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phase 2a mine > catch up (phase 1) > Flashcards

catch up (phase 1) Flashcards

neuro, endo

1
Q

layer of meninges

A

dura - adherent to skull
arachnoid
pia - cannot be seperated from brain

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2
Q

parasympathetic vs sympathetic

A

these are the two types of autonomic (unconcious) motor

parasymp = rest/digest
symp = fight/flight/fright/fuck
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3
Q

what myelinates in brain

A

oligodendrocytes

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4
Q

what myelinates in peripheral nerves

A

schwann cells

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5
Q

three planes

A

coronal plane - think cut ear to ear (Crown)

saggital plane - arrow fired face on. parasaggital = parralel to this

transverse/axial plane - horizontal

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6
Q

efferent/ afferent

A 
afferent = sensory
efferent = motor
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7
Q

is it somatic motor or somatic sensory where all vessels are myelinated

A

somatic motor

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8
Q

somatic/autonomic

A

somatic = concious, of it

autonomic = not concious, involuntary

applies to both motor and sensory

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9
Q

brachial nerves =?

A

theses are skeletal (somatic) efferent motor nerves that supply
- mandible+ ear

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10
Q

tell me about somatic vs autonomic nerve supply - distribution of supply

A

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

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11
Q

which horn of the vertebra do sensory and motor travel in respectively

A

sensory – dorsal horn (back)

motor – ventral horn

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12
Q

why is UMN lesion spastic

A

is UMN is cut, LMN can get stimulation from other neurones, so is spasms, and contracts

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13
Q

what layer does a lumbar puncture reach

A

between pia mater and subarachnoid space

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14
Q

why is a blunt needle used for epidural

A

does not peirce the dura, just pushes it so you can feel when you have reached the right spot as there is resistance

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15
Q

with epidural local anaesthetic what is the ideal effect

A

sensory loss below level
motor function maintained

think perfect for childbirth

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16
Q

spinothalamic tract carries what

A 
nasty sensations
pain
extreme temperature
tickling
pressure
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17
Q

spinocerebellar tract carries what

A

non concious sensory info – eg muscle length (to feed back to motor for adjustment)

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18
Q

dorsal column carries what

A

fine touch
vibration
two point discrimination
proprioception

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19
Q

which cranial nerves are parasympathetic

A

3,7,9,10

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20
Q

Brown sequard lesion on R side effect

A

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

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21
Q

where does spinothalamic tract decussate

A

spinal cord

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22
Q

where does dorsal tract medial leminiscus decussate

A

medulla

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23
Q

where does corticospinal tract decussate

A

medulla

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24
Q

what does spinothalamic tract carry

A

nasty sensations - crude touch, pain, temp

ascending . sensory

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25
Q

what does corticospinal tract carry

A

descending voluntary motor

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26
Q

what does dorsal tract medial leminiscus carry

A

ascending sensations of fine touch, vibrations, 2 point deiscrimination, proprioception

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27
Q

horner’s syndrome symtpoms

A
  • Hypohydrosis (Reduced sweating on face)
  • Meiosis (pupil constriction)
  • Ptosis (upper eyelid droop)
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28
Q

Horner’s syndrome + neck stiffness

A

vertebral artery or carotid artery dissection (carotid artery dissection is more common)

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29
Q

UMN and LMN signs

A 
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
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30
Q

UMN = where

A

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

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31
Q

LMN = where

A

synapse with UMN in anterior horn of vertebra then travel to effector site (neuromuscular junction)

and in cranial nerve nuclei in brainstem

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32
Q

motor unit

A

LMN and axon and the muscle fibres it supplies

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33
Q

vasopressin

  • aka
  • made where
  • released from where, based on what
A
  • 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)
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34
Q

when is vasopressin released

A

released from the posterior pituitary
when osmoreceptors (day to day) and baroreceptors (extreme stress/trauma) detect:
when high osmolality (concentrated particles) = low water levels

