SSS FunMed2 Flashcards

1
Q

After activation, which type of immunity do CD4 Th1 cells and CD4 Th2 cells trigger? [2]

which cytokines causes this to happen for each?

A
  1. CD4+ Th1 Cell: IFN-y & TNFa: - triggers cell mediated immunity (to target intracellular pathogens, using CD8+, NK & macrophages)
  2. CD4+ Th2 Cell: IL-4, IL5, IL-13: triggers humoral immunity (extracellular pathogens - B cells & lots of proteins)
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2
Q

what do both MHC Class I & Class II have on them? [1]

A

Both have peptide-binding cleft: but the fit between the amino acid side chains inthe peptide and the grove of MHC molecule determine binding

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3
Q

what is Th1 vs Th2 response to allergies?

A
  • Th2 responses lead to IL-4, which leads to IgE, which causes allergies
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4
Q

how do cytokines drive the recruitment of immune cells (when endothelium is damaged)? (3)

what do TNFa and chemokines do specifically?

A
  • *1. tethering:** cytokines make the lining the BV more sticky
  • *2. rolling and activation:** chemokines activated adhesion molecules and allow rolling arrest
  • *3 diapedesis & migraton:** cause cells to flow in to cells within tissues
  • *TNFa**: increaes stickiness of endothelium by increasing expression of adhesion molecules:
  • rapid release from Weibal-Palade bodies (WP) (adhesion molecules)
  • new synthesis of TNF molecules
  • *Chemokines**: activate adhesion molecules to increase binding
  • causes rearangement of adhesion molecules on surface of cell, to bind more strongly to vessel wall.
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5
Q

how does a cyotkine storm occur?

A

cytokine production becomes uncontrolled to a potentially fatal positive feedback loop:

  • *- cytokine stimulates immune cell
  • immune cell produces cytokine**
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6
Q

what is difference between immune reponse in normal v asthma / allergy ?

A

normal:

  • niave CD4+ T cell in presence of IL-4 = Th2 cell
  • Th2 cell produces more IL-4, which induces B cell to class swich to make IgE
    ​- IgE binds to mast cells, which, if comes into contact with antigen that induced B cells, causes degranulation

asthma:

  • overproduction of IL-4 -> drives allergies and asthma
  • its the release of the degranulation by mast cells that causes response
  • if have an allergy: subsequent exposure are rapidly released (why get really quick response)
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7
Q

what granules do basophils contain? [2]

A

Large dark purple cytoplasmic granules that often obscure the bilobed nucleus

The granules contain:

Histamine (vasoactive substance which promotes vasodilation during inflammation)

Heparin (an anticoagulant which prevents clotting

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8
Q

Q

acid / base disorders:

If the problem is with the respiratory system, the kidneys can compensate by altering HCO3-. How is this altered for acidosis & alkalsosi?

A

A

If the problem is with the respiratory system, kidneys:

  • In acidosis: increases HCO3-
  • In alkalosis: ¯ HCO3-
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9
Q

innate immunity tries to take out pathogens. the system uses complement blood proteins. name 2 that do this and their role [2]

A

Uses complement blood proteins that

  • opsonise (act as markers for phagocytes)
  • cytolyse (directly attack via membrane attack complex (MAC))
  • enhance inflammation
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10
Q

Q

acid / base disorders:

If the problem is metabolic, the lungs can compensate by altering Co2 levels. How is this altered for acidosis & alkalsosi?

A

•the lungs can compensate by altering CO2 Levels

•In acidosis: increases­ RR (decreases CO2)

•In alkalosis: decreaeses¯ RR (increases CO2)

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11
Q

which nuclei in the hypothalamus recieve information regarding:

a) warm temperatures [1]
b) cold temperatures [2]

A

- preoptic area (POA) monitors core temperature: recieves input from warm receptors from skin and and internal receptors

- paraventricular (PVN) and dorsomedial hypothalamic (DMH) nuclei: recieve input from cold

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12
Q

what are the products of Krebs cycle? [4]

A
  • produces: Co2, 3NADH, 1 FADH2, 1GTP. feeds into oxidative phosphorylation pathway
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13
Q

label A-D stages of cancer development:

A
B
C
D

A

label A-D stages of cancer development:

A: hyperplasia
B: metaplasia
C: dysplasia
​D: anaplasia

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14
Q

what can type 2,3, & 4 hypersensitivty be

A

Type II: IgG/IgM to patients own RBCs due to M. pneumonia

Type III: complement activation causing inflammation e.g. S. pyogenes causing glomerulonephritis

Type IV: T cell mediated e.g. TB granulomas

1-4: ACID

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15
Q

what are the spectrums for antiobiotics? (2)

A

Broad: both aerobes and anaerobes

Narrow: either aerobes or anaerobes or a specific gram +/-

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16
Q

name two ways that cancer can be caused by mutations to transcription factors [2]

A

C-MYC overexpression: breast / colon cancer
C-MYC translocation: burkitt lymphoma

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17
Q

what are the two types of venules?

how do u distinguish them?

A
  • Postcapillary venules collect blood from the capillary network and are characterized of pericytes (contractible cells wrapped around the endothelial cells). Made up of endothelial, basal lamina and pericytes.
  • Muscular venules can be distinguished by the presence of tunica media. Distal to the postcapillary venules and have one to two SMC layers.

(picture on right = postcapil, on left; muscular venules)

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18
Q

** which method of calculating HR do you use if the ECG is irregular? **

A

A

QRS X 6

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19
Q

what does the phrenic nerve cause during inhalation / exhalation? [2]

A

The motor innervation activation will cause the diaphragm to contract with inspiration, resulting in a flattened diaphragm and increased intrapleural space.

During exhalation, the diaphragm relaxes and returns to the dual dome shape.

The phrenic nerve also provides touch and pain sensory innervation to the mediastinal pleura and the pericardium in addition to the intercostal nerves.

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20
Q

trachea runs from where to where?

at which structures in trachea does the aorta cross over?

levels of oesphagus? [1]

A

trachea: c6-t4
- aorta arches over left main bronchus and lung root
- C6-T10 = oesphagus

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21
Q

Q

where do posterior intercostal arteries 1&2 orginate?

where do posterior intercostal arteries 3-12 orginate?

A

A

where do posterior intercostal arteries 1&2 orginate: costocervical trunk (branch that comes off subclavian arteries)

​where do posterior intercostal arteries 3-12 orginate: desecending aorta

22
Q

describe the paths of th coronary arteries - what do they both anastmose with?

A

RCA: anastomoses with circumflex branch of LCA: gives rise to posterior interventricular artery

LCA: loops around apex and branches into left anterior descending (LAD). anastamoses with posterir interventricular artery

23
Q

Q

calmodulin is assocaited with which type of muscle contraction? [1]

tropinin C is associated with which type of muscle contraction? [1]

A

A

calmodulin is assocaited with smooth muscle muscle contraction

tropinin C is associated with cardiac muscle muscle contraction

24
Q

what is S like on normal ECG for V1-V6?

which precoridal leads should T wave be largest on?

A
  • *S wave:**
  • large on V1 & V2
  • progessively smaller to V5
  • should be gone by V6

T wave: large on V2 and V3

25
Q

what do the qrs individually show?

A

Q wave representing interventricular septal depolarisation

R wave representing ventricular depolarisation

S wave representing depolarisation of the Purkinje fibres / signifies the final depolarization of the ventricles, at the base of the heart

26
Q

what is polycythaemia? what is absolute polycythaemia? what is relative polycythaemia?

A

Polycythaemia is a disease state in which the haematocrit increases. It can be due to an excessive production of red blood cells, absolute polycythaemia, or to a decrease in the volume of plasma, relative polycythaemia

27
Q

where in the medulla is the NTS located?

what does the NTS connect to ? (2) - which one of these is linked to parasympathetic output and sympathetic output

A

The Nucleus of the solitary tract (NTS) lies near the dorsal surface of the medulla

NTS connects to:

  • the vasomotor centre in the rostral medulla: sympathetic output to increase BP
  • nucleus ambiguus in the nearby lateral medulla: parasympathetic output to decrease BP
28
Q

BP is detected in the carotid and aortic sinus, afferent nerve fibres come via CNIX and CNX to the NTS centre in brain.

Describe the efferent nerve fibre outflow and effect if:

a) BP is too low (3)
b) BP is too high (2)

A
  • *a) BP is too low:**
  • NTS, via the vasomotor centre, activates SNS: noradrenaline acts on alpha 1 adrenoreceptors on vascular smooth muscle = vasoconstriction
  • increase in HR - raises CO
  • constriction of veins
  • *b) BP is too high:**
  • NTS, via the nucleus amibguus, actvates PNS: SAN inhibiting muscarinic receptors to cause hyperpolarisation of the cardiac muscle cells and therefore slow the heart down
  • vasomotor centre inhibited
29
Q

how do u measure clearance?

A
30
Q

Diabetes insipidus is caused by what?

A

Diabetes insipidus; damage to the hypothalamus or posterior pituitary leading to loss of ADH secretion. Result high volume of dilute urine.

31
Q

what are Hasssals corpsucles?
function?
location?

