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Important processes Flashcards

1
Q

3 stage viral replication (include sub stages

A
  1. Entry (fusion with membrane via virus receptor > endocytosis).
  2. Replication (uncoating > genome replication >mRNA synthesis > protein synthesis.
  3. release (non enveloped accumulate til cell lysis, enveloped bud out (some secreted out)).
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2
Q

explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?

A
  1. Transformation - DNA fragments of a lysed cell are taken up by a competent bacteria and incorporated into its genome
  2. Phage mediated - infection of bacteria by abnormal bacteriophage
  3. Plasmid mediated - 2 bacteria form cytoplasmic bridge>
    plasmid DNA replicates> is taken up by new bacteria> cells seperate.
    Worrying because bacteria don’t need to be related to receive plasmids
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3
Q

function MOA of aminoglycosides

A

cause the bacteria to misread the genetic code.
binds to the 30S subunit of bacterial ribosomes > cause distortion of the region where mRNA is translated > incorporation of incorrect amino acids or the premature termination of protein synthesis

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4
Q

overall function of a Beta LActam? one example. MOA

A

inhibit cell wall synthesis. Penicillin
Bind cell wall at the d-ala, d-ala terminal >inhibit cell wall synthesis.> abnormal synthesis induces autolytic enzymes > weakens the cell wall > allows water in >bacteria will rupture.

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5
Q

how do bacteria often penetrate the epithelium? what initiates this

A

pathogen-mediated endocytosis. Initiated by bacterial surface proteins

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6
Q

how do viral genomes evolve. give examples of each (3)?

A

mutation - esp. RNA virus
If 2 viruses infect same cell can either:
Recombination - exchange stretches of nucleic acid (esp. DNA virus).
Reassortment - swapping segments of genome (influenza).

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7
Q

typical course of viremia?

A

virus infects epithelial cells and multiples > regional lymph node(more replication) > enters blood stream (primary viraemia)> spleen and liver (multiplcation) > enter blood again (2ndary viremia) > focal infection

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8
Q

targets of flu vaccine (2)?

A

antibody to HA blocks attachment. antiobdy to NA blocks release

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9
Q

MOA of MAO inhibitors

A

they inhibit the activation of monoamine oxidase which breaks down monoamine neurotransmitters (eg. NA, dopamine), thereby increasing their availabilty

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10
Q

triple response of histamine? explain cause

A

Redness (vasodilation at site).
Wheal (oedema from vascular permeability).
Flare (spread through sensory fibres)

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11
Q

mechanism of NO activation

A

AcH, bradykinin or mechanical stress act on endothelial cell > increase calcium > activate NO synthase > turns arginine into NO

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12
Q

increase in cardio output does what to venous pressure and why?

A

decrease it - more blood in arteries

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13
Q

how does the body infer the adequacy of cardiac output?

A

pressure, pO2, pH, pCO2

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14
Q

describe Virchow’s triad

A

there are 3 components to blood clotting: The vessel wall, the blood composition and the blood flow

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15
Q

what are the 3 stages of coagulation. describe them

A

Initiation - TF is exposed and binds to FVII. The complex then turns 9 and 10 to 9a and 10a.
Amplification - the 10a/5a complex (on vessel wall) converts small amounts of prothrombin to thrombin. The thrombin activates some factors and platelets (which bind to the factors).
Propagation - the complexes create a large amounts of thrombin from prothrombin (thrombin burst) which then turns fibrinogen into fibrin to clot the bleeding

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16
Q

describe the arachidonic acid metabolism pathway (include enzymes)

A

Cell membrane phospholipids >(phospholipase A2) Arachidonic acid > sideways to leukotrienes (5 lipoxygenase) or downwards to eventual prostaglandins (COX

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17
Q

describe the action potential of a ventricular myocyte

A

resting at -90.

  1. Na comes in so depolarizes.
  2. K+ out so starts to dip
  3. Ca+ in (K still going out) so plateaus
  4. Only K out so repolarizes
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18
Q

name the drug suffixes of the angiotensin renin-system antihypertensives. What is their MOA?

A

“pril” = ACE inhibitor so reduce cardiac hypertrophy, vascular tone and aldosterone production.
Also prevent Bradykinin breakdown (ACE degrades bradykinin) which vasodilates.

