Review posters 18/05/2016 Flashcards Preview

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Flashcards in Review posters 18/05/2016 Deck (90):
1

What composes the upper respiratory tract?

Two nasal cavities
Oral cavity
Oropharynx, laryngopharynx, nasopharynx
Larynx

2

What composes the lower respiratory tract?

Trachae, main bronchi, lobar bronchi, segmental bronchi, terminal bronchioles and alveoli.

3

Describe the arrangement of the trachae, the oesophagus and the larynx in the neck.

The oesophagus lies most posteriorly. Then the trachae is just anterior to this. Then the ithmus of the thyroid gland lies in front of the trachae.

4

The chest wall consists of

Skin, fascia, skeletal muscle, bone/joints, parietal pleura.

5

What is the role of the chest wall?

Protect the chests internal organs

6

Chest cavity consists of

RIght and left pleural cavities and the mediastinum.

7

Which fissure do both lungs have?

The oblique fissure

8

How many lobes does each lung have?

Right- three lobes- superior, middle and inferior
Left- two lobes- superior and inferior.

9

Lobar bronchi supply

lung lobes

10

segmental bronchi supply

lung segments

11

How many lung segments does each lung have?

10

12

Describe the bony features of the sternum

At the top- manubrium. This goes down to the sternal angle. Then the body of the sternum and then the xiophoid process.

13

What is the joint that attaches the ribs to the sternum?

sternocostal joint.

14

True ribs

1-7

15

False ribs

8-10

16

Floating ribs

11 and 12

17

What joints are in false ribs?

costochondral attaching the rib to the costal cartilage
Sternochondral attaching the cartilage to the sternum

18

Which joint attaches the ribs to the vertebrae and where do they articulate?

The costovertebral joint.
The tubercle of the rib articulates with the transverse process of the vertebrae.
The head of the rib articulates with body of the vertebrae and the body of the vertebrae superior.

19

What sits in the costal groove?

The neurovascular bundle.

20

Where do the layers of intercostal muscles attach?

To the adjacent ribs

21

Describe the blood supply to the intercostal spaces.

Posteriorly-
The abdominal aorta's lateral branches are called the posterior intercostal arteries. These supply the posterior aspect of the intercostal spaces.
It is drained by the azygous vein.
Anteriorly- supplied by the internal thoracic artery. This branches into the anterior intercostal arteries which supply the anterior of the intercostal spaces. Drained by the internal thoracic vein.

22

Describe the branches of the abdominal aorta supplying the thorax.

Laterally- posterior intercostal arteries.
Anteriorly- bronchial arteries that supply the lung tissue.

23

Where do the internal thoracic arteries run in comparison to the sternum.

Laterally

24

The seratus anterior attaches:

To the anterior medial border of the scapula and between ribs 1-8

25

What happens in the seratus anterior becomes detached?

Winged scapula.

26

Attachments of the diaphragm

The sternum, the lower 6 ribs and costal cartilages.

27

Draw ALL the vessels of the heart

---

28

Name the branches of the aorta.

Brachiocephallic which splits into right subclavian and right common carotid.
Left common carotid
Left subclavian

29

What drains into the SVC?

The internal jugular vein and right subclavian vein.

30

What is an auricle?

They increase the capacity of the atrium.
Look like a wrinkled sac on the outside of the heart.

31

Describe the coronary artery supply to the heart.

The coronary arteries arise from the root of the aorta at the coronary ostia.
The right coronary artery runs along the right side of the heart, branching into the marginal artery before going posteriorly. When it gets to the base (posterior) part of the heart it branches to give the posterior interventricular artery.
The left coronary artery branches into the left anterior descending, the left marginal and the left circumflex artery.

32

What is the coronary sinus?

The venous drainage from the heart into the right atrium.

33

Describe the openings in the right atrium.

The SVC, IVC and coronary sinus. Also the oval fossa makes an indentation.

34

All the valves have three cusps except:

mitral valve- only has two.

