3rd Yr 2nd Sem Oral Rev

1.
Schizophrenia
DEFINITION Schizophrenia is defined as a serious mental illness that affects how a person
thinks, feels, and behaves. Schizophrenia causes distorted and bizarre thoughts,
perceptions, emotions, movements, and behavior.It cannot be defined as a
single illness; rather, schizophrenia is thought of as a syndrome or as a disease
process with many different varieties and symptoms.
Schizophrenia is a chronic illness requiring long-term management

strategies and coping skills. It is a disease of the brain, a clinical syndrome
characterized by a person's thoughts, perceptions, emotions, movements,
and behaviors.
(galing sa notes ni maam apol)
PHASES OF SCHIZOPHRENIA ah yess
The pattern of development of schizophrenia may be viewed in four phases: the

premorbid phase, the prodromal phase, the active psychotic phase
(schizophrenia), and the residual phase.
Phase I: The Premorbid Phase

The premorbid personality often indicates social maladjustment, social
withdrawal, irritability, and antagonistic thoughts and behavior. Premorbid
personality and behavioral measurements that have been noted include being
very shy and withdrawn, having poor peer relationships, doing poorly in school,
and demonstrating antisocial behavior.
In the typical, but not invariable, premorbid history of schizophrenia, patients had
schizoid or schizotypal personalities characterized as quiet, passive, and
introverted; as children, they had few friends. Pre-Schizophrenic adolescents
may have no close friends and no dates and may avoid team sports. They may
enjoy [solitary activities] to the exclusion of social activities.
Phase II: The Prodromal Phase

The prodrome of an illness refers to certain signs and symptoms that precede
the characteristic manifestations of the acute, fully developed illness. The
prodromal phase of schizophrenia begins with a change from premorbid
functioning and extends until the onset of frank psychotic symptoms. This phase
can be as brief as a few weeks or months, but most studies indicate that the
average length of the prodromal phase is between 2 and 5 years.
During the prodromal phase the person experiences substantial functional

impairment and nonspecific symptoms such as a sleep disturbance, anxiety,
irritability, depressed mood, poor concentration, fatigue, and behavioral deficits
such as deterioration in role functioning and social withdrawal. Positive
symptoms such as perceptual abnormalities, ideas of reference, and
suspiciousness develop late in the prodromal phase and herald the imminent
onset of psychosