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Summary NURP 404 Exam 2 Study Guide

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This is a comprehensive and detailed study guide on Exam 2 for Nurp 404.

Institution
Simmons College
Course
NURP 404









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Uploaded on
December 29, 2024
Number of pages
13
Written in
2021/2022
Type
Summary

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1
Patho Exam 2 Need to Know Content (Class and Case Study combined)

NEURO SYSTEM

Diencephalon – “least clear”, where
all the thalamus anatomy lies
- Hypothalamus
- Thalamus
- Epithalamus
- Limbic system




Blood Brain Barrier – Semi permeable barrier that really does not allow a lot of substance or molecules through, and so
the blood brain barrier is very strong protective mechanism for the brain to prevent drugs, medications and other
substances from passing into the brain and harming the brain




Nervous System
- Central Nervous System (CNS) – brain and spinal cord
- Peripheral Nervous System (PNS) –
o Somatic Pathway – muscle movement, neuromuscular junction, voluntary movement of skeletal muscle
o Autonomic – autonomically regulated, controls self-regulated action of internal organs and glands
 Sympathetic (arousing)
 Parasympathetic (calming)
 Neurotransmitters (receptor type determine response to neurotransmitter)
 Cholinergic Receptors – using acetylcholine as primary neurotransmitter
 Nicotinic: the ones that we most familiar with in the neuromuscular junction, activity w/
muscle contraction, etc
 Muscarinic: slow things down, more associated w/ parasympathetic nervous system.
o When you bind acetylcholine to the muscarinic receptor in the heart (Sa Node), it
slows down the heart rate. Therefore when it is too slow we give Atropine.
 Adrenergic Receptors – using noradrenaline or norepinephrine as neurotransmitter

, 2
Patho Exam 2 Need to Know Content (Class and Case Study combined)

 Alpha-adrenergic: vasoconstriction of blood vessels of skin and viscera, not in airway
smooth muscle
 Beta-adrenergic: (beta1, beta2) vasodilation of blood vessels in skeletal muscle, increase
heart rate and contractility, relaxation of airway smooth muscle – blocked by propranolol

MENINGITIS

Meninges – three connective tissue membranes that cover the brian and protect the central nervous system
- Dura mater, Arachnoid mater, Pia mater… then there is also the subarachnoid space
Meningitis: inflammation of the meninges
- Causes are viral, bacterial, or noninfectious origin
- Clinical characteristics: fever, headache, stiffness of neck, N/V, photophobia, AMS, brain, brain swelling,
petechiae/purpura (non-blanchable)
Due to meningitis inflammatory and infectious process going in, it causes cardiac consequences.
- The heart is trying to compensate so it’s going to try to hypertrophy or enlarge
- But is also won’t be efficient in pumping, so we will see decreased EF and hypotension. Then we will get a
backup back into pulmonary vascular bed and then we will see pulmonary edema.

STROKE

Stroke: sudden focal neurological deficit from a vascular disorder. Either ischemic or hemorrhagic, it’s a non-traumatic
disruption of blood supply to an area of the brain
- S&S: facial droop, arm/leg weakness, pain, slurred speech, word finding issues
Ischemic Stroke: a cerebral vascular obstruction from either a thrombus or emboli that leads to a lack of oxygen to areas
of the brain tissue
Intracerebral Hemorrhage (hemorrhagic stroke): is the destruction of the cerebral vessels, commonly in the frontal and
temporal lobes, where bleeding causes increased intracranial pressure
Subarachnoid Hematoma: is an accumulation of blood in subarachnoid space which is caused by rupture of cerebral
aneurysm
TIA – transient ischemia attach – “mini stroke
Stroke – permanent ischemic nature

Risk Factors
- Non-Modifiable: age, gender, race, family history, prior history of stroke
- Modifiable: smoking, ETOH, HLD
Deficit on one side of brain leads to deficits on opposite side of body
MORE THAN ONE RIGHT ANSWER ON QUESTION REGARDING STROKE FINDINGS ON EXAM

MULTIPLE SCLEROSIS

Multiple Sclerosis: originates in the central nervous system. So we have oligodendrocytes here that have produced the
myelin and we have some autoimmune process that triggers the destruction of the myelin sheaths.
- This is not primarily a sclerosing condition (hardening/calcification, may occur but not central)
- It is an autoimmune destruction of myelin sheaths that starts in the nervous system
- CNS origin
Amyotrophic Lateral Sclerosis (ALS) – originates with the myelin production of the Schwan cells, and you get the
destruction of the myelin in the peripheral nervous system

MS disease Process – Epstein Barr Virus, Herpes Simplex Virus, locations that are further from equator have higher
prevalence (? Vitamin D exposure/levels)
S&S: numbness, tingling. Burning, pressure on feet/extremities, abnormal gait, visual field issues, nystagmus, speech
issues, sexual dysfunction
Progressive- Relapsing MS – steady decline since onset w/ super-imposed attacks

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