35

Mitral valve has:

anterior and posterior cusps

36

Tricuspid valve has

anterior, posterior and septal

37

Pulmonary valve has

left, right and anterior. (left and right attached to septum)

38

Aortic valve has

left, right and anterior

39

Signs of immune deficiencies

S- serious infections. Unresponsive to oral antibiotics
P- persistant infections- early structural damage, chronic infections
U- unusual infections- unusual organisms at unusual sites
R- recurrent infections (1 or more major infection per year)

40

Classifications of immunodeficiency

Secondary- common. Often subtle. Often involves more than one component of the immune system.
Primary- born with it. Relatively uncommon

41

Conditions associated with immune deficiency

Physiological immune deficiency- ageing, prematurity
Infection- HIV, measles
Treatment interventions- immunosuppressive therapies, anti cancer agents, corticosteroids
Malignancy- lymphoma, leukaemia, myeloma
Biochemical and nutritional disorders- malnutrition, diabetes, renal insufficiency

42

Phagocyte deficiencies

Could be failure in production, mobilisation/ recruitment or function of phagocytes.

43

Reticular dysgenesis

Failure to produce neutrophils

44

Kostmann syndrome

Severe congenital neutropenia
Rare autosomal recessive disorder.

45

Clinical presentation of Kostmann syndrome

Infections usually within 2 weeks of birth. Recurrent bacterial infections. Could be both localised or systemic.
Fever
Mouth ulcers
Irritability
Failure to thrive

46

Supportive treatment of Kostmann syndrome

Prophylactic antibiotics
Prophylactic antifungals
mortality 70% within first year.

47

Definitive treatment of Kostmann syndrome

Stem cell transplantation- the defect is in the neutrophil precursor- by replacing this you should hopefully solve the issue.
Granulocyte colony stimulating factor- specific growth factor to assist maturation of neutrophils.

48

Leukocyte adhesion deficiency

Failure of white blood cells to adhere/recognise activation markers expressed on endothelial blood vessel cell surfaces.
Rare primary immune deficiency- genetic defect in leukocyte integrins.

49

Presentation of leukocyte adhesion deficiency

Recurrent infections occur
Very high neutrophil counts in the blood
Deep tissue infections- no pus.

50

Defect of phagocyte function

Defect in pathogen recognition receptor
Defect in opsonins
Defect in complement or antibodies

51

Chronic granulomatous disease

Failure of oxidative killing mechanisms.
Absent respiratory burst- deficiency of intracellular killing mechanisms of phagocytes.

52

Commonest phagocyte function deficiency

p47phox
Component of NADPH oxidase
Inability to generate free radicals.

53

Features of chronic granulomatous disease

Recurrent deep bacterial infections- especially staph, aspergillus, mycobacterium, atypical mycobacterium, psudemononas and cepacia.
Recurrent fungal infections
Failure to thrive
Lymphadenopathy (massive enlargement of lymph nodes)
Granuloma formation

54

Investigations into chronic granulomatous disease

NBT test- nitroblue tetrozulum test
Asks whether neutrophils can kill through the production of free radicals. Feed the patients neutrophils a source of ecoli. Then add hydrogen peroxide sensitive dye. if they are working, the dye will turn blue.

55

treatment of chronic granulomatous disease

Supportive- prophylactic antibiotics.
prophylactic antifungals
Definitive- stem cell transplant
Gene therapy

56

Why are diseases like TB especially hard for the immune system to get rid of?

They hide in the immune cells themselves.

57

Infection with Tb

Infected macrophages produce IL12
IL12 induces T cells to produce gamma interferon
Gamma interferon feeds back to macrophage and neutrophils
Stimulates production of TNF
Stimulates oxidative pathways.

Any defect in this will result in TB infection.

58

Risk factors for cardiovascular diseases.
Out of these select the modifiable ones and non modifiable ones

Oral contraceptive pill- M
Age- NM
Previous MI- NM
High blood pressure- M
Smoking-M
Alcohol-M
Obesity-M
Diabetes-M
Previous strokes/TIA's -NM
Inactivity-M
Family history-NM
Ethnicitiy-NM
Gender-NM

59

HDL cholesterol

Has a protective effect for risk of atherosclerosis and CHD. Lower HDL means higher risk.
HDL tends to be low when triglycerides are high.

60

LDL cholesterol

Primary target of drugs to try to prevent CHD.

61

Triglycerides

Increase CHD risk. Normal level 2.3.

62

What does smoking do to your cholesterol?

Increases BP
Lowers HDL

63

What does diabetes do to your cholesterol?

Decreases HDL
Increases VLDL

64

Hypercholesterolaemia

excess cholesterol in the blood stream

65

Dyslipidaemia

elevation of cholesterol

66

Membrane potential Em is maintained by

Seperation of opposite charges across the membrane in mV. The membrane itself is not charged.

