Important processes Flashcards
1
Q
3 stage viral replication (include sub stages
A
- Entry (fusion with membrane via virus receptor > endocytosis).
- Replication (uncoating > genome replication >mRNA synthesis > protein synthesis.
- release (non enveloped accumulate til cell lysis, enveloped bud out (some secreted out)).
2
Q
explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?
A
- Transformation - DNA fragments of a lysed cell are taken up by a competent bacteria and incorporated into its genome
- Phage mediated - infection of bacteria by abnormal bacteriophage
- 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
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
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.
5
Q
how do bacteria often penetrate the epithelium? what initiates this
A
pathogen-mediated endocytosis. Initiated by bacterial surface proteins
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).
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
8
Q
targets of flu vaccine (2)?
A
antibody to HA blocks attachment. antiobdy to NA blocks release
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
10
Q
triple response of histamine? explain cause
A
Redness (vasodilation at site).
Wheal (oedema from vascular permeability).
Flare (spread through sensory fibres)
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
12
Q
increase in cardio output does what to venous pressure and why?
A
decrease it - more blood in arteries
13
Q
how does the body infer the adequacy of cardiac output?
A
pressure, pO2, pH, pCO2
14
Q
describe Virchow’s triad
A
there are 3 components to blood clotting: The vessel wall, the blood composition and the blood flow
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
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
17
Q
describe the action potential of a ventricular myocyte
A
resting at -90.
- Na comes in so depolarizes.
- K+ out so starts to dip
- Ca+ in (K still going out) so plateaus
- Only K out so repolarizes
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
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.
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
21
Q
MOA of aortic dissection
A
tear in intima> blood enters and splits media
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
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
24
Q
MOA of SOB in angina
A
insufficient oxygen to myocyte> => muscle cant contract and relax => increase LV Diastolic Volume=> pulmonary congestion => dyspnea
25
most common cause of SCD
coronary athersclerosis + thrombus accusing acute ischaemia
26
MOA of symptoms in unstable angina
Unstable plaque => Acute Plaque Event => blood exposed to sub-endothelium => cascade gets going=> thrombus + vasoconstriction
27
3 types of cardiac infarctions with respect to the wall. give reasons for each
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.
28
describe the physiological concepts of treating stable angina (basically describe diagram form lecture).
can either increase oxygen supply to myocardium (decrease HR) or decrease oxygen demand (decrease HR, SV, afterload and preload)
29
dif in causes b/w concentric and eccentric hypertrophy. how dif in wall thickness
concentric is caused by hypertension and aortic stenosis. larger wall thickness.
Eccentric is caused by volume overload or mitral or aortic regurgitation
30
3 cardiac failure mechanism and 2 reasons for each
loss of muscle - Infarction or myopathy.
Pressure overload - hypertension or aortic stenosis.
Volume overload - valve regurgitation or septal shunts
31
clinical signs of LH failure (3) and right(1)
SOB, fatigue, tachycardia. RH failure = oedema
32
compensation of Aortic Stenosis?
LV concentric hypertrophy due to pressure overload
33
compensation of Aortic or Mitral Regurgitation?
LV dilatation due to volume overload
34
compensation of mitral stenosis
both dilatation and hypertrophy
35
how does Hb enhance oxygen diffusion
also carries NO which it releases simultaneously with oxygen to dilate vascular smooth muscle
36
hyperactivity of HMG-CoA reductase may lead to what
atherosclerosis by making more cholesterol and thus more blood LDL
37
cholesterol is thought to be made in 4 stage, what are the 3 key intermediates
HMG-CoA, isoprene and squalene
38
examinable scheme for cholestorol
acetyl-CoA > acetoacetyl-Coa > HMG-CoA >(enzyme = HMG-Coa Reductase. Cofactors = 2NADPH + 2H+ > 2NADP+) Mevalonic acid + Coa > 6x Mevalonic Acid > Cholestorol
39
describe how the volume of the thorax is increased
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.
40
histamine does what to the airways?
constricts
41
a large Pulmonary embolism may cause what compared to a medium size
```
large = SCD or acute cor pulmonale.
Medium = acute pulmonale or pulmonary infarct
```
42
describe the dif in immediate and late phase in an asthma attack
immediate = increased vascular permeability (oedema), mucus production and bronchospasm.