Sartan = blocks angiotensin 2

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19
Q

what do ACE and angiotensin 2 do

A

ACE converts Angiotensin1 to Angiotensin2.

A2 induces aldosterone secretion from kidneys, vasoconstriction, cardiac cell growth and increases sympathetic activity.

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20
Q

what is an aneurysm explain 2 types and give 4 risk causes

A 
weakening in media of a vessel. saccular (one side) or fusiform both sides
ATHEROSCLEROSIS.
CONGENITAL WEAKNESS IN WALL.
SYSTEMIC HYPERTENSION.
INFECTION IN WALL
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21
Q

MOA of aortic dissection

A

tear in intima> blood enters and splits media

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22
Q

MOA of athersclerosis

A

disruption to endothelium => LDLs enter > oxidised by ROS > cytokines recruit macrophages > ingest lipid to become foam cells > recruitment of smooth muscle cells from media > produce more ECM > some plaque degenerates forming necrotic lipid core > Eventually variable combination of vessel stenosis, impaired vasodilation, plaques vulnerable to rupture, local prothrombotic environment

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23
Q

dif b/w stable and unstable angina

A

stable will occur on exertion and caused by stable athero plaque whereas unstable will occur at rest and probs get worse over time - caused by unstable athero plaque

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24
Q

MOA of SOB in angina

A

insufficient oxygen to myocyte> => muscle cant contract and relax => increase LV Diastolic Volume=> pulmonary congestion => dyspnea

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25
Q

most common cause of SCD

A

coronary athersclerosis + thrombus accusing acute ischaemia

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26
Q

MOA of symptoms in unstable angina

A

Unstable plaque => Acute Plaque Event => blood exposed to sub-endothelium => cascade gets going=> thrombus + vasoconstriction

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27
Q

3 types of cardiac infarctions with respect to the wall. give reasons for each

A

Regional Transmural:
99% caused by thrombosis in an atherosclerotic coronary artery after an Acute Plaque event.

Subendocardial:
early intervention or spontaneous lysis of thrombus.

Circumferential:
triple vessel narrowing
systemic perfusion reduction eg; shock.

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28
Q

describe the physiological concepts of treating stable angina (basically describe diagram form lecture).

A

can either increase oxygen supply to myocardium (decrease HR) or decrease oxygen demand (decrease HR, SV, afterload and preload)

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29
Q

dif in causes b/w concentric and eccentric hypertrophy. how dif in wall thickness

A

concentric is caused by hypertension and aortic stenosis. larger wall thickness.
Eccentric is caused by volume overload or mitral or aortic regurgitation

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30
Q

3 cardiac failure mechanism and 2 reasons for each

A

loss of muscle - Infarction or myopathy.
Pressure overload - hypertension or aortic stenosis.
Volume overload - valve regurgitation or septal shunts

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31
Q

clinical signs of LH failure (3) and right(1)

A

SOB, fatigue, tachycardia. RH failure = oedema

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32
Q

compensation of Aortic Stenosis?

A

LV concentric hypertrophy due to pressure overload

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33
Q

compensation of Aortic or Mitral Regurgitation?

A

LV dilatation due to volume overload

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34
Q

compensation of mitral stenosis

A

both dilatation and hypertrophy

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35
Q

how does Hb enhance oxygen diffusion

A

also carries NO which it releases simultaneously with oxygen to dilate vascular smooth muscle

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36
Q

hyperactivity of HMG-CoA reductase may lead to what

A

atherosclerosis by making more cholesterol and thus more blood LDL

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37
Q

cholesterol is thought to be made in 4 stage, what are the 3 key intermediates

A

HMG-CoA, isoprene and squalene

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38
Q

examinable scheme for cholestorol

A

acetyl-CoA > acetoacetyl-Coa > HMG-CoA >(enzyme = HMG-Coa Reductase. Cofactors = 2NADPH + 2H+ > 2NADP+) Mevalonic acid + Coa > 6x Mevalonic Acid > Cholestorol

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39
Q

describe how the volume of the thorax is increased

A

Diaphragm going up and down alters Vertical volume.Upper ribs are like pump handle and move sternum superior and anterior, increasing AP volume.Lower ribs are like bucket handles so increase Lateral Volume.

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40
Q

histamine does what to the airways?

A

constricts

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41
Q

a large Pulmonary embolism may cause what compared to a medium size

A 
large = SCD or acute cor pulmonale.
Medium = acute pulmonale or pulmonary infarct
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42
Q

describe the dif in immediate and late phase in an asthma attack

A

immediate = increased vascular permeability (oedema), mucus production and bronchospasm.

Late = epthelial damage from ongoing inflammation

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43
Q

what happens to airways in severe chronic asthma?

A

remodelling with irreversible obstruction

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44
Q

what is emphysema and main type causes?

A

destruction of alveolar walls without fibrosis. Centrolobular - smoking

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45
Q

how does smoking destroy alveoli?

A

increase in elastase destroys elastin and thus the alveoli cell wall

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46
Q

dif b/w primary and 2ndary TB. Where in lung is 2ndary?

A

Primary usually subclinical.
2ndary - reactivation of dormant infection or reinfection.
Apical Areas of Upper Lobe.
can spread to other organs

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47
Q

CO2 is transported in blood in 3 forms. what are they and what % of CO2 for each way

A

60% bicarbonate, 30% attached to proteins (inc. Hb), 10% dissolved

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48
Q

CO2 + H2O equation? enzyme involved

A

CO2 + H2O → H2CO3 → H+ + HCO3-

Enzyme = CA (carbonic Anhydrase)

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49
Q

eqaution of A-a gradient? what is normal

A

PAO2 - PaO2.

Where PAO2 = PiO2 – PACO2 / RQ
RQ=.8 and Pi02 = 150 (at sea level).

PACO2 & PaO2 Will be given in Blood gases. (Normal < 15-30)

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50
Q

2 main causes of Pulmonary Oedema. Give 2 reasons for 1st and 1 for 2nd

A
  1. Increased capillary hydrostatic pressure (mitral stenosis, fluid overload).
  2. Increased capillary permeability (toxins)
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51
Q

3 reasons why obstruction could occur during sleep?

A

– Airway muscles relax (floppy throat - esp REM).
– Throat already narrowed (obesity, tonsils etc).
– Tongue falls backwards ( esp if supine).

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52
Q

why shouldnt give large amount of supplemental oxygen to someone with chronic hypercapnea?

A

they dependant on low oxygen to breath

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53
Q

6 reasons for dyspnea (body systems)

A

resp, cardiac, muscle weakness, metabolic, anaemia, psychogenic

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54
Q

5 respiratory causes of dyspnea? give 2 reasons for each class

A

1) AIRWAYS DISEASE -
a) Upper airways - tumour, foreign body
b) Lower airways - asthma, COPD, bronchiolitis.
2) ALVEOLAR DISEASE -
Pneumonia, lung collapse, pulmonary odema, pulmonary fibrosis.
3) PULMONARY VASCULAR DISEASE -
Pulmonary embolism, vasculitis, primary pulmonary hypertension.
4) PLEURAL and CHEST WALL DISEASE - Pleural effusion, pneumothorax, chest wall deformity.
5) RESPIRATORY MUSCLE DISEASE - Respiratory muscle weakness, phrenic nerve palsy

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55
Q

what are the results of an increase and decrease of NaCl respectively and when do these occur?

A

increase in NaCl (occurs at higher GFR as blood flow is too fast giving less time for NaCl to pass into blood) -vasoconstricts.

A decrease in sodium chloride concentration (occurs at lower GFR as blood flow is too slow giving more time NaCl to pass into blood) initiates a signal from the macula densa that vasodilates the afferent arteriole (increasing GFR).

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56
Q

what releases renin and when is it released? (3)

A

Juxtaglomerular cells (from signalling by macula densa).

  1. Decrease in NaCl at Macula Densa
  2. In response to Blood volume or Pressure decrease
  3. Sympathetic innervation
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57
Q

how do the afferent and effernt arteriole modulate GFR? For what range of MAP is GFR constant

A

If afferent arteriole constricts GFR Decreases.
If Efferent constricts GFR Increases.
80-180

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58
Q

how can NSAIDS cause pre renal failure

A

they reduce prostaglandins that vasodilate - hence less blood to kindey

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59
Q

name 3 non drug causes of pre-renal acute failure

A

haemorrhage, renal stenosis and hypoalbuminaemia

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60
Q

why do proteins stay in blood and not filter in to kidneys? (2)

A

negative charge of proteins and neg charge of glomerular basement membrane repel.
physical structure of membrane (tight pores)

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61
Q

does atheorsclerosis cause hypertension

A

only in renal atherosclerosis

62
Q

what is Hyaline arteriolosclerosis? where is it often seen? most common association?

