Immune system : blood, fever etc. Flashcards

1
Q

Briefly discuss the different causes of anaemia

A
  • Haemorrhage : wounds, heavy bleeding
  • Iron deficiency : BM needs iron to make RBC, poor diet, Chronic slow
  • Chronic disease: ongoing disease, cancer, chronic infection
  • Kidney disease: decrease EPO production
  • Poor nutrition: e.g. decreased B12
  • sickle cell anaemia: poor B12 absorption
  • Pernicious anaemia: production of abnormal haemoglobin molecules
  • Thalassemia: hereditary, quantitative haemoglobin
  • BM related: leukaemia alter RBC production
  • Haemolytic anaemia
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2
Q

How is anaemia classfiied?

A

Microcytic: MCV is less than 80, people may have iron deficiency or anaemia of chronic disease.

Nomocytic: - Reticulocyte count is done, this may be Leukaemia or Haemorrhage

Macrocytic: MCV more than 100 Megalocytes and segmented neutrophils are looked at, this then shows if it is vitamin B12 deficiency or drug induced, or Alcohol abuse, liver disease, bone marrow failure

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3
Q

What are common clinical manifestations of anaemia?

A

faster heart beat, pale, dizziness, fatigue, fainting (severe), shortness of breath, low blood pressure, muscular weakness, yellowing of the eyes, cold to touch.

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4
Q

How is Anaemia treated?

A
  • treatment depends on the underlying cause
  • give Iron or B 12
  • Blood transfusion
  • Oxygen
  • antibiotics
  • prevent bleeding
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5
Q

Describe the pathophysiology of Disseminated intravascular coagulation.

A
  • DIC begins with the formation of blood clots throughout the body followed by bleeding
    Two mechanism may trigger DIC:
    1. release of tissue factor or thromboplastin substances into circulation
    2. wide spread injury to endothelial cells
  • causing wide spread microvascular thrombosis in organs> ischemic tissue damage, activation of plasmin, consumption of clotting factors and platelets.
    = Bleeding ( increase blood in urine and blood stools)
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6
Q

What changed may you observe in WBC numbers and function during infection?

A
  • WBC is used to determine specific cause of illness
    WBC increases at first
    then WBC might decrease = neutropenia due to infection and sepsis (the WBC move into the tissue)
  • neutrophils numbers will increase during inflammation
  • neutrophils will release chemotactic factors that recruit macrophages
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7
Q

Define Fever and how it develops.

A
  • Fever is a temp above 36-37 due to an increase in the hypothalamic set point
  • Pyrogens cause the release of Prostaglandin which causes Hypothalamus to raise temp
  • Pryogens can be endogenous or exogenous
  • used to combat infection
  • increases mobility of leukocytes
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8
Q

What is lymphadenopathy?

A

disease of the lymph nodes
they enlarge and swell
enlarged lymph nodes are commonly associated with infection disease

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9
Q

What is multiple Myeloma?

A
  • Malignant proliferation of plasma cells of the bone marrow
  • cause = unknown
  • may have anaemia, back pain , fatigue, SOB, high risk of infection
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10
Q

Discuss the predominant cells types and their function in the acute and chronic inflammatory response

A

White blood cells are the most predominant, they include:
Acute inflammation:
- Neutrophils- active in non specific phagocytosis (non specific defence). Low neutrophil count leads to life threatening infections. They are the first on scene in ACUTE inflammatory response. They release cytokines = recruiting and activating other cells and inflammation response.
- Basophil: release heparin and histamine- least common cell

Chronic inflammation

  • lymphocytes: T and B are involved in specific/acquired immunity such as B cells which produce antibodies, T cells release toxins to kill pathogenic cells.
  • macrophages:
  • Eosinophil: important in allergic reactions (acute and chronic response? ) and in the control of Helminths
  • Monocyte: important in non specific phagocytosis, migrate into the tissues to become macrophages. (monocyte in blood, macrophage in tissue)
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11
Q

Discuss the function of the innate immune system in preventing invasion by
pathogens.

