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40 Cards in this Set
- Front
- Back
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WHAT IS PERICARDITIS? |
Acute pericarditis is where the pericardium becomes inflamed, roughened with possible exudate. Sudden chest pain, worse on inspiration and lying down, pericardial friction rub by the outside layer getting roughened so it affects smooth movement. Pericardial effusion: fluid in pericardial cavity, compression of heart may cause cardiac tamponade. Constrictive pericarditis: visceral and parietal layers adhere obliterating the pericardial cavity. Compresses the heart, decrease cardiac output which causes perfusion and blood pressure to drop. The exudate makes fibrin and scarring build and the layers stick together |
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WHY IS SOMEONE WITH SLE OR CIRRHOSIS AT HIGHER RISK OF PERICADITIS? |
SLE this is due to the antigen-antibody complexes that are produced during active lupus. |
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AORTIC STENOSIS? WHAT HAPPENS? WHAT HAPPENS WITH A MITRAL STENOSIS? |
Aortic stenosis is a blockage in the aorta. It diminishes blood from the left ventricle into aorta which can result in ischemia, arrhythmias and heart failure. This back flow can cause pulmonary oedema and pulmonary hypertension which will decrease in cardiac output, low blood pressure and perfusion. Mitral stenosis is the blood from the left atrium cannot travel too the left ventricle. This increases pressure in the left atrium which will go backwards into the pulmonary vein and back into the lungs leading to pulmonary hypertension or pulmonary oedema. The valve leafets become fibrous and duse, chordae tendineae shorten, atrial arrhythmias and thromboemboli, increased left ventricle pressure leading to pulmonary hypertension, oedema and perfusion problems |
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WHAT IS AORTIC REGURGITATION? WHAT IS MITRAL REGURGITATION? MITRAL VALVE PROLAPSE SYNDROME? |
Aortic regurgitation: aortic valve should allow blood to go out. The back flow of blood into the left ventricle causes it to dilate and can get left ventricular hypertrophy, drop in perfusion, higher risk of embolus can lead to death of tissues Mitral Valve: back flow of blood from left v to LA which puts pressure on the atrium. Goes back into pulmonary vein, lungs, pulmonary hypertension and possibly oedema. LV dilate and hypertrophy to maintain cardiac output. Mitral valve prolapse: valve billow upwards into atrium, replace with porcine or mechanical valve |
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RHEUMATIC HEART DISEASE AND WHAT HAPPENS IF ITS UNTREATED |
Caused by B-hemolytic streptococci. Causes inflammation of joints, skin, nervous system and heart, require antibiotics within first 9 days, if untreated it leads too rheumatic heart disease which means the valves become deformed and scarring. Because tissue in joints is similar to endocardium valves so it causes stiffening. |
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ARTERIOSCLEROSIS AND ATHEROSCLEROSIS |
Arteriosclerosis a chronic disease with abnormal thickening and hardening of arterial walls, smooth muscle cells and collagen migrate into tunica intima which decreases elasticity Atherosclerosis form of arteriosclerosis that is caused by an accumulation of lipid-laden macrophages which results in plaque formation. Main cause of CAD and CVA, 1/2 western world deaths, inflammatory disorder by injury to the endothelium. Higher chance from smoking, hypertension, diabetes, high LDL, low HDL, chronic infection |
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WHAT IS THE SEQUENCE OF ATHEROSCLEROSIS |
Injured endothelium becomes inflamed & fails to produce normal antithrombotic & vasodilatory cytokines --> growth factors are released e.g. angiotensin which causes smooth muscle cell proliferation (overgrowth) --> macrophages adhere to endothelium & generate free radicals that oxidise LDL. Platelets aggregate. --> Macrophages engulf oxidised LDL and become foam cells which are enlarged, not useful & not active. This causes more inflammation & scar tissue is laid down because macrophages bring fibrin to repair things which affects the elasticity in the vessel wall --> Foam cells encourage atherosclerosis further resulting in fatty streak --> further proliferation & collagen deposition results in fibrous plaque which can lead to thrombus --> calcification can lead to protrusion into vessel --> plaque may erode or tissue, rupture can cause thrombus formation which can then lead to embolisms |