67

Ena

+61mv

68

Ek

-90

69

resting potential of a cell

-70mv

70

The nernst equation:

calculates the equilibrium potential for any given ion.
For a monovalent ion at 37 degrees this is
Eion= 61 log [ion]o/[ion]i

71

The goldman Hodgkin Katz equation

Determines membrane potential taking into account all the ions.

72

What cells make up the innate immune response?

Macrophages
Neutrophils
Eosinophils
Basophils
Dendritic cells
Mast cells.

73

Describe the innate immune response.

Immediate, non-selective response.

74

First line of defence

The skin

75

Properties of the skin

Sebacious glands secrete
Ammonia keeping the pH low.
Antimicrobial peptides
Hydrophobic oils
Lysozymes

Mucus glands secrete- IgA antibodies
Lysozymes

76

How do macrophages react to pathogens?

If the pathogen gets inside the body it expresses PAMPS (pathogen associated molecular patterns) which are not present on human cells. Pathogen recognition receptors (PRR) on macrophages recognise these and therefore begin to phagocytose them.

77

Describe the process of phagocytosis

Perfomed by macrophages, dendritic cells, neutrophils and monocytes.
The pathogen is recognised
Receptor (PRR) binds to it
Rearrangement of the cytoskeleton to form phagosome
Fusion with lysozyme to form phagolyzosome
Release of oxidative radicals- kills pathogen
MHC class II presents it on cell surface.

78

What is the role of antibodies?

Increase toxic reactivity of oxygen and hydrogen
Opsonise- making it more obvious to the phagocytes where the pathogens are aiding phagocytosis.

79

What do natural killer cells do?

Cells infected with pathogens express MHC Class I on their surface. The natural killer cell recognises these and forms a membrane attack complex. It also releases pro-inflammatory mediators.

80

What do mast cells do?

Mast cells reside in tissues. They degranulate and release inflammatory mediators. They also express genes and create new pro-inflammatory mediators.

81

Examples of pro-inflammatory mediators.

Cytokines- TNFalpha, IL-1, IL-6, IFN gamma
Chemokines
Nitric oxide
Prostaglandins
Histamine

82

Describe the process of the inflammatory response in full.

1) A screw covered with manure has broken through the epidermis. This screw is covered with bacteria that get into the interstitial fluid.
2) When the skin is pierced, some of the cells will die. The ones that are still in a position to do so will release chemokines. These are small proteins that cells release as a signalling mechanism
3)Mast cells can be activated by direct contact with the bacteria or by chemokines. The mast cells then release histamine
4)Histamine and thrombin act on the endothelial cells in the cappilary walls. These cause vasodilation increasing the space between the endothelial cells.. The capillary also gets larger (swelling). The histamine and thrombin also increase selectin expression meaning that white blood cells bind more strongly to vessel walls
5)When the blood vessel dilates- the rate of blood flow slows. The white blood cells migrate to the periphery of the vessel in a process called white cell margination. On the white blood cell, there are things expressed called integrins. During inflammation, the endothelial walls become sticky and the white blood cells roll along its surface. This is due to weak binding between integrins expressed by the WBC and the selecting on the endothelial surface.
6)TNF and interleukin 1 increase endothelial cell of expression of VCAM (vascular cell adhesion molecule) and ICAM (intracellular adhesion molecule). Chemokines also asssist in stopping the WBC from rolling.
7) The vessels become leaky and proteins escape- water follows causing swelling
8) WBC's move out of the vessel by diapedesis
9) Dendritic cells also become activated and present the MHC class II with the bacteria. B cells and T cells also come through the vessel and recognise the MHC class II and activate.

83

Acute phase proteins

Cytokine release stimulates the liver to produce these.

84

CRP

Inflammation- prevents spread of infection
lower than 10mg is normal
Can opsonise bacteria
Activates complement system

85

Serum amyloid protein

Prevents spread of infection

86

Complement proteins

Diagnostic markers

87

Fibrinogen

Wound healing, coagulation

88

Resolution

Good as new- occurs because the tissue has good capacity to regenerate with good blood supply. Means white blood cells can reach the area and injurous agent is removed.

89

Supparation

PUS- contains living and dead cells. Also neutrophils, bacteria and inflammatory debris. May be termed an abscess.
If a cavity is filled with pus- empyema

90

Granulomatous tissue

Defect is slowly infiltrated by capillaries and then myofibroblasts which lay down collagen and smooth muscle cells. The tissue looks red.