A

thickening of the walls of arterioles by the deposition of homogeneous hyaline, lumen narrowed. kidneys. Aging

63
Q

3 brainstem tests (include afferent and efferent)

A

Midbrain: pupil light (afferent 2, efferent 3).
Pons: Corneal blink (afferent 5, efferent 7).
Medulla: Gag (afferent 9, efferent 10)

64
Q

innervation of tongue

A

Motor: vagus does palatoglossus and hypoglossal does all other muscles.
Sensory: Posterior 3rd CN9 does all general and special sensory except. CN10 (internal laryngeal does all sensory just behind).
Anterior 2/3s CN5(lingual nerve) does general sensory and CN7 (chorda tympani) does taste.

65
Q

functional pathway of retina

A

photoreceptor > bipolar (in put from horizontal) > ganglion (input form amacrine).

66
Q

why do cones have a greater visual acuity than rods?

A

Cones have a much lower convergence ratio to bipolar cells than rods

67
Q

compare b/w dark and light for photoreceptor bipolar cell communication

A

In the dark, a photoreceptor (rod/cone) cell will release glutamate, which inhibits (hyperpolarizes) the ON bipolar cells and excites (depolarizes) the OFF bipolar cells. In light, however, light strikes the photoreceptor which causes the photoreceptor to be inhibited (hyperpolarized), causing less glutamate to be released. This causes the ON bipolar cell to lose its inhibition and become active (depolarized), while the OFF bipolar cell loses its excitation (becomes hyperpolarized) and becomes silent.

68
Q

main visual pathway from ganglion cells

A

GC > optic nerve >LGN (in thalamus) > optic radiations > visual cortex

69
Q

apart from the LGN name 4 other targets of Ganglion cells and their function

A
  1. midbrain (pupil response).
  2. Suprachasmaitc nucleus (circadian rhythm).
  3. superior colliculus (eye movement).
  4. other part of thalamus (photophobia)
70
Q

what is the MLF and what is it involved in

A

white matter tracts that connect cranial nerves. controls the co-ordiantion of eye movement.

71
Q

neural pathway of sound

A

CNVIII > cochlea nucleus (medulla) > superior olive > lateral lemniscus > inferior colliculus (midbrain) > MGN (thalamus) > cortex (auditory centre in temporal lobe).

72
Q

pathway of sound travelling through ear

A

→sounds travels down auditory canal
→tympanic membrane vibrates
→this causes the Malleus, Incus and then Stapes to vibrate
→stapes transfers force to oval window
→force causes fluid in cochlea (perilymph) to vibrate
→vibration causes Basilar membrane (BM) moves up and down
→ the hair cells on the Organ of Corti (located on BM) bend on the tectorial membrane resulting in the firing of an AP

73
Q

describe the main mechanosensory path. What it is also known as

A

DCML (dorsal Column Medial Lemniscus pathway).
mechanoreceptor > travels up ipsilateral spinal cord to Medial Lemniscus in medulla (gracile(more medial) for lower body and cuneate for upper body) > decussates! 2nd synapse in thalamus > 3rd synapse in primary somatosensory cortex

74
Q

MOA of benzodiazepenes. why cant one overdose?

A

bind to GABA A ion channel and increase affinity for GABA so that the channel increases frequency of opening (allosteric modulation). This enhances sensitivity of receptor with no change in maximum response

75
Q

pathogenisis of bacterial meningitis? (8)

A

Colonisation of nasopharyngeal mucosa> Invasion of bloodstream> Survival & multiplication> Crossing of BBB> Invasion of meninges & CNS> Increased permeability of BBB> Release of proinflammatory compounds causes Neuronal injury

76
Q

pathway to make adrenaline

A

L-DOPA > Dopamine > noradrenaline > adrenaline

77
Q

whats is a Haemmorahic infarction? MOA

A

reperfusion has occurred in an area of infarcted brain resulting in haemorrhage.

Embolus lodges in brain>infarction>the body lyses the embolus in the brain → infarcted tissue is reperfused → haemoorhagic infarcts (reperfusion injury)

78
Q

how can CI cause death? MOA

A

CI > brain swell > increased ICP > herniation> cruches other cerebral arteries> 2ndary haemorrhage of vital centres (brainstem).

79
Q

a legion in the supplementary motor cortex would differ how from one in the primary motor cortex

A 
supp = can't sequence events (brushing teeth).
primary = specific muscle issue
80
Q

describe what happens neurnonally in an epileptic fit

A

disturbance in balance b/w excitatory and inhibitory neurons results in networks firing in an uncontrolled manner

81
Q

pathogenesis of alzheimer’s

A

accumulation of abeta protein (beta amyloid) and tau protein cause deposits of amyloid plaques and neurofibrillary tangles

82
Q

describe the path for lateral corticospinal tract. What is it for?

A

voluntary movement.

cortex > medulla-spinal cord junction (pyramidal decussation) > LMN

83
Q

normal pathway of growth hormone? what 2 other factors can come from hypo to be additive or antagonistic at Ant. Pituitary?

A

GHRH (hypo) > GH (A. Pit) > IGF-1 (liver) > cells.

Ghrelin stimulates GH release, whilst somatostatin inhibits.

84
Q

Pathway of Hormones from Hypothalamus to Anterior Pituitary Gland? what is it called?

A

hypothalmic-hypophyseal portal system.
Trophic hormones made in Hypothalamus → capillaries of portal system →ant pituitary → endocrine cells release hormones into 2nd set of capillaries > body

85
Q

pathway of Posterior Pituitary?

A

Hormone is made and packaged in hypothalamus → transported to post pituitary via vesicle → hormones released into blood upon when necessary.

86
Q

effects of thyroid hormone? (4)

A

increase BMR (thermogenisis), sympathomimetic effect (by increasing adrenoceptors), increase protein, carb and fat metabolism, permissive for growth and development

87
Q

describe thyroid hormone production (put the diagram into words)

A

TSH binds to follicular cell > stimulates thyrglobulin synthesis for colloid > I- enters via NIS symport > Thyroid perioxidase makes I- to I > Iodine is added by enzymes to tyrosine to make MIT or with MIT to make DIT > DIT + DIT = T4 or DIT + MIT = T3 > taken back into follicular cell via vesicles > enzymes separate T3 and T4 from protein into bloodstream

88
Q

normal cortisol pathway?

A

CRH (hypo) > ACTH (ant. pit) > Cortisol (adrenal cortex -zona f).

89
Q

where doe cortisol act (4) and what does it do at each part?

A

immune system (suppress), Liver (gluconeogenisis), Adipocytes (lipolysis), Muscle (protein catabolism)

90
Q

MOA of cortisol to Immunospupression?

A

cortisol> decrease pro-inflammmatory cytokine production + increase anti inflammatory molecules > immune suppresion

91
Q

MOA of cortisol to neutrophilia

A

cortisol> increase bone marrow production + decrease neutrophil adhesion molecules (demargination)

92
Q

cortisol is an immunosupressant. why might there be an overall leukocytosis despite this fact

A

the neutrophilia (due to ncrease bone marrow production + decrease neutrophil adhesion molecules) is greater than the lymphocytopaenia caused by the decrease in pro-inflammmatory cytokine production.

93
Q

Describe type 1 Diabetes and it’s presentation.

A

Type 1 is autoimmune destruction of beta cells causing absolute deficiency of insulin.
Presents as weight loss with appetite, polyuria and polydipsia. Can be fruity breath (ketoacifosis)

94
Q

What main pathwas that hyperglycaemia damages the tissue.

A

Advanced glycation end products(AGEs)

95
Q

Describe how AGEs damage tissue in each of the specific cell to which they bind

A

Pro inflammatory cytokines (macrophages)
ROS in endothelial cells
Matrix production in vascular smooth muscle

96
Q

explain why NSAIDs cause GIT problems

A

inhibits mucosal secretion of PGE2 and PGI2.

PGE2 induces mucus secretion, inhibits gastric acid secretion

97
Q

explain how NSAIDs cause increase bleeding time

A

inhibit Thromboxane A2 (TXA2) synthesis which will result in impaired platelet aggregation

98
Q

why is aspirin special. explain MOA

A

increase the PGI2 TXA2 ratio as TXA2 levels are reduced more and for longer than PGI2. Platelets have no nucleus so cant synthesise COX

99
Q

explain biological consequences of physical inactivty

A

increase abdo adiposity > macrophage infiltration of visceral fat > chronic systemic inflammation > insulin resistance, atherosclerosis, neural degeneration, tumour growth

100
Q

Carb digestion?

A

salivary amylase>pancreatic a-amylase (in duodenum)> enzymes in bursh border break down oli and disaccharides > absorbed (SGLT then GLUT2)

101
Q

protein digestion?

A

pepsin (in stomach) > pancreatic proteases (in duodenum/jejunum) > tri, di and free amino acids co-transported at brush border, small peptides by transcytosis

102
Q

fat digestion

A

salivary lipase> bile +pancreatic lipolytic enzymes (duodenum - CCK stimulates) > free fatty acids taken up in mucosa > converted to TAGs > converted to chylomicrons > travel via lymph or blood > deposit fat (myocyte or adipocyte)

103
Q

what happens to red blood cells when die?

A

globin is broken down into free AA to be reused from protein synthesis.
Haem broken down into iron or billiverdin. Iron goes to liver then Red bone marrow for more Red Cell production.
Billverdin > billrubin(spleen - unconjugated) > binds to albumin and transported to liver > conjugated in liver by adding glucouronic acid >secreted in blie to SI > stercobilin in poo (makes it brown) or urobilin in pee (makes it yellow - got here from urobiligen from blood to kidneys)

104
Q

why do bruises change colour through their course

A

intially red due to blood > then purple due to deoxy and met-Hb > then green due to billiverdin > then yellow due to billirubin

105
Q

what happens to urobiligen

A

most goes back to liver to be conjugated, rest is excreted in urine

106
Q

alc metabolism?

A

ethanol > acetylaldehyde (via ADH) > acetate (via ALDH)

107
Q

why can only clear approx 2 drink/hr

A

coz at this stage alcohol dehydrogenase is working at Vmax

108
Q

pathogensis of cirrhosis

A

chronic hepatocyte inflammation/apoptosis > fibrosis b/w cells > vascular remodelling

109
Q

pathogenesis of portal hypo in cirrhosis:

A

heaptic vein compressed by regenrating nodules > sinusoids damaged and narrowed by fibrosis > hepatic artery shunts blood to portal vein

110
Q

describe the biochemical pathway of vitamin D to D3. describe any points of stimulation

A

diet or sunlight make give vitamin D>lliver enzymes>kidney enzymes (PTH stimulates)> Calcitrol

111
Q

describe the 5 layers of the growth plate.

A
  1. Resting - normal hyaline cartilage
  2. Proliferative - dividing chondrocytes
  3. Maturing - chondrocytes mature
  4. Hypertrophic - chondrocytes hypertrophy and die
  5. Ossification - degenerating cartilage is destroyed and new bone laid.
112
Q

describe the haversian system

A

osteoclasts form a cavity in the bone> blood vessel comes in> osteoblasts line cavity> add layers inwardly toward vessel with collagen alternating directions.
Osteocytes present in layers

113
Q

stages of bone repair?

A

inflammation, reparative (soft and hard callus), remodelling.

114
Q

describe the imflammation stage of repair. give time frame.
describe the repartive stage of repair. give time frame.
describe the remodelling stage of repair. give time frame

A

Haematoma formation, then Granulation tissue formation. first few days.
soft callus (cartliage formation. Holds fractured ends together.) days to weeks.
Hard callus - osteoid formation and ossification creates woven bone. Weeks to months.
woven bone to lamellar bone along lines of stress. months to years.

