Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMB 2 > BMB 2 > Flashcards

BMB 2 Flashcards

1
Q

Subarachnoid hemorrhage cause and sx

A

Caused by berry aneurysm leaking (most feared)
-shows up as blood in subarach space (white), neuro sx and neck stiffness, maybe had smaller headaches in weeks prior, THUNDERCLAP HEADACHE lasting a few sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Subdural hemmorrhage

A
  • Concave crescent, tearing of bridging veins

- slow changes in mobility and cog, dizziness/sleepiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Epidural hematoma

A
  • Convex lens, tearing of middle meningeal artery
  • lucid period after trauma then decline
  • e.g. athlete who got a concussion
  • Requires EMERGENT SURGERY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intercerebral hemorrhage appearance and cause

A
  • Looks like weird brain tumor on CT (white shape)

- Can be from HTN or anti-coag or anything that leas to bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Migraine sx

A

-few hours to few days, unilat, pulsating pain, N/V avoidance of light/sound, prodromal period with aura (eg scotoma, pins and needles, dysarthria/aphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Meds for migraines

A
  • abortive meds, triptans (5-HT blockers), etc.

- prevent with BBs, botox etc, NOT opiates !

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tension headache

A

Bilateral dull, non-pulsating, no nausea

tx by removing triggers eg stress, phys ther, NSAIDs etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Trigeminal Autonomic Cephalgia types (5)

A 
These include:
Cluster headaches
Paroxysmal hemicranias
SUNCT
SUNA
Hemicrania continua
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cluster headache

A

Worst pain, can awaken from sleep, occur in winter, men, weeks to months, UNILATERAL PAIN AROUND ORBIT, several times a day, minutes to hours

  • tearing of eyes and conjunctivitis
  • various tx (verapamil, Li etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Paroxysmal hemicrania

A

Affects V1 opthalmic region

  • short 2-30 min, 2-40x/day
  • can also have tears/conjuct
  • tx with indomethacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SUNCT

A

SHORT UNILATERAL NEURALGIFORM headache with ipsilateral CONJUCTIVITIS AND TEARS
-like cluster headaches but shorter ~30 s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SUNA

A

short unilat neuralgform headache with cranial AUTONOMIC sx

  • also has NASAL CONGESTION and eyedrip during short attacks
  • give lidocaine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hemicrania continua

A

Persistent, autonomic sx like PTOSIS, lacrimation, sweating, nasal congestion, eyelid edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Psuedotumor cerebri sx

A

whooshing, vision issues, maybe CN 6 palsy, but normal MRI/CSF lvl
-dx by MEASURING OPENING PRESSURE OF SPINAL TAP (lumbar puncture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

General adaptation sydnrome and stages

A

-response of body to threatening demand: shock phase with sudden decr in resistance to stressor, resistance phase (anti shock phase) where resistance incr and peaks, then exhaustion when resistance is depleted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Reactive stress vs anticipatory stress involves…

A

reactive- ASCENDING SENSORY PATHWAYS

anticipatory- anticipated by LIMBIC SYSTEM

17
Q

Reactive stress response general path

A

Bottom up: sensory input from outside world synpases on locus coeruleus or solitary tract nucleus (in midbrain/pons/medulla) before going to hypothalamus to signal NE release

18
Q

Anticipatory stress path

A

Top down:
Starts in limbic forebrain bc reliant on memo/conditioning, goes to bed nucleus of STRIA TERMINALIS (BST), and then to hypothal to activate hpa or ans

19
Q

SYMP STRESS PATHWAY

A

stress > pregang symp neurons activated in IML column T1-L2 of SC > synpase onto ganglia that go to viscera and chromaffin cells of ADR MEDULLA to release EPI (FAST)

20
Q

HPA STRESS PATHWAY

A

stress > activates PVN of hypothal > secr CRH/AVP into median eminance circ > then RFs at ant pit cause release of ACTH > goes to zona fasc of ADR CORTEX to rel gluco/mineralocorticoids (CORTISOL AND ALDO) (SLOW)

21
Q

CV, GI, and met response to stress

A

symp:
incr HR, vasoconstriction to incr BP, incr blood vol because vasopressin causes water absorption in kidneys
-inhib of salivation and contractility, incr acid/enz
-energy mobilization from inhib pancr insulin, conv prot to gluc in muscle, conv glyco to clug in liver, conv fatty acid to energy

22
Q

From limbic sys to HPA axis, what structures are involved and where do neurons synapse? (excit/inhib)

A

GABA goes to BST to inhib hypothal from rel stress hormones (eg inhib rel of CRH into med eminence)

  • but amyg/pfc/hc modifies GABA relay
  • amygdala has GABA output to BST, so inhibiting the inhibitory affects of BST on hypothal, thus overall positive (amygdala heightens fear resp)
  • PFC and HC stimulate BST via glutamate, so further inhibits rel from hypothal
23
Q

Acute stress short term benefits

A

-acute: energy mobilization, immune suppr, CNS arousal, moderate lvls inv incr memo retention of emotionally charged events, long term potentiation, adaptive (more dendritic spines and neurogenesis, interconnectivity, branching, incr in learning/memo in hc)

24
Q

Chronic stress long term consequences

A

-chronic: met disease, obesity, msk atrophy, immune issues, depr/anx/ptsd, maladaptive (can exacerbate psych issues and limit resp to disease or lead to substance abuse) (decr in above fxns, hypertrophy of amygdala causing chronic activation of HPA axis bc cant inhibit it, and PFC atrophy, causing constant fear response and may contr to anxiety)

25
Q

When does cortisol peak?

A

8am

26
Q

PTSD/ Depr hyper/hyposensitivity to cortisol in chronic stress

A

depr- high cortisol bc not sensitive enoguh to coritsol

ptsd- low cortisol bc hypersens to cortisol

27
Q

What part of the brain acts as the central clock?

A

the SCN (suprachiasmatic nuclei) (above optic chiasm)

28
Q

light pathway to SCN

A

light goes to retinal gang cells with melanopsin, sends info dir to SCN via retinohypothalamic tract
-after, SCN transfers this info to PVN of hypothal, PVN sends tract down cerv spinal cord to IML which sends info to sup cervical gang which sends info to pineal gland to make melatonin in dark (or prevent it in light)

29
Q

two process model for regulation of sleep wake cycle

A

process s- sleep drive, rises throughout day, and falls one asleep (curve correl with amount of adenosine which is made when we use up ATP_

process c- wake drive, falls at end of day, mimics orexin curve (molec in hypothal which keeps u awake) around 11 is biggest gap between process s and c

30
Q

what NT is needed to make serotonin into melatonin?

A

NE!
(melatonin can be found in blood vessels in all parts of body and CSF, peaks in early childhood, can enhance chemo drugs and slow tumors)

BMB 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions