NURS 5315 Shock, Shock
Advanced Path QUESTIONS
AND ANSWERS LATEST
UPDATE 2026
Brain hernation - ANSWERPressure in brain moves brain tissue
Potentially deadly
,Subarachnoid hemorrhage (bleeding deep in the brain) - ANSWER-Bleeding in the subarachnoid space,
the space between the pia mater and the arachnoid matter
-Innermost bleeding in the brain
-Bleeding causes inflammatory reaction of meninges (MENINGITIS)
-Increased risk: patients with hypertension, ANEURYSMS (they burst and bleed), head injuries
-S/sx: "Thunderclap headache" (feels like being kicked in the head), changs in LOC, Kernig's &
Brudzinski's signs, motor deficits.
-Cerebral vasopasms are a complication & can lead to delayed cerebral ischemia
Kernig's Sign - ANSWERSevere *stiffness of hamstrings*
(Can't *K*ick = *K*ernig's)
Sign of MENINGITIS (possibly secondary to subarachnoid hemorrhage)
Brudzinski's Sign - ANSWERSevere *neck stiffness*
(*Bruh, I can't move my neck = Brudzinski's*) Sign of MENINGITIS (possibly secondary to subarachnoid
hemorrhage)
Post Concussive Syndrome - ANSWER-Affects about 80% of people with mild-moderate traumatic brain
injuries
-Women are at higher risk
-Age increases risk
-Symptoms may occur 3-12 months post injury
-Symptoms: Headaches, dizziness, anxiety, difficulties with learning/memory/attention, depression
Signs: Global brain atrophy on imaging & signs of organic brain injury (changes not r/t mental illness) on
imaging 1 year post injury
Chronic Traumatic Encephalopathy (CTE) - ANSWER-Results from from *repeated* trauama to brain
,-*Hallmark sign: Deposition of tau protein throughout the brain
-Tau proteins are associated with synaptic dysfunction and neural cell death
-Patients may initially present with chronic symptoms: mood, cognitive, behavioral, motor disturbances
(Side note: Tau proteins are associated w/ Alzheimer's and clinical presentation is similar with
Alzeheimer's & CTE)
-Gene Apolipoprotein Ee4 increases risk for CTE
-Mortality from CTE & Alzheimer's is 3x higher in NFL players than general public
-Patho: Cerebral atrophy (remember this also follows post-concussive syndrome and CTE patients likely
have had lots of concussions), extensive tau-immunoreactive degenerative changes such as
neurofibrillary tanges, neutrophil threads, astrocytic tangles
4 stages of Chronic Traumatic Encephalopathy - ANSWERThe higher the number, the more widespread
the tau protein accumulation & worse the disease
Stage I: p-tau neurofibrillary tangles are isolated to cerebral cortex
Stage 4: p-tau proteins are widespread throughout brain
Cushing's Triad - ANSWER-Sign of increasing intracranial pressure (ICP)
1. Hypertension
2. Bradycardia
3. Widening pulse pressure (difference between systolic & diastolic pressure)
ICP & CPP - ANSWERIntracranial Pressure & Cerebral Perfusion Pressure have an inverse relationship -
when one is high the other is low
Normal CPP (cerebral perfusion pressure) - ANSWER60-100
, Low CPP (cerebral perfusion pressure) - ANSWER-Causes: *hypovolemia, hypotension*
Either of these can *cause brain ischemia*, then cellular hypoxia, then *cell injury & death*. Cell dies
and *intracellular contents are released*, leading to cellular edema and *increased ICP*. The increased
ICP further lowers CPP (cerebral perfusion pressure).
Remember: ICP & CPP have an inverse relationship; when one is high the other is low.
Elevated CPP (cerebral perfusion pressure) - ANSWERCause: *Hypertension*
Hypertension leads to increased hydrostatic pressure, which *pushes fluid out of the blood vessels* and
*into the brain* & causes *increased ICP*, which in turn causes decreased CPP (lower pressure due to
less volume in the blood vessels)
Example of CPP (cerebral perfusion pressure) and ICP (intracranial pressure) interacting - ANSWER1.
Head injury occurs
2. Inflammation of brain
3. Swelling of brain increases intracranial pressure
4. Cerebral perfusion pressure decreases (it's more difficult for new blood flow to get to the brain &
perfuse due to the high pressure in the brain; there's not enough room for all the fluid building up in the
brain AND for new blood to get in and perfuse)
5. Lowered cerebral perfusion pressure (CPP) leads to brain ischemia & cell death.
6. Intracellular contents are released, further increasing ICP.
7. ICP blocks flow of CSF in the cerebral ventricles and meninges, which causes them to swell. This
further decreases cerebral perfusion pressure (CPP) and increases ICP, causing more brain ischemia.