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AN ANEURYSM, CAUSES, COMMON SITES, 2 TYPES AND CLINICAL MANIFESTATIONS |
Localised dilation or out pocketing of a vessel wall or cardiac chamber. Grows bigger because of tension building up, can put pressure on surrounding organs, rupture or dissect. Causes atherosclerotic plaque erodes and weakens tunica media, syphillis, chronic hypertension, marfans. Common sites: aorta, post infarct Two types: True: involves all three layers either fusifrom; entire circumference of vessel or saccular: part of circumference, sac like False: break in tunica intima which bleeds in between layers, dissecting, saccular Manifestations: related to pressure, most AAA asymptomatic, pulsating/calcified mass, pain is mild to severe mid-abdominal, lumbar or back region, stasis of blood favours thrombus and peripheral emboli |
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WHAT IS REYNAUD'S PHENOMENON |
Bilateral spasms in arteries and arterioles of hands, skin colour and sensation changes, prolonged attacks affect cell metabolism in hands. May be secondary to systemic disease e.g. scleroderma (excessive collagen deposition), smoking, exposure to cold or vibrating machinery, triggered by brief exposure to cold, common in young females, cause is unknown |
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WHAT IS THROMBOANGIITIS OBLITERANS |
Buerger disease which is an inflammatory disease. It obliterates the arteries in the hands and feet. Causes pain, tenderness, reynaud's phenomenon, cyanosis, redness, ulcers and possibly gangrene |
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WHAT ARE THE TREATMENTS FOR HYPERTENSION? |
Beta blockers by blocking andronergic receptors, slow down heart, cause dilation e.g. metoprolol Diuretics strip fluid off and take water level down in body e.g. spironolactone ACE inhibitors stop ACE functioning e.g. captopril Calcium channel blockers block calcium from smooth muscle cells and they can't contract so they get relaxation e.g. nifedipine Centrally-acting drugs which affect the brain/sympathetic nervous system to cause vessel dilation e.g. clonidine Vasodilators cause vessels to relax e.g. hydralazine |
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HOW DO ACE INHIBITORS WORK |
Angiotensinogen is constantly produced by the liver, low renal blood flow, low sodium and/or potassium levels and B adrenergic stimulation all cause renin release from kidneys. Renin converts angiotensinogen to angiotensin 1, ACE converts angiotensin 1 to angiotensin 2 which affects aldosterone secretion,smooth muscle constriction and sodium and water retention. ACE inhibitors prevent conversion of Angiotensin 1 to Angiotensin 2. Results in decreasing fluid retention, after load e.g. captopril |
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WHAT HAPPENS WITH HIV? WHAT PART OF THE IMMUNE SYSTEM IS AFFECTED? |
It is a retrovirus. The protein on the virus coat (GP12) can bind to CD4 molecules on T helper cells. The virus is engulfed and then the cell makes DNA using reverse transciptase and it integrates the genome, impairing the cell function. Can lay dormant or make may virus particles. Infect monocytes and the CNS. |
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WHAT ARE THE TREATMENTS FOR HIV? HOW DO THEY WORK? |
Triple therapy = reverse transcriptase inhibitors - azidovudine Protease inhibitors - a viral protease important for coat assembly In developing countries only <5% of those infected are getting anti-retroviral drugs Immune regulating hormone = immunitin or HE 2000, it is not clear how it works, decreases levels of inflammatory mediators and boosts immune response. Appears to stimulate key parts of the immune system. Maintain or increase number of T-cells by cell expansion (individual cells multiple outside the body then transferred back), cell transfer (immune tissue transplant of twins or HIV negative relative, cytokines (interleukin-2 can lead to large increases in CD4+ cells, gene therapy (change bone marrow cells so they become immune to HIV infection) |
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ANTI-RETRO VIRAL DRUGS |
Anti-retro viral: give 2 or 3 types. Fusion inhibitors bind to GP120 of HIV virus to prevent it binding to CD4. CCR5 antagonists that bind to CCR5 as in most cases CCR5 is needed to bind too to infect cells. Nucleoside reverse transciptase inhibitor form a bond that cannot be binded too by the HIV which means they can't make the strand longer. Non-nucleoside reverse transciptase inhibitors they work on the enzyme, not the nucleoside. Intergrase inhibitors block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell. Protease inhibitor binds to the protease enzyme to make sure it can't make the viral polyprotein. |