115
Q

what is osteoporosis. give 2 MOAs

A

decreased bone mass that increases likelihood of fracture.
Menopause - decreased estrogen & increase osteoclast
Aging - decease osteoblast

116
Q

describe how osteoporosis affects bone

A

loss of bone cells and matrix. The loss of trabeculae reduce the cross-sectional area resulting in a relatively greater load on the bone

117
Q

pathogenisis of haem osteomyeltitis (5)

A
  1. slow flow through looped capillaries and venous sinusoids.
  2. Bacteria seed in metaphyseal-epiphyseal junction
  3. Poor penetration of WBCs
  4. Pressure from pus further limits blood supply
  5. infection spreads to subperiosteal space ( can invade shaft)
118
Q

pathogenesis of R Arthritis

A

Unknown Stimulus> Thelper cells (1 & 17) release cytokines (IL-1,6,17 +TNFa)> induce ifbroblasts, macrophages, osteoclasts and b cells> Pannus (granulation like tissue) in joints

119
Q

Morphology of RA (3)

A

villous hyperplasia, mononuclear infiltrate, germinal centre

120
Q

morphology of a rheumatoid nodule

A

typical granulomatous inflammation. Central necrosis, surrounded by epithelioid macrophages then lymphocytes and fibrosis.

121
Q

pathogenies of gout

A

build up of uric acid > crystal formation >Acute inflammation > IL-1, complement and neutrophil lysis (neutrophils phagocytosing the crystal)

122
Q

describe the hormone cascade in male repro

A

Route 1: GnRH > LH > leydig cells > Testosterone > sertoli cells and body for secondary effects. Test feedback on Ant Pit and hypo
Route 2: GnRH> FSH> secondary messenger to Sertoli Cells> sprematocyte maturation. Inhibin feedback on Ant Pit

123
Q

describe the uterine cycle

A

Menses
– when no pregnancy the endometrium of uterus sheds causing bleeding.
• Proliferative phase
– New layer of endometrium in preparation of pregnancy.
• Secretory phase
– Conversion of endometrium to secretory structure to promote implantation.

124
Q

describe the ovarian hormone levels

A

estrogen steadily rise, peaks at ovulation, drops then mini peak at 3/4s then drops again.
Progesterone constant til ovulation then slowly rises, peaks at 3/4s tehn declines.
Inhibin mini surge at ovulation, slow rise with peak at 3/4s then declines

125
Q

physiological cause of menopause

A

ovaries stop responding to LH and FSH > low estrogen and progesterone > eggs stop developing

126
Q

describe what happens to the sperm in fertilisation

A

sperm membrane fuses with egg membrane > sperm nucleus enters cytoplasm of egg > oocyte nucleus completes meiotic division > egg and sperm form zygote

127
Q

describe what happens as a result of cervical stretch during parturation

A

stretch induces 2 things. uterine contractions and oxytocin from ant pituatary. Oxytocin does 2 things. induces more contraction and prostaglandins form uterine wall. prostaglandins induce contraction. ALL POSITIVE FEEDBACK

128
Q

describe The hormonal control of milk secretion and release

A

suckling or crying inhibit PIH (prolactin inhibiting hormone) which increases prolactin release from anterior pituitary, increasing milk secretion. Simultaneously from the hypothalamus oxytocin stimulates smooth muscle contraction in breast.

129
Q

what is the main MOA of estrogen working as a contraceptive?

A

inhibits FSH

130
Q

main MOA of progesterone as contraceptive

A

make endometrium unfavourable for implantation

and alters cervical mucus to create unfavourable environment for sperm. Also can inhibit LH

131
Q

how do aromatase inhibitors work?

A

block synthesis of oestrogen from testosterone. Also block the conversion of a pre-testosterone to a dif oestrogen.

132
Q

write a word equation for STI epi?

A

basic reproductive rate = probability of transmission per sexual partnership X rate of partner change X duration of infection

133
Q

S. aureus produces a vast array of virulence factors to enable it to overcome immunity. name 5

A
  1. Binds to damaged tissues via adhesins
  2. inhibits chemotaxis
  3. Inhibits phagocytosis
  4. If ingested by PMNs, can resist killing
  5. forms biofilms
134
Q

3 ways venom causes death. explain each

A
  1. haemotoxicity - can contain a v powerful pro coagulant → localized clotting → strips the body of clotting factors (fibrin) → vulnerable to catastrophic bleed.Can also can also be a very powerful anti-coagulant → vulnerable to catastrophic bleed.2. neurotoxicity - paralysis3. Myotoxicity - Rhabdomyolosis causing renal failure. (muscle breakdown > increase myoglobin > damage kidney)
135
Q

Describe, using examples, how SNPs can change Pharmacokinetic and Pharmacodynamic behavior of drugs.

