catch up (phase 1) Flashcards
neuro, endo
layer of meninges
dura - adherent to skull
arachnoid
pia - cannot be seperated from brain
parasympathetic vs sympathetic
these are the two types of autonomic (unconcious) motor
parasymp = rest/digest symp = fight/flight/fright/fuck
what myelinates in brain
oligodendrocytes
what myelinates in peripheral nerves
schwann cells
three planes
coronal plane - think cut ear to ear (Crown)
saggital plane - arrow fired face on. parasaggital = parralel to this
transverse/axial plane - horizontal
efferent/ afferent
afferent = sensory efferent = motor
is it somatic motor or somatic sensory where all vessels are myelinated
somatic motor
somatic/autonomic
somatic = concious, of it
autonomic = not concious, involuntary
applies to both motor and sensory
brachial nerves =?
theses are skeletal (somatic) efferent motor nerves that supply
- mandible+ ear
tell me about somatic vs autonomic nerve supply - distribution of supply
somatic (concious) - arranged adjacently like somites = area all supplied by a single somatic nerve
- dermatomes / myotomes = skin/muscle supplied by a single nerve
there is overlap between different ones
autonomic is less clear - they are mixed in with somatic
which horn of the vertebra do sensory and motor travel in respectively
sensory – dorsal horn (back)
motor – ventral horn
why is UMN lesion spastic
is UMN is cut, LMN can get stimulation from other neurones, so is spasms, and contracts
what layer does a lumbar puncture reach
between pia mater and subarachnoid space
why is a blunt needle used for epidural
does not peirce the dura, just pushes it so you can feel when you have reached the right spot as there is resistance
with epidural local anaesthetic what is the ideal effect
sensory loss below level
motor function maintained
think perfect for childbirth
spinothalamic tract carries what
nasty sensations pain extreme temperature tickling pressure
spinocerebellar tract carries what
non concious sensory info – eg muscle length (to feed back to motor for adjustment)
dorsal column carries what
fine touch
vibration
two point discrimination
proprioception
which cranial nerves are parasympathetic
3,7,9,10
Brown sequard lesion on R side effect
AT LEVEL OF LESION
loss of R crude sensations
BELOW THE LESION
loss of R voluntary motor
loss of R fine touch
loss of L crude sensations
where does spinothalamic tract decussate
spinal cord
where does dorsal tract medial leminiscus decussate
medulla
where does corticospinal tract decussate
medulla
what does spinothalamic tract carry
nasty sensations - crude touch, pain, temp
ascending . sensory
what does corticospinal tract carry
descending voluntary motor
what does dorsal tract medial leminiscus carry
ascending sensations of fine touch, vibrations, 2 point deiscrimination, proprioception
horner’s syndrome symtpoms
- Hypohydrosis (Reduced sweating on face)
- Meiosis (pupil constriction)
- Ptosis (upper eyelid droop)
Horner’s syndrome + neck stiffness
vertebral artery or carotid artery dissection (carotid artery dissection is more common)
UMN and LMN signs
UMN- everything upped increased muscle tone--> spasticity hyper-reflexes increased plantar (minimal muscle atrophy ) positive babinksi sign (big toe goes up rather than down when sole is stroked)
LMN - everything lowered! muscle tone reduced --> flaccid muscle atrophy (wasting) hypo- reflexia fassiculation (brief spontaneous contraction) negative babinski sign
UMN = where
cell body in motor cortex. axon travels down through internal capsule, through midbrain, pons and medulla spinal cord and synapse with LMN in anterior horn of vertebra
LMN = where
synapse with UMN in anterior horn of vertebra then travel to effector site (neuromuscular junction)
and in cranial nerve nuclei in brainstem
motor unit
LMN and axon and the muscle fibres it supplies
vasopressin
- aka
- made where
- released from where, based on what
- ADH
- paraventricular nucleus of the hypothalamus
- transported to the posterior pituitary via the axoplasm of neurons. then released from here. stimulated by osmoreceptors (day to day) and baroreceptors (extreme stress/trauma)
when is vasopressin released
released from the posterior pituitary
when osmoreceptors (day to day) and baroreceptors (extreme stress/trauma) detect:
when high osmolality (concentrated particles) = low water levels
vasopressin action
Binds to G protein receptors:
V1a- in vasculature → vasoconstriction
V1b- in pituitary → ACTH release (cause glucocorticoid steroid hormones release from adrenal cortex → increase in glucose levels)
V2- in renal collecting ducts→ reabsorption of water
- Aquaporin 2 vesicles move to and fuse with the apical membrane of the collecting duct, creating channels that allow water to move from collecting duct lumen to collecting duct wall cells.
- This water then moves from here to blood via aquaporin 3 and 4 channels
- Water reabsorbed
- serum osmolality decreases
what is osmolality
high/low osmolality
= concentration of dissolved particles in serum.
High = lots of particles, concentrated (not so much watah)
Low = few particles, dilute (lotsa watah)
normal glucose blood level
3.5-8 mmol/L
- what stimulates insulin release
- released from where
- mechanism of release
- type of release
- fed/fasting state
- rising glucose stimulates
- released from beta cells of islets of langerhans of the pancreas. Glucose enters cell so they know glucose levels. When high levels, then they release insulin in response
- this then enters portal circulation to the liver
- biphasic : rapid release and second phase if glucose levels still high
- fed state
glucose converted to what
- glycogenesis
- lipogenesis
to glycogen (glycogenesis) to triglycerides (lipogenesis)
in fed state, does glucose go more to liver or to the periphery?
peripheral glucose transporters
- where?
- sensitive to what
- effect
40% liver
60% periphery (mainly muscle)
muscle and fat
have insulin- responsible glucose transporters to absorb glucose post prandially due to high glucose and high insulin
stored as glycogen inside
what energy source does brain use
glucose
unable to use (free fatty acids→ ketones → acetyl coA because free fatty acids can not cross the blood brain barrier
GLUT transporters
glucose cannot pass membrane, needs transporter
GLUT1 - non-insulin stimulated
GLUT2- beta cells of the pancreas. Glucose enters cell so they know glucose levels. When high levels, then they release insulin in response
GLUT3- non insulin stimulated in brain neurons and placenta
GLUT4 - mediates peripheral action of insulin - muscle and adipose tissue following stimulation of insulin receptor as insulin binds to it
insulin action
- insulin:
- –Decreases gluconeogenesis and glycogenolysis (hepatic output)
- –Increases glucose uptake into periphery - lipogenesis and glycogenesis
- –Inhibits lipolysis
- –Inhibits protein/muscle breakdown / ketogenesis
+glucagon secretion (due to insulin/glucose)
cortisol function
Lipid and glycogen deposition
Muscle and carb catabolism
Na retention
growth hormone secretion
- what stimulates/ inhibtis
- type of secretion
- secreted from where
GHRH stimulates
Ghrelin stimulates
somastostatin inhibits
glucose inhibits
pulsatile secretion from anterior pituitary
what stimulates thyroid hormones to be released
Hypothalamus → TRH Thyrotropin Releasing Hormone → anterior pituitary → TSH Thyroid Stimulating Hormone → Thyroid → T3 (Triiodothyronine) and T4 (thyroxine)
thyroid hormones - differences
t3 (triiodothyronine) and t4 (thyroxine)
- more t4 produced than t3
- t4 inactive, needs to be converted to t3 (using TPO thyroglobulin peroxidase enzyme)
- so slow release
what is needed for thyroid hormone synthesis
and why
iodine
in follicular cells
Iodine binds to tyrosine (which is on the thyroglobulin molecules), with the help of thyroid peroxidase enzyme (TPO). Tyrosine + 1 iodine = T1 (monoiodotyrosine). Tyrosine + 2iodines = T2 (diiodotyrosine). T3=T1+T2 and T4=T2+T2
thyroid location, shape, and vascular status
Anterior neck C5-T1
Two lobes joined by isthmus
highly vascular- hormones secreted directly into blood
where is angiotensinogen made
liver
where is renin made
juxtoglomerular cells in kidney
where is ACE made
vascular endothelial cells in lung
what causes renin to be released
low blood pressure
renin action
angiotensinogen to angiotensin 1
ACE action
angiotensin 1 to 2
angiontensin 2 action
- vasoconstriction
- causes adrenal cortex to release aldosterone
aldosterone action
- channel proteins produced so more Na and water reabsorbed into the blood
- K+ excreted (electrolyte balance)
distal tubules primarily