Late = epthelial damage from ongoing inflammation
43
what happens to airways in severe chronic asthma?
remodelling with irreversible obstruction
44
what is emphysema and main type causes?
destruction of alveolar walls without fibrosis. Centrolobular - smoking
45
how does smoking destroy alveoli?
increase in elastase destroys elastin and thus the alveoli cell wall
46
dif b/w primary and 2ndary TB. Where in lung is 2ndary?
Primary usually subclinical.
2ndary - reactivation of dormant infection or reinfection.
Apical Areas of Upper Lobe.
can spread to other organs
47
CO2 is transported in blood in 3 forms. what are they and what % of CO2 for each way
60% bicarbonate, 30% attached to proteins (inc. Hb), 10% dissolved
48
CO2 + H2O equation? enzyme involved
CO2 + H2O → H2CO3 → H+ + HCO3-
| Enzyme = CA (carbonic Anhydrase)
49
eqaution of A-a gradient? what is normal
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)
50
2 main causes of Pulmonary Oedema. Give 2 reasons for 1st and 1 for 2nd
1. Increased capillary hydrostatic pressure (mitral stenosis, fluid overload).
2. Increased capillary permeability (toxins)
51
3 reasons why obstruction could occur during sleep?
– Airway muscles relax (floppy throat - esp REM).
– Throat already narrowed (obesity, tonsils etc).
– Tongue falls backwards ( esp if supine).
52
why shouldnt give large amount of supplemental oxygen to someone with chronic hypercapnea?
they dependant on low oxygen to breath
53
6 reasons for dyspnea (body systems)
resp, cardiac, muscle weakness, metabolic, anaemia, psychogenic
54
5 respiratory causes of dyspnea? give 2 reasons for each class
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
55
what are the results of an increase and decrease of NaCl respectively and when do these occur?
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).
56
what releases renin and when is it released? (3)
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
57
how do the afferent and effernt arteriole modulate GFR? For what range of MAP is GFR constant
If afferent arteriole constricts GFR Decreases.
If Efferent constricts GFR Increases.
80-180
58
how can NSAIDS cause pre renal failure
they reduce prostaglandins that vasodilate - hence less blood to kindey
59
name 3 non drug causes of pre-renal acute failure
haemorrhage, renal stenosis and hypoalbuminaemia
60
why do proteins stay in blood and not filter in to kidneys? (2)
negative charge of proteins and neg charge of glomerular basement membrane repel.
physical structure of membrane (tight pores)
61
does atheorsclerosis cause hypertension
only in renal atherosclerosis
62
what is Hyaline arteriolosclerosis? where is it often seen? most common association?
thickening of the walls of arterioles by the deposition of homogeneous hyaline, lumen narrowed. kidneys. Aging
63
3 brainstem tests (include afferent and efferent)
Midbrain: pupil light (afferent 2, efferent 3).
Pons: Corneal blink (afferent 5, efferent 7).
Medulla: Gag (afferent 9, efferent 10)
64
innervation of tongue
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
functional pathway of retina
photoreceptor > bipolar (in put from horizontal) > ganglion (input form amacrine).
66
why do cones have a greater visual acuity than rods?
Cones have a much lower convergence ratio to bipolar cells than rods
67
compare b/w dark and light for photoreceptor bipolar cell communication
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
main visual pathway from ganglion cells
GC > optic nerve >LGN (in thalamus) > optic radiations > visual cortex
69
apart from the LGN name 4 other targets of Ganglion cells and their function
1. midbrain (pupil response).
2. Suprachasmaitc nucleus (circadian rhythm).
3. superior colliculus (eye movement).
4. other part of thalamus (photophobia)
70
what is the MLF and what is it involved in
white matter tracts that connect cranial nerves. controls the co-ordiantion of eye movement.
71
neural pathway of sound
CNVIII > cochlea nucleus (medulla) > superior olive > lateral lemniscus > inferior colliculus (midbrain) > MGN (thalamus) > cortex (auditory centre in temporal lobe).
72
pathway of sound travelling through ear
→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
describe the main mechanosensory path. What it is also known as
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
MOA of benzodiazepenes. why cant one overdose?