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35
Q

vasopressin action

A

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
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36
Q

what is osmolality

high/low osmolality

A

= concentration of dissolved particles in serum.
High = lots of particles, concentrated (not so much watah)
Low = few particles, dilute (lotsa watah)

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37
Q

normal glucose blood level

A

3.5-8 mmol/L

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38
Q
  • what stimulates insulin release
  • released from where
  • mechanism of release
  • type of release
  • fed/fasting state
A
  • 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
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39
Q

glucose converted to what

  • glycogenesis
  • lipogenesis
A 
to glycogen (glycogenesis)
to triglycerides (lipogenesis)
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40
Q

in fed state, does glucose go more to liver or to the periphery?

peripheral glucose transporters

  • where?
  • sensitive to what
  • effect
A

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

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41
Q

what energy source does brain use

A

glucose

unable to use (free fatty acids→ ketones → acetyl coA because free fatty acids can not cross the blood brain barrier

42
Q

GLUT transporters

A

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

43
Q

insulin action

A
  • 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)

44
Q

cortisol function

A

Lipid and glycogen deposition
Muscle and carb catabolism
Na retention

45
Q

growth hormone secretion

  • what stimulates/ inhibtis
  • type of secretion
  • secreted from where
A

GHRH stimulates
Ghrelin stimulates
somastostatin inhibits
glucose inhibits

pulsatile secretion from anterior pituitary

46
Q

what stimulates thyroid hormones to be released

A

Hypothalamus → TRH Thyrotropin Releasing Hormone → anterior pituitary → TSH Thyroid Stimulating Hormone → Thyroid → T3 (Triiodothyronine) and T4 (thyroxine)

47
Q

thyroid hormones - differences

A

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
48
Q

what is needed for thyroid hormone synthesis

and why

A

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

49
Q

thyroid location, shape, and vascular status

A

Anterior neck C5-T1
Two lobes joined by isthmus
highly vascular- hormones secreted directly into blood

50
Q

where is angiotensinogen made

A

liver

51
Q

where is renin made

A

juxtoglomerular cells in kidney

52
Q

where is ACE made

A

vascular endothelial cells in lung

53
Q

what causes renin to be released

A

low blood pressure

54
Q

renin action

A

angiotensinogen to angiotensin 1

55
Q

ACE action

A

angiotensin 1 to 2

56
Q

angiontensin 2 action

A
  • vasoconstriction

- causes adrenal cortex to release aldosterone

57
Q

aldosterone action

A
  • channel proteins produced so more Na and water reabsorbed into the blood
  • K+ excreted (electrolyte balance)

distal tubules primarily

58
Q

where is aldosterone made

A

zona glomerulosa in adrenal cortex

59
Q

RAAS response to low blood pressure

A
  • 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
60
Q

water-soluble vs lipid-soluble hormones

  • bound to what
  • clearance
  • how does it affect
  • half life
  • pre-done or done on demand
A

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
61
Q

endocrine vs exocrine

A 
endocrine = secrete into bloodstream directly
exocrine= secrete into ducts
62
Q

endocrine
paracrine
autocrine

A

endocrine- acts distantly
paracrine - acts on nearby cells
autocrine- acts on cell that secreted the hormone

63
Q

location of…

peptide hormone receptor
steroid hormone receptor
thyroid hormone receptor

A

peptide hormone receptor = cell membrane

steroid hormone receptor= cytoplasm

thyroid hormone receptor= nucleus

64
Q

types of stimulation for hormone secretion

A
  • humoral stimulation- detect change in environment
  • nerve stimulation
  • hormonal stimulation
65
Q

pituitary stalk connects what

A

posterior pit and hypothalamus

66
Q

what hormones do ant/post pit secrete

A 
anterior pit:
GH
TSH
LH
FSH
ACTH
Prolactin

post pit:
oxytocin
vasopressin (ADH)

67
Q

what hormones do post pit make

A

none. oxytocin and vasopressin made in hypothalamus, stored and secreted from post pit

68
Q

oxytocin effect

A

cervix, uterus, breast milk

labour etc

69
Q

where does spinal cord end at cauda equina begin?

what is at the end of the spinal cord at the level

A

L1/2.
so cauda equina is L2 and below

conus medullaris

70
Q

filum terminale=

A

delicate strand of fibrous tissue proceeding down from the apex of the conus medullaris (non-neural)

71
Q

FEV1

A

amount of air forced out of lungs in 1 second

72
Q

FVC

A

amount of air expelled after the deepest breath in (no time limit)

73
Q

PEFR

A

peak expiratory flow rate - exhale as fast as poss

74
Q

which cells dont pass through the glomerulus

A

large negative molecules

cells

75
Q

what is the kidneys net excretion

A 
Na 
phosphate
acid 
k
uraemic toxins
76
Q

reabsorption in kidney

  • where mainly
  • what
A 
Majority in PCT
Na
Phosphate
Glucose
Amino acids
77
Q

where are do diuretics act

A

loop - loop of henle

thiazides - DCT

78
Q

K in kidney

  • filtration, reabsorption
  • what determines its level
A

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
79
Q

how do they kidneys contribute to RBC production

A
  • kidneys produce EPO

- And produce substance (?hepcidin) that allow iron to be absorbed in the duodenum

80
Q

vitamine D acitvation

A

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

81
Q

calcitrol action

A

= 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
82
Q

how does kidney balance acid-base

A

excrete h+

reabsorb bicarbonate

83
Q

creatinine measures kidney function

  • why
  • drawbacks
A
  • 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

84
Q

urine dipstick measures what for kidney function

drawbacks

A

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

85
Q

GFR is controlled by what vessels. what effects these vessels

A

afferent and efferent arteriole

Prostaglandin dilates afferent arteriole (increase GFR)
Angiotensin 2 constricts efferent arteriole (increase GFR)

86
Q

3 ureteric narrowings

A 
Pelviureteric junction (leave kidneys)
Pelvic brim (cross iliac vessels)
Vesicoureteric junction (enter bladder)
87
Q

enterohepatic circulation

A
  • 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
88
Q

bile =

constitution
role

A

= bile acids (cholic acids, cheondeoxydolic acid) + phospholipids + cholesterol

Helps fat digestion (emulsifies) → absroption of fat + fat soluble vitamins (ADEK)

89
Q

when does alcohol withdrawal start?
how long does it last?
symptoms:

A 
6-24h after last drink
up to a week
Tremor
Insomnia
nausea/vom
Agitation
Seizure
90
Q

delerium tremens =

A 
24-72h after last drink - withdrawal
Hyperadrenergic state
Symptoms
- Disorientation
- Tremors
- Impaired attention /consciousness
- Visual and auditory hallucinations
- Diaphoresis = sweating
91
Q

wernicke’s encephalopathy

  • =?
  • triad
  • treatment
A
  • 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
92
Q

korsakoff syndrome

A
  • Follows on from untreated wernicke’s encephalopathy
  • Memory impairment, confabulation
  • Chronic and irreversible
93
Q

platelet shape, what does this allow

A

Disc shape allows them to flow close to endothelium

94
Q

how many nuclei do platelets have

A

0

95
Q

lifespan of platelets

  • what stimulates production inc how this works
  • how they are made
  • how they die
A

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

96
Q

thromboxane induces

A

induces platelet aggregation and vasoconstriction

97
Q

P2Y12 =

- what is their role

A

P2Y12 = platelet receptors that is activated by ADP, causing platelet amplification/ activation and activates glycoprotein IIb/IIIa

98
Q

what is glycoprotein IIb/IIIa? and what is their role

A

Glycoprotein IIb/IIIa = platelet receptor for fibrinogen and vwF → platelet adherence and aggregation

99
Q

physiology of calcium / phosphate regulation

A
  • 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)
100
Q

where is intrinsic factor made

A

gastric parietal cells

phase 2a mine (38 decks)

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