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WHAT IS A TYPE 1 HYPERSENSITIVITY REACTION |
Type 1: Most common, reaction to environmental antigens, IgE mediated (on surface of mast cells and basophils), histamine release, prostaglandins, leukotrienes and kinins, mast cells abundant (skin, GIT, reap tract e.g. hay fever, asthma, anaphylaxis. Antihistamines or noradrenaline in anaphylaxis. Allergy: environmental antigens. Cause atypical immunologic responses in predisposed individuals e.g. pollens, molds and fungi, food, animals. Allergen is contained within particles to large to be phagocytosed. Manifestations are urticaria, conjunctivitis, rhinitis, hypotension, bronchospasm, dysrhythmias, GI cramps and malabsorption |
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WHAT IS A TYPE 2 HYPERSENSITIVITY REACTION AND WHAT ARE THE 5 MECHANISMS |
Tissue specific. Specific cell or tissue is the target of an immune response. Tissue specific antigens on surface of cell become targets during an immune response e.g. rH, ABO incompatibility, autoimmune haemolytic anaemia. 5 Mechanisms: Cell is destroyed by antibodies and complement --> cell destruction through phagocytosis --> soluble antigen may enter the circulation and deposit on tissues --> antibody-dependent cell-mediated cytotoxicity --> causes target cell malfunction |
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WHAT IS A TYPE 3 HYPERSENSITIVITY |
Immune complex mediated. Antigen-antibody complexes formed in circulation deposited in vessel walls or other tissues, not organ specific. Immune complex clearance: Large = macrophages. Small = renal clearance. Intermediate = deposit in tissues Immune Complex Disease: presents with wide variety of symptoms. Serum sickness: soluble antigens cause systemic immune reaction Arthus reaction: localised tissue reaction to antigen, celiac disease, allergic alveolitis, skin tests |
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WHAT IS TYPE 4 HYPERSENSITIVITY |
Delayed 24-72 after exposure to antigen, cell mediated, direct killing of Tcells or recruitment of phagocytic cells by T helper cells. E.g. contact allergic reactions, autoimmune diseases, acute graft reaction. Fixed with corticosteroids |
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WHAT IS THE DIFFERENCE BETWEEN AUTOSOMAL DISORDERS AND SEX LINKED DISORDERS |
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AUTOSOMAL DOMINANT AND RECESSIVE |
h |
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WHAT IS HUNTINGTONS DISEASE |
h |
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MACROCYTIC-NORMOCHROMIC ANAEMIA |
Magrocytic: Meaning large cell, has normal haemoglobin and normal colour. Normochromic: has normal haemoglobin and normal colour. Pernicious anemia: caused by lack of intrinsic factor inside the body, made in the stomach to absorb B12 properly which results in a deficiency. Which can cause ulcers, inflammation. Folate deficiency anaemia: always caused by lack of folate in diet, similar symptoms to pernicious anaemia, folate deficiency also causes neural tube defects in the foetus (spinal cord and brain). |
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MICROCYTIC-HYPOCHROMIC ANAEMIA |
Small cell, too little haemoglobin. Related to iron metabolism disorders, disorders of porphyrin and heme synthesis (needed to make haemoglobin), disorders of glob in synthesis. Iron deficiency anaemia: most common. Nutritional iron deficiency. Causes brittle, thin, coarsely ridged and spoon shaped nails, a red sore, painful tongue. Sideroblastic anemia: altered mitochondrial metabolism causing ineffective iron uptake and resulting in dysfunctional haemoglobin synthesis. Erythropoietic hemochromatosis or iron overload is present due to sideroblasts (erythroblasts that contain iron granules that have not been synthesised into haemoglobin.) |
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NORMOCYTIC-NORMOCHROMIC ANAEMIA |
Characterized by red cells that are relatively normal in size and haemoglobin content but insufficient in number. Aplastic anaemia: pancytopenia (reduction or absence of all 3 blood cell types), results from failure or suppression of bone marrow. Treatment is immunotherapy and bone marrow transplant Posthaemorrhagic anemia: acute blood loss Hemolytic anemia: accelerated destruction of red blood cells. Inherited or acquired conditions e.g. dysfunctional RBC, destroy them quicker Sickle cell: inherited autosomal recessive disorder, cells go into crescent shape Anaemia of chronic inflammation: mild to moderate anaemia seen in AIDS, lupus, hepatitis, renal failure, rheumatoid arthritis. Pathologic mechanisms decreased erythrocyte life span, ineffective bone marrow response to erythropoietin, altered iron metabolism |