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
pathogenisis of bacterial meningitis? (8)
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
pathway to make adrenaline
L-DOPA > Dopamine > noradrenaline > adrenaline
77
whats is a Haemmorahic infarction? MOA
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
how can CI cause death? MOA
CI > brain swell > increased ICP > herniation> cruches other cerebral arteries> 2ndary haemorrhage of vital centres (brainstem).
79
a legion in the supplementary motor cortex would differ how from one in the primary motor cortex
```
supp = can't sequence events (brushing teeth).
primary = specific muscle issue
```
80
describe what happens neurnonally in an epileptic fit
disturbance in balance b/w excitatory and inhibitory neurons results in networks firing in an uncontrolled manner
81
pathogenesis of alzheimer's
accumulation of abeta protein (beta amyloid) and tau protein cause deposits of amyloid plaques and neurofibrillary tangles
82
describe the path for lateral corticospinal tract. What is it for?
voluntary movement.
| cortex > medulla-spinal cord junction (pyramidal decussation) > LMN
83
normal pathway of growth hormone? what 2 other factors can come from hypo to be additive or antagonistic at Ant. Pituitary?
GHRH (hypo) > GH (A. Pit) > IGF-1 (liver) > cells.
| Ghrelin stimulates GH release, whilst somatostatin inhibits.
84
Pathway of Hormones from Hypothalamus to Anterior Pituitary Gland? what is it called?
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
pathway of Posterior Pituitary?
Hormone is made and packaged in hypothalamus → transported to post pituitary via vesicle → hormones released into blood upon when necessary.
86
effects of thyroid hormone? (4)
increase BMR (thermogenisis), sympathomimetic effect (by increasing adrenoceptors), increase protein, carb and fat metabolism, permissive for growth and development
87
describe thyroid hormone production (put the diagram into words)
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
normal cortisol pathway?
CRH (hypo) > ACTH (ant. pit) > Cortisol (adrenal cortex -zona f).
89
where doe cortisol act (4) and what does it do at each part?
immune system (suppress), Liver (gluconeogenisis), Adipocytes (lipolysis), Muscle (protein catabolism)
90
MOA of cortisol to Immunospupression?
cortisol> decrease pro-inflammmatory cytokine production + increase anti inflammatory molecules > immune suppresion
91
MOA of cortisol to neutrophilia
cortisol> increase bone marrow production + decrease neutrophil adhesion molecules (demargination)
92
cortisol is an immunosupressant. why might there be an overall leukocytosis despite this fact
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
Describe type 1 Diabetes and it's presentation.
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
What main pathwas that hyperglycaemia damages the tissue.
Advanced glycation end products(AGEs)
95
Describe how AGEs damage tissue in each of the specific cell to which they bind
Pro inflammatory cytokines (macrophages)
ROS in endothelial cells
Matrix production in vascular smooth muscle
96
explain why NSAIDs cause GIT problems
inhibits mucosal secretion of PGE2 and PGI2.
| PGE2 induces mucus secretion, inhibits gastric acid secretion
97
explain how NSAIDs cause increase bleeding time
inhibit Thromboxane A2 (TXA2) synthesis which will result in impaired platelet aggregation
98
why is aspirin special. explain MOA
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
explain biological consequences of physical inactivty
increase abdo adiposity > macrophage infiltration of visceral fat > chronic systemic inflammation > insulin resistance, atherosclerosis, neural degeneration, tumour growth
100
Carb digestion?
salivary amylase>pancreatic a-amylase (in duodenum)> enzymes in bursh border break down oli and disaccharides > absorbed (SGLT then GLUT2)
101
protein digestion?
pepsin (in stomach) > pancreatic proteases (in duodenum/jejunum) > tri, di and free amino acids co-transported at brush border, small peptides by transcytosis
102
fat digestion
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
what happens to red blood cells when die?
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
why do bruises change colour through their course
intially red due to blood > then purple due to deoxy and met-Hb > then green due to billiverdin > then yellow due to billirubin
105
what happens to urobiligen
most goes back to liver to be conjugated, rest is excreted in urine
106
alc metabolism?
ethanol > acetylaldehyde (via ADH) > acetate (via ALDH)
107
why can only clear approx 2 drink/hr
coz at this stage alcohol dehydrogenase is working at Vmax
108
pathogensis of cirrhosis
chronic hepatocyte inflammation/apoptosis > fibrosis b/w cells > vascular remodelling
109
pathogenesis of portal hypo in cirrhosis:
heaptic vein compressed by regenrating nodules > sinusoids damaged and narrowed by fibrosis > hepatic artery shunts blood to portal vein
110
describe the biochemical pathway of vitamin D to D3. describe any points of stimulation
diet or sunlight make give vitamin D>lliver enzymes>kidney enzymes (PTH stimulates)> Calcitrol
111
describe the 5 layers of the growth plate.