where is aldosterone made
zona glomerulosa in adrenal cortex
RAAS response to low blood pressure
- renin produced (juxtaglomerular cells in kidney)
- this converts angiotensinogen to angiotensin 1
- angiotensin 1 converted to 2 by ACE (made in lung vascular endothelial cells)
- angiotensin 2 causes vasoconstriction and aldosterone release (from zona glomerulosa in adrenal gland)
- aldosterone causes sodium and water to be reabsorbed and K+ to be excreted
- the volume increase plus the vasoconstriction causes BP to rise, correcting the low blood pressure
water-soluble vs lipid-soluble hormones
- bound to what
- clearance
- how does it affect
- half life
- pre-done or done on demand
WATER-SOLUBLE - peptide
- unbound
- quick clearance
- bind to cell receptor
- short half life
- pre synthesised and stored
FAT SOLUBLE - hormone
- protein bound
- slow clearance
- diffuses through membrane
- long half life
- synthesised on demand
endocrine vs exocrine
endocrine = secrete into bloodstream directly exocrine= secrete into ducts
endocrine
paracrine
autocrine
endocrine- acts distantly
paracrine - acts on nearby cells
autocrine- acts on cell that secreted the hormone
location of…
peptide hormone receptor
steroid hormone receptor
thyroid hormone receptor
peptide hormone receptor = cell membrane
steroid hormone receptor= cytoplasm
thyroid hormone receptor= nucleus
types of stimulation for hormone secretion
- humoral stimulation- detect change in environment
- nerve stimulation
- hormonal stimulation
pituitary stalk connects what
posterior pit and hypothalamus
what hormones do ant/post pit secrete
anterior pit: GH TSH LH FSH ACTH Prolactin
post pit:
oxytocin
vasopressin (ADH)
what hormones do post pit make
none. oxytocin and vasopressin made in hypothalamus, stored and secreted from post pit
oxytocin effect
cervix, uterus, breast milk
labour etc
where does spinal cord end at cauda equina begin?
what is at the end of the spinal cord at the level
L1/2.
so cauda equina is L2 and below
conus medullaris
filum terminale=
delicate strand of fibrous tissue proceeding down from the apex of the conus medullaris (non-neural)
FEV1
amount of air forced out of lungs in 1 second
FVC
amount of air expelled after the deepest breath in (no time limit)
PEFR
peak expiratory flow rate - exhale as fast as poss
which cells dont pass through the glomerulus
large negative molecules
cells
what is the kidneys net excretion
Na phosphate acid k uraemic toxins
reabsorption in kidney
- where mainly
- what
Majority in PCT Na Phosphate Glucose Amino acids
where are do diuretics act
loop - loop of henle
thiazides - DCT
K in kidney
- filtration, reabsorption
- what determines its level
Freely filtered in glomerulus
Most reabsorbed in PCT and loop of henle
K determined by
- Na in collecting duct- Na pumped out and K in (to lumen)
- Aldosterone
how do they kidneys contribute to RBC production
- kidneys produce EPO
- And produce substance (?hepcidin) that allow iron to be absorbed in the duodenum
vitamine D acitvation
vitamin D from sun (skin) and diet
converted to 25(OH)- vitamin d in liver
converted to 1, 25(OH)2- vitamin d in kidney = calcitrol
calcitrol action
= activated vitamin d
- Suppresses PTH
- Increases calcium and phosphate gut absorption
- Lack of it → secondary hyperparathyroidism
- – Not enough calcium in bone
- – Bone tumours
- – Salt and pepper skull
- – Etc
how does kidney balance acid-base
excrete h+
reabsorb bicarbonate
creatinine measures kidney function
- why
- drawbacks
- Waste product of muscle metabolism
- Purely excreted by kidney
- increased creatinine = decreased GFR. So an equation works out eGFR from creatinine, race, age, gender
BUT varies with muscle mass - differs for some people. more inaccurate for liver disease, body builders and amputees
creatinine is secreted from tubules as well as filtered. so creatinine clearance >GFR. this is more prominent at low GFR so you may overestimate someones kidney condition
urine dipstick measures what for kidney function
drawbacks
proteinuria (albuminuria)
Score /colour = +/ ++/+++ - based on concentration
BUT varies with volume, so Albumin-creatinine ratio
Creatinine is excreted at constant rate, so this ratio is constant, irrespecitve of urine volume
GFR is controlled by what vessels. what effects these vessels
afferent and efferent arteriole
Prostaglandin dilates afferent arteriole (increase GFR)
Angiotensin 2 constricts efferent arteriole (increase GFR)
3 ureteric narrowings
Pelviureteric junction (leave kidneys) Pelvic brim (cross iliac vessels) Vesicoureteric junction (enter bladder)
enterohepatic circulation
- Bile salts made in liver
- Gallbladder stores it
- Released for food intake (digestion of fat)
- Reabsorbed in terminal ileum
- Into portal circulation
- To liver
- Reconjugated and secreted back into bile
bile =
constitution
role
= bile acids (cholic acids, cheondeoxydolic acid) + phospholipids + cholesterol
Helps fat digestion (emulsifies) → absroption of fat + fat soluble vitamins (ADEK)
when does alcohol withdrawal start?
how long does it last?
symptoms:
6-24h after last drink up to a week Tremor Insomnia nausea/vom Agitation Seizure
delerium tremens =
24-72h after last drink - withdrawal Hyperadrenergic state Symptoms - Disorientation - Tremors - Impaired attention /consciousness - Visual and auditory hallucinations - Diaphoresis = sweating
wernicke’s encephalopathy
- =?
- triad
- treatment
- Medical emergency
- Thiamine reserves exhausted - malnutrition, alcoholism
- Triad (most don’t have all 3)
- – Ataxia
- – Nystagmus (involuntary eye movements)/ ophthalmoplegia (paralysis / weakness of eye muscles)
- – Confusion
- Acute onset
- Reversible : treat with IV thiamine
korsakoff syndrome
- Follows on from untreated wernicke’s encephalopathy
- Memory impairment, confabulation
- Chronic and irreversible
platelet shape, what does this allow
Disc shape allows them to flow close to endothelium
how many nuclei do platelets have
0
lifespan of platelets
- what stimulates production inc how this works
- how they are made
- how they die
TPO (liver) stimulates production of platelets
- So liver damage reduces platelet production
- TPO binds to platelets and megakaryocyte receptors, so when there are low platelets, less TPO is bound so more can bind to megakaryocyte receptors and stimulate platelet production
Formed by fragmentation of megakaryocytic cytoplasm in bone marrow
At end of life, are phagocytosed by macrophages in spleen
thromboxane induces
induces platelet aggregation and vasoconstriction
P2Y12 =
- what is their role
P2Y12 = platelet receptors that is activated by ADP, causing platelet amplification/ activation and activates glycoprotein IIb/IIIa
what is glycoprotein IIb/IIIa? and what is their role
Glycoprotein IIb/IIIa = platelet receptor for fibrinogen and vwF → platelet adherence and aggregation
physiology of calcium / phosphate regulation
- LOW serum calcium stimulates parathyroid PTH production
- Increased PTH increases calcium by…
- – Reabsorption of calcium in KIDNEY
- – Absorption of calcium in GUT - driven by vitamin D
- – Release of calcium from BONE - increased bone remodelling – increased bone resorption (osteoclast) and decreased bone formation (osteoblast)
- Negative feedback loop - with exaggerated response- small inc/decrease of calcium causes a large de/increase of PTH
- Increased PTH decreases phosphate by…
- – Less reabsorption in kidney
- – (slight increase of serum phosphate though gut absorption and bone resorption but doesn’t outweigh)
where is intrinsic factor made
gastric parietal cells