Causes of Increased ICP - ANSWERAnything that increases intracranial contents: tumors, edema, excess
CSF, hemorrhage
Increased Intracranial Pressure: First method of cerebral compensation - ANSWERDumping of CSF
Advanced Path QUESTIONS
AND ANSWERS LATEST
UPDATE 2026
Brain hernation - ANSWERPressure in brain moves brain tissue
Potentially deadly
,Subarachnoid hemorrhage (bleeding deep in the brain) - ANSWER-Bleeding in the subarachnoid space,
the space between the pia mater and the arachnoid matter
-Innermost bleeding in the brain
-Bleeding causes inflammatory reaction of meninges (MENINGITIS)
-Increased risk: patients with hypertension, ANEURYSMS (they burst and bleed), head injuries
-S/sx: "Thunderclap headache" (feels like being kicked in the head), changs in LOC, Kernig's &
Brudzinski's signs, motor deficits.
-Cerebral vasopasms are a complication & can lead to delayed cerebral ischemia
Kernig's Sign - ANSWERSevere *stiffness of hamstrings*
(Can't *K*ick = *K*ernig's)
Sign of MENINGITIS (possibly secondary to subarachnoid hemorrhage)
Brudzinski's Sign - ANSWERSevere *neck stiffness*
(*Bruh, I can't move my neck = Brudzinski's*) Sign of MENINGITIS (possibly secondary to subarachnoid
hemorrhage)
Post Concussive Syndrome - ANSWER-Affects about 80% of people with mild-moderate traumatic brain
injuries
-Women are at higher risk
-Age increases risk
-Symptoms may occur 3-12 months post injury
-Symptoms: Headaches, dizziness, anxiety, difficulties with learning/memory/attention, depression
Signs: Global brain atrophy on imaging & signs of organic brain injury (changes not r/t mental illness) on
imaging 1 year post injury
Chronic Traumatic Encephalopathy (CTE) - ANSWER-Results from from *repeated* trauama to brain
,-*Hallmark sign: Deposition of tau protein throughout the brain
-Tau proteins are associated with synaptic dysfunction and neural cell death
-Patients may initially present with chronic symptoms: mood, cognitive, behavioral, motor disturbances
(Side note: Tau proteins are associated w/ Alzheimer's and clinical presentation is similar with
Alzeheimer's & CTE)
-Gene Apolipoprotein Ee4 increases risk for CTE
-Mortality from CTE & Alzheimer's is 3x higher in NFL players than general public
-Patho: Cerebral atrophy (remember this also follows post-concussive syndrome and CTE patients likely
have had lots of concussions), extensive tau-immunoreactive degenerative changes such as
neurofibrillary tanges, neutrophil threads, astrocytic tangles
4 stages of Chronic Traumatic Encephalopathy - ANSWERThe higher the number, the more widespread
the tau protein accumulation & worse the disease
Stage I: p-tau neurofibrillary tangles are isolated to cerebral cortex
Stage 4: p-tau proteins are widespread throughout brain
Cushing's Triad - ANSWER-Sign of increasing intracranial pressure (ICP)
1. Hypertension
2. Bradycardia
3. Widening pulse pressure (difference between systolic & diastolic pressure)
ICP & CPP - ANSWERIntracranial Pressure & Cerebral Perfusion Pressure have an inverse relationship -
when one is high the other is low
Normal CPP (cerebral perfusion pressure) - ANSWER60-100
, Low CPP (cerebral perfusion pressure) - ANSWER-Causes: *hypovolemia, hypotension*
Either of these can *cause brain ischemia*, then cellular hypoxia, then *cell injury & death*. Cell dies
and *intracellular contents are released*, leading to cellular edema and *increased ICP*. The increased
ICP further lowers CPP (cerebral perfusion pressure).
Remember: ICP & CPP have an inverse relationship; when one is high the other is low.
Elevated CPP (cerebral perfusion pressure) - ANSWERCause: *Hypertension*
Hypertension leads to increased hydrostatic pressure, which *pushes fluid out of the blood vessels* and
*into the brain* & causes *increased ICP*, which in turn causes decreased CPP (lower pressure due to
less volume in the blood vessels)
Example of CPP (cerebral perfusion pressure) and ICP (intracranial pressure) interacting - ANSWER1.
Head injury occurs
2. Inflammation of brain
3. Swelling of brain increases intracranial pressure
4. Cerebral perfusion pressure decreases (it's more difficult for new blood flow to get to the brain &
perfuse due to the high pressure in the brain; there's not enough room for all the fluid building up in the
brain AND for new blood to get in and perfuse)
5. Lowered cerebral perfusion pressure (CPP) leads to brain ischemia & cell death.
6. Intracellular contents are released, further increasing ICP.
7. ICP blocks flow of CSF in the cerebral ventricles and meninges, which causes them to swell. This
further decreases cerebral perfusion pressure (CPP) and increases ICP, causing more brain ischemia.
Causes of Increased ICP - ANSWERAnything that increases intracranial contents: tumors, edema, excess
CSF, hemorrhage
Increased Intracranial Pressure: First method of cerebral compensation - ANSWERDumping of CSF