A

Kinetics - with statins - a SNP in one of the liver transport genes will decrease statin uptake and increase toxicity.Dynamics - SNP in the 5-lipoxygenase gene is predicitve of poor response to anti-luekotriene therapy in asthma

136
Q

single most important physiological equation related to blood?Measurements

A

Tissue oxygen delivery = CO x Hb x %sat x 1.34. l/min x g/l x % x mls/g = mls/min

137
Q

lack of B12 or folate can cause macrocytic anaemia, why?

A

they needed for DNA replication. cells grow big coz cannot produce DNA quickly enough to divide at the right time

138
Q

4 things that athero may cause to vessel.

A

narrowed lumen, prothrombotic environment, impaired vasodilation, plaque vulnerable to rupture

139
Q

what does aldosterone do? how? where?

A

increases Na reabsorption into blood and increases K secretion into nephron lumen.
Distal tubule + collecting duct by increasing Na/K ATPase (na out K in) and increasing ENaC (Na passive out)

140
Q

describe the 3 main types of dementia (age of onset, progression and deficits

A

alzheimers (senile age, insidious onset, memory loss first),
Frontotemporal (pre-senile, insidious, behavioural changes),
Vascular (anytime - associated with CVD risk factors, fast step wise progression, focal deficits

141
Q

what is uncal herniation?

A

the innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the brainstem, most notably the midbrain

142
Q

Areas of the brain affected in dementia?

A 
Alzheimer's = atrophy mainly hippocampus but also parietal and temperal lobes.
Frontotemporal = frontal and temporal atrophy.
Vascular = depends which vessel.
143
Q

Peripheral signs of a man who died of coning?

A

loss of all brainstem reflexes (pupil, corneal and gag), respiratory arrest, loss of consciousness, coma, cardiac arrest

144
Q

Structures at risk in hemithyroidectomy

A

parathyroids and laryngeal nerve (particuallar recurrent).

para will cause hypocalcaemia. nerve damage can cause hoarse voice

145
Q

how does severe anxiety of medical procedures differ from normal anxiety?

A

Blood-injury phobias differ from all other phobias in that the initial sympathetic activity underpinning the flight/fight response is soon overtaken by vagal activation. Thus, initially there may be a transient rise in heart rate and blood pressure, however, this is followed my marked vasovagal slowing of heart rate, a drop in blood pressure, there is nausea, sweating and pallor, and the individual may faint.
It is worth noting that people without a blood phobia also also show vagal inhibition in response to blood-injury stimuli despite sympathetic activation. Thus individuals with blood-injury phobias differ in the degree of cardiovascular response to blood or injury, rather than the type.

146
Q

treatment for phobia? how differ for blood/injury?

A
  1. relaxation to reduce physiological arousal and muscle tension.
  2. exposure therapy - exposure to the phobic stimulus in a controlled (relaxed) manner will allow habituation of the fear to occur. By pairing a competing response, such as relaxation, with the conditioned fear response, the fear response is ultimately ‘deconditioned’.

**relaxation should be avoided in blood phobias as the vasovagal activity may be exacerbated.

147
Q

Describe the coronary blood supply. include ventricles and nodes

A

Main three are LAD, Left circumflex and RCA. LAD does ant wall of LV and IV septum. L circumflex does posterior LV and in 40% ppl SA node
RCA does right ventricle and inferior LV and SA node in 60% ppl. also does AV node in high majority

148
Q

describe the types of MI with respect to wall and causes

A

Transmural - 99% form thrombosis - full thickness of wall.
Subendocardial - portion of wall just beneath the
endocardium (ie. furtherest away from blood supply) - will occur if thrombus is lysed.
Circumferential - severe triple vessel narrowing or systemic hypoperfusion - shock

149
Q

Cholesterol – what is it needed for?

A

steroids, bile, membranes

150
Q

Familial hypercholesterolaemia?

A

inherited dominant disorder with mutation in LDL receptor - results in more LDLs in circulation and atherosclerosis begins before puberty

151
Q

what can cause pansystolic murmur

A

Mitral or tricuspid regurgitation. or ventricular septal defect

SAQs (13 decks)

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