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
describe the haversian system
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
stages of bone repair?
inflammation, reparative (soft and hard callus), remodelling.
114
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
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
what is osteoporosis. give 2 MOAs
decreased bone mass that increases likelihood of fracture.
Menopause - decreased estrogen & increase osteoclast
Aging - decease osteoblast
116
describe how osteoporosis affects bone
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
pathogenisis of haem osteomyeltitis (5)
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
pathogenesis of R Arthritis
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
Morphology of RA (3)
villous hyperplasia, mononuclear infiltrate, germinal centre
120
morphology of a rheumatoid nodule
typical granulomatous inflammation. Central necrosis, surrounded by epithelioid macrophages then lymphocytes and fibrosis.
121
pathogenies of gout
build up of uric acid > crystal formation >Acute inflammation > IL-1, complement and neutrophil lysis (neutrophils phagocytosing the crystal)
122
describe the hormone cascade in male repro
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
describe the uterine cycle
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
describe the ovarian hormone levels
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
physiological cause of menopause
ovaries stop responding to LH and FSH > low estrogen and progesterone > eggs stop developing
126
describe what happens to the sperm in fertilisation
sperm membrane fuses with egg membrane > sperm nucleus enters cytoplasm of egg > oocyte nucleus completes meiotic division > egg and sperm form zygote
127
describe what happens as a result of cervical stretch during parturation
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
describe The hormonal control of milk secretion and release
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
what is the main MOA of estrogen working as a contraceptive?
inhibits FSH
130
main MOA of progesterone as contraceptive
make endometrium unfavourable for implantation
| and alters cervical mucus to create unfavourable environment for sperm. Also can inhibit LH
131
how do aromatase inhibitors work?
block synthesis of oestrogen from testosterone. Also block the conversion of a pre-testosterone to a dif oestrogen.
132
write a word equation for STI epi?
basic reproductive rate = probability of transmission per sexual partnership X rate of partner change X duration of infection
133
S. aureus produces a vast array of virulence factors to enable it to overcome immunity. name 5
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
3 ways venom causes death. explain each
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
Describe, using examples, how SNPs can change Pharmacokinetic and Pharmacodynamic behavior of drugs.
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
single most important physiological equation related to blood?Measurements
Tissue oxygen delivery = CO x Hb x %sat x 1.34. l/min x g/l x % x mls/g = mls/min
137
lack of B12 or folate can cause macrocytic anaemia, why?
they needed for DNA replication. cells grow big coz cannot produce DNA quickly enough to divide at the right time
138
4 things that athero may cause to vessel.
narrowed lumen, prothrombotic environment, impaired vasodilation, plaque vulnerable to rupture
139
what does aldosterone do? how? where?
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
describe the 3 main types of dementia (age of onset, progression and deficits
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
what is uncal herniation?
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
Areas of the brain affected in dementia?
```
Alzheimer's = atrophy mainly hippocampus but also parietal and temperal lobes.
Frontotemporal = frontal and temporal atrophy.
Vascular = depends which vessel.
```
143
Peripheral signs of a man who died of coning?
loss of all brainstem reflexes (pupil, corneal and gag), respiratory arrest, loss of consciousness, coma, cardiac arrest
144
Structures at risk in hemithyroidectomy
parathyroids and laryngeal nerve (particuallar recurrent).
| para will cause hypocalcaemia. nerve damage can cause hoarse voice
145
how does severe anxiety of medical procedures differ from normal anxiety?
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.
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treatment for phobia? how differ for blood/injury?
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
Describe the coronary blood supply. include ventricles and nodes
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
describe the types of MI with respect to wall and causes
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
Cholesterol – what is it needed for?
steroids, bile, membranes
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Familial hypercholesterolaemia?
inherited dominant disorder with mutation in LDL receptor - results in more LDLs in circulation and atherosclerosis begins before puberty
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what can cause pansystolic murmur
Mitral or tricuspid regurgitation. or ventricular septal defect