A

hassals corpuscles: concentric layers of flattened reticular epithelial cells filled with keratohyalin granules and keratin.

activate dendritic cells

only found in thymus

32
Q

what are the names and locations of the pleural recesses? [2]

A
  1. costadiaphragmatic: located between the costal pleurae and diaphragmatic pleura
  2. costomedialstinal: located betweeen the costal pleurae and the mediastinal pleurae, behind the sternum
33
Q

how do calcium channel blockers work?

what are the two major types? & mech of action for each

A
  • block Ca entry to vascualr smooth muscle and myocardial cells: interrupt excitation-contraction coupling

types:

  • *1. dihydropyridine CCBs**: vasodilate dominately. reduced systemic vascular resistance
  • *2. non dihydropyridine CCBs:** reduce HR, contractility, conduction. may worsen heart failure tho
34
Q

what is the green?

A

costodiaphragmatic recess :)

36
Q

what is liddle syndrome / disease?

A
  • enac channels undergo ubiquitination
  • this causes inappropriately elevated sodium reabsorption in the distal nephron
  • this makes have too much water retention and hypertension
37
Q

how can sympathetic action of JGA cause a positive feedback of reninn release?

A

This raises the possibility of positive feedback; sympathetic stimulation increases renin release, angiotensin then increases noradrenaline release which in turn increases renin release leading to hypertension

38
Q

at which structure does ithe internal laryngeal nerve and superior laryngeal artery enter larnyx?

A

Internal laryngeal nerve and superior laryngeal artery come through thyrohyoid membrane.

39
Q

what does activation of AT1 receptors cause to occur? [3]

A

AT1:

i) GCPR which increases Ca entry into smooth muscle & constriction to occur
ii) stimualtes noradrenaline release from sympathetic nerve terminlas (can increase BP via SNS too)
iii) found in cells of adrenal cortex: secretes aldosterone

41
Q

calculate the o2 and co2 exchanges for the below values. assume alveolar ventilation is 4.2 l/min

Room o2 = 21%
alveolar o2 = 14%

Room Co2 = 0.04%
alveolar Co2 = 5.5%

A

Co2 output = 4.2 X (5.5 - 0.04 / 100) = 0.231 L/min

O2 input: 4.2 X (21 - 14 / 100) = 0.294 L/min

42
Q

what is intrapleural pressure a balance of? [2]

what is intrapleural pressure normally? [1]

A
  • the chest wall and lungs are locked together by the intrapleural fluid in the intrapleural space
  • at the end of exipration get opposing forces:
  • *a) lungs: elasticity is causing them to collapse
    b) chest wall: elasticity is causing to spring outwards**
  • generates a pressure = PPl

intrapleural pressure usually negative with respect to the atmosphere and the air pressure in the alveoli

43
Q

how do you calculate compliance in respiratory physiology?

A

compliance = change in volume / change in pressure

44
Q

label these parts of thymus histology :)

A
45
Q

which two factors cause an increase in resp workload? [2]

A

compliance
airway resistance

46
Q
A
47
Q

name 3 types of cells that monocytes can differentiate into [3]

A

monocytes:
- differentiate into macrophages & phagocytose stuff, Kupffer cells, Langerhan cells, alveolar marcophages

49
Q

what are the two branches found in palmar arches?
where do they come from?^

A

superficial & deep palmar arches

  • Branches of both radial and ulnar arteries
    i) Superficial arch mainly from ulnar artery.
    ii) Deep arch mainly from radial artery.
50
Q

Which histological landmarks of the sarcomere shrink when a muscle contracts? [3]

A

The I-band and the H-band decrease in size; [2]

the A-band remains the same.

51
Q

what type of cells line the nasal cavity respiratory system - respiratory mucosa?
what are the 3 different types?^

what is role? (2)

A

respiratory mucosa:
- ciliated, pseudostratified columnar epithelium
a) goblet cells - tall columnar cells producing mucous
b) brush cells - bear short microvilli
c) basal cells - stem cells

role:
warms, moistens and filters the inspired air

53
Q
A

1 = hyoid bone

2 = epiglottis

3 = thyroid cartilage

4 = arytenoid cartilage

5 = cricoid cartilage

54
Q

what cell type makes true and false vocal cords? [1]

A

non k stratified squamous

55
Q

how can you tell the difference histologically between PCT and DCT? [1]

A

PCT has brush border on luminal surface, DCT does not / The DCT is lined with simple cuboidal cells that are shorter than those of the proximal convoluted tubule (PCT

57
Q

which muscle and which nerve supplies the muscle that gives tone to voice? [2]

A

cricothyroid muscle
external laryngeal muscle