased keratin and sebum production during adolescence are thought to be important contributory factors

- the increased amount of keratin leads to blockages of the follicles and the formation of microcomedones.

- the microcomedones can develop into a non-inflammatory lesion (comedone) , which may be open (blackhead) or closed ( whitehead) or into an inflammatory lesion( papule, pustule or nodule) .

- excess sebum encourages the growth of bacteria , particularly propionibacterium acnes, which are involved in the development of inflammatory lesions.

Management

- The general aim of therapy are to remove follicular plugs so that sebum is able to flow freely and to reduce the number of bacteria on the skin.

- therefore reduce comedone formation

- lotions, creams and gels ( gels with an alcoholic base dry quickly but can be irritating. those with aqueous base dry shower but are less likely to irritate the skin.) comedogenic moistuiser.

Benzoyl peroxide (BP)

• has both antibacterial and anticomedogenic actions and is the 1st-line OTC treatment for inflammatory and no inflammatory acne.
  
• Antiflammatory action occurs at all strengths but anticomedogenic action is low and has the greatest effect at higher strengths.
  
• it has a keratolytic action, which increases the turnover of skin cells, helping the skin to peel.
  
• Regular application can result improvement of mild acne.
  

1. BP is very like to produce reddening and soreness of the skin. and patient should be warned of this.
   
2. so, treatment should start with a 2.5 or 5%product. moving gradually to 10% strength if needed.
   
3. Oily skin: Gels
   
4. Dry skin: Creams
5. Washing the skin with a mild soap or cleansing help by reducing the amount of sebum on the skin.
   
6. BP prevents new lesions forming rather than shrinking existing area. Therefore it needs to apply on the whole of affected area. and it is best to apply after washing.
7. first use: the skin is like to redden and sore. Stinging, drying and peeling to occur. - lowest strength preparation to begin and to apply cream, lotion...on the first week of treatment.
   
8. Application once daily or on alternate day could be tried for a week and then frequency of use increased to twice daily. After 2 or 3 weeks, a higher strength preparation may be introduced. if irritant affects do not improve after 1 week or are severe. Discontinued.

Acne rosacae

- over 40s
-broken blood vessels


Fungal skin infection

- caused by Tinea

Types:

1. T.Pedis
   
2. T.cruris
   
3. T. corporis
   
4. T. unguium
   
5. T. capitis
   

- Dermatophytes invade stratum corneum ( not living tissus)
- Intertrigo ( rash in skin fold)

T.Corporis : anywhere on the body. Red edge , satellite spots surrounding and clearance in the middle.

T. pedis : affects toe webs- bits in between the toes.

T. Cruris: Affects the groin.

Treatment

• Benzoic acid ( + salicylic acid= Whitefield's ointment)
• Undecanoates
  
• tolnaftate -less evidence
  
• imidazoles
  
• Allyamines
  
• Canesten HC ( with hydrocortisone 1%)
  
• Griseofulvin (1%) spray
  

Onychomycosis

• Amorolfine (OTC)
  
• use weekly
• take 8-12 weeks
  
• Curanail - 3 months treatment and 2 nails only
  

Dry skin

• use emolients
• Apply 4 times a day + after bathing
  

Eczema

• Irritant contact dematitis
  
• Allergic contact dermatitis
  
• Atopic eczema

Treatment

Hydrocortisone ( 0.1 and 1% OTC and 0.25% with crotamiton)

• mild topical steroid
  
• over 10 years of age only
• contact and allergic dermatitis and mild to moderate eczema
  
• Apply sparingly once or twice a day
  
• Max 7 days
  

Clobetasone

• NB Chobetasone butyrate 0.05%
  
• Moderately potent steroid
  
• over 12 years of age only
  
• contact and allergic dermatitis and mild to moderate eczema
• Apply sparingly twice a day
  
• Max 7 days
  

Warts / verrucae
- Growths of the skin caused by human papilloma virus (HPV)
- Verrucae: warts on the foot. Plantar warts

Refer:

• Eczema or broken skin
  
• facila or anogenital
• Diabetic / poor circulation
  
• large area affected
  

Treatment

• 1st line: Salicylic acid for 12 weeks
  
• 2nd line: Gluteraldehyde. formaldehyde

Corns ( Helomas ) and calluses
- caused by friction and pressure ( hyperkeratoses )
- corns: against bony prominences
- hard corns : top tops
- soft corns: between toes, macerated

Calluses: Flattened yellowed white hardened skin

Treatment

• relieve pressure and friction
• shoes that fit
  
• cushioning
  
• Keratolytics
  

Bunions
- caused by inappriate footwears ( sky-high heels etc)

Cold Sores

- infection caused by herpes simplex virus type 1 ( HSV)
- after primary contact virus lays dormant in root nerve
Triggers:
- sunlight
- cold weather
- infection
- menstruation

• start as burning, pricking, tingling
  
• then a painful blisters develop
  
• scab over in a couple of days
  

Treatment

Aciclovir 2% cream
Penciclovir 1% ( fenistill )

• they inhibit HSV DNA polymerase
  
• if applied at prodromal stage can reduce healing time by day.
  

Aciclovir

• apply 5 times a day for 5 days
  

Penciclovir :

• 2 hourly for 4 days