A

Innate = first line
non specific, initiates inflammatory response

Physical and chemical barriers:
· Skin prevents entry
· Stomach acids low pH kills microbes
· Mucous traps dirt and microbes
· Tears contain antibacterial enzymes
· Saliva has enzyme and is antibacterial
· Ciliated respiratory epitheliums remove debris

(2nd line) Internal defences:
· Fight pathogens that invade deeper tissues
· Includes: phagocytes, antimicrobial proteins, fever and inflammatory response, no memory

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12
Q

Compare and contrast lymphocytic leukaemia with lymphoma.

A

leukaemia is increased WBC in the bone marrow and blood. can be acute, chronic, lymphatic or non lymphatic .
lymphoma usually starts in the lymphoid tissues like lymph nodes and tissues. Can be Hodgkins or non Hodgkins.

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13
Q

Review meningococcal case study from tutorial and describe meningococcal meningitis and meningococcal septicaemia.

A

Meningitis which is bacterial or viral infection of the meninges can turn into septicaemia when the infected blood goes into the blood stream and multiplies causing blood poisoning .

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14
Q

Describe the pathophysiological processes that may lead to disseminated intravascular
coagulation

A

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Two main mechanisms trigger DIC:
1. release of tissue factor or thromboplastic substances into the circulation
2. widespread injury to endothelial cells
- begins with the formation of
blood clots through out the body and bleeding once all of the clotting factors have been consumed.

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15
Q

Review the different types of shock and their cause.

A

In all types of shock, the cell either is not receiving an adequate amount of oxygen or is unable to use oxygen
different types of shock:
- cardiogenic: ‘myocardial dysfunction and tissue hypoxia in the presence of adequate intravascular volume’ and most cases follow acute myocardial infarction. (causes= myocardial dysfunction, tissue hypoxia).
- hypovolaemic: large loss of fluid volume, whether it be blood, plasma or interstitial fluid. (cause= loss of fluid volume)
- neurogenic: result of vasodilation that results from parasympathetic overstimulation and sympathetic under stimulation (causes = trauma to spinal cord or medulla, severe stress, lack of oxygen to medulla, depressive drugs).
- anaphylactic: results as an allergic reaction to an allergen and leads to similar physical alterations as neurogenic shock. (cause= anaphylaxis)
- septic shock: It begins with an infection that progresses to bacteraemia, then sepsis, severe sepsis and septic shock. (cause= micro organism)

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16
Q

Describe the vascular and cellular responses that promote healing following a wound in the skin

A

Vascular and cellular responses are seen in the inflammatory reaction at the site of a wound.
Vascular responses is where vasodilation and vascular permeability occurs.
The vessels adjacent to the injury, dilate and blood flow increases, swelling occurs, increased blood clotting.
Tissue fluid also increases and acts as a medium for inflammatory proteins, it also helps remove pathogens and cell debris through lymphatic drainage.
Cellular response is where leukocytes/neutrophils infiltrate the site.
chemotaxis = migration, formation of inflammatory barrier, phagocytosis; to get rid of pathogens.

17
Q

Discuss innate/specific immunity.

A

innate immunity: a natural resistance that is present at birth and protects the individual by providing a natural barrier, activating cells and molecules that limit and destroy the capacity of foreign substances to enter and spread throughout the body. includes the skin (first line) and second line of defence. = no memory

specific: develops as the individual is exposed to foreign substances. It is a slower performing system than the innate system, yet is more powerful and precise, as it selectively targets foreign substances that it has identified. = third line of defence e.g. T and B cells.

18
Q

Discuss the active/passive immunity

A

Active immunity is attained by exposure to a pathogen. This leads to the production of antibodies in the body. The antigens present on the surface of the pathogens act as markers that bind to the antibodies.

Passive: is acquired when antibodies are introduced into the body from an external source. It provides a quick response to the infection. However, passive immunity is short-lived because the antibodies are not continually replenished as they would be in an individual whose immune system is responding directly e.g. maternally acquired as a foetus.