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WHAT IS INFECTIOUS MONONUCLEOSIS? |
Acute, self limiting infection of B Lymphocytes transmitted by saliva through personal contact. Commonly caused by the Epstein-Barr virus (EBV)-85%. Other viral agents resembling IM --> influenza, HIV, hepatitis Symptoms: fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count, and atypical (activated) lymphocytes. Serious complications are infrequent <5%. Diagnostic test: monospot qualitative test for heterophillic antibodies |
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WHAT IS LEUKEMIA? WHAT ARE THE 4 CLASSIFICATIONS? |
Malignant disorder of the blood and blood forming organs. Excessive accumulation of leukemic cells. Acute leukaemia: presence of undifferentiated or immature cells, usually blast cells, most immature cells Chronic: predominant cell is mature but does not function normally 4 classifications: acute lymphocytic leukemia most immature cells/cancer of lymphocytes or lymphoblasts Myelid (bone marrow) = acute myelongenous leukaemia = under developed cells with bone marrow Acute (immature cells) - chronic myelogenous leukaemia Chronic (mature, dysfunctional cells) = Chronic lymphocytic leukaemia = lymphoid tissue, large cells in lymph node tissues |
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WHAT ARE THE SIGNS AND SYMPTOMS OF LEUKEMIAS? |
Anemia, bleeding purpurea, petechiae (red spots) and ecchymosis (bruise), thrombosis, haemorrhage and DIC, infection, weight loss, bone pain, elevated uric acid, liver/splee/lymph node enlargement, anorexia |
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WHAT IS DISSEMINATED INTRAVASCULAR COAGULATION? WHAT CAN CAUSE IT |
OBGYN COMPLICATIONS: When tissue is damaged = tissue factor enters circulation and sets off coagulation cascade. INFECTION: gram negative organisms. They release an endotoxin that generates and exposes tissue factor --> coagulation cascade CANCER: tumor cells can express/release tissue factor. Presenting symptom with slowly evolving DIC is blood clots, DVT and PE. More commonly is severely rapidly evolving DIC which is bleeding. Depletion of coagulation factors, fibrinogen Complex, acquired disorder in which clotting and haemorrhage occur simultaneously. Results from increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis. Endothelial damage is the primary initiator of DIC in the presence of sepsis. Amount of activated thrombin exceeds antithrombins; does not remain localised, the widespread thromboses created widespread schema, infarction and organ hypo perfusion. Clinical signs: bleeding from venipuncture sites, bleeding from arterial lines, purpurea, pertechiae and haematomas, symmetric cyanosis of the fingers and toes. Treatment is to: remove the stimulus, restore haemostasis, maintain organ viability |
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PHARMACOLOGICAL TREATMENT FOR HEPARIN OVERDOSE |
Protamine. |
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WHAT IS A SEIZURE? |
Sudden, transient alteration of brain function caused by an abrupt, explosive, disorderly discharge of cerebral neurons Tonic: muscle tone/muscle stiffness Clonic: when muscle relaxes Myoclonis: little twitches in muscle |
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WHAT TYPES OF SEIZURES ARE THERE? |
Generalized seizures: conciosuness always lost - not always LOC, can become unresponsive, have an absence of consciousness Partial (focal) seizures: uncontrolled movement --> seizures in one part of the body e.g. eyes. Consciousness is retained and a focal effect so they can lay down memory Complex partial: consciousness impaired but focal origin. Can be confused, stay conscious but not remember 100% of the seizure, only one part of the body is involved Secondary generalisation: if a partial seizure becomes generalised Status epilepticus: multiple seizures with no period of consciousness in between or a single seizure lasting more than 1-2 minutes. |
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WHAT ARE THE SEIZURE STAGES |
Aura: may precede some seizures but not everyone has this. Epileptogenic focus, group of neurone that appear to be hypersensitive to paroxysmal depolarisation Tonic phase: initial loss of consciousness and muscle rigidity Clonic: alternating contraction and relaxation of muscles Postictal state follows the seizure -- altered consciousness |
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WHAT DRUG TREATMENTS ARE USED FOR SEIZURES? |
Sites on the synapse have receptors for drugs to bind too e.g. glycine site for NDMA receptor, glutamate site for AMPA and NDMA receptor, GABA receptor has barbiturate site, GABA site and the benzo site. Glutamate site/NDMA receptor: stops glutamate from glutamanuric neurone which stops the epileptic action potentials to not work. Otherwise glutamate will be released into the synaptic cleft and binds to the site causing an influx of Na+ GABA RECEPTOR: GABA is taken up by neurone and packaged into vesicles and some is released into the synaptic cleft to bind to the GABA site and chlorine ions enter the post synaptic cleft causing hyper polarisation and inhibition, decreasing the likelihood of seizures. BARBITUATE AND BENZO: PHENOBARBITAL AND DIAZEPAM: allow chlorine ions to enter the post synaptic neurone causing hyperpolarisation and inhibition. SODIUM CHANNEL BLOCKERS: When Na+ channels are open it causes depolarisation of the cell which causes to excitation. Phenytoin and Carbamazepine block these channels CALCIUM CHANNEL BLOCKERS: Ca+ causes depolarisation and excitation. A Calcium Channel Blocker blocks T type calcium channels so it can't enter the neurone. |
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WHAT IS HUNTINGTON DISEASE? |
"Chorea" a type of hyperkinesia. Presents as abnormal movements and progressive cognitive dysfunction. It is autosomal dominant, hereditary degenerative disorder. Severe degeneration of the basal ganglia and frontal cerebral cortex. |
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WHAT IS PARKINSON'S DISEASE? WHAT IS THE TREATMENT? |
A form of hypokinesia. Unknown cause. Severe degeneration of the basal ganglia (make large amounts of dopamine which means people with Parkinsons lack dopamine). Parkinson rigidity (lots of resistant), parkinson bradykinesia, tremor at rest, postural abnormalities, cognitive affective symptoms. Precursor of dopamine = levodopa combined with a dopa decarboxylase inhibitor to prevent conversion to dopamine at periphery. Monoamine oxidase metabolise noradrenaline, adrenaline and dopamine --> break down dopamine |
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WHAT IS MULTIPLE SCLEROSIS? |
A progressive, inflammatory, demyelinating disorder of the CNS. Twice as common in females. Cause unknown, genetic link mixed with environmental factors leading to autoimmune response to single myelin protein - scarring of myelin producing cells. Relapsing-remitting: disease flares, gets better, back to normal and continuous. Primary progressive disease slowly gets worse and worse. Secondary progressive: relapsing and then after flares you get words and worse, normally starts as RR. Progressive relapsing relapses where disease flares and then you are much worse, get worse in between then have a flare and get worst. |
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WHAT TYPES OF MS ARE THERE? WHAT TREATMENTS? |
Mixed (general): signs of optic, brain stem and cerebella involvement Spinal: peripheral sensory changes, spastic ataxia, bladder and bowel symptoms, skeletal muscle changes and deficits Cerebralla: spastic ataxia, weakness, hypotonia. Treatments: corticosteroids are other immunosuppresants are used during acute attacks. Antispastic drugs (diazepam, baclofen), antidepressants and anticonvulsants (for pain and sensory disturbances) are used symptomatically |
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WHAT IS GUILLAIN-BARRÉ SYNDROME |
Aquired inflammatory disease causing demolition of the peripheral nerves w/ relative sparing of axons. Humoral and cellular immunologic reaction. Acute onset, ascending motor paralysis. Symptoms can vary from leg weakness to quadriplegia. Weakness usually plateaus by Week 4 and condition usually improves over time, 10-30% require ventilatory support from respiratory muscle weakness |
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WHAT IS SLE |
Destorys connective tissue in skin, blood vessels and organs. Arthralgias or athritis, vasculitis and rash, renal disease, haematological changes, cardiovascular disease. At least 4 of the following symptoms: facial rash, discoid rash, photosensitivity, oral or nasopharyngeal ulcers, nonreosive arthritis, serositis, renal disorder, neurologic disorder, hematologic disorders, immunologic disorders and presence of antinuclear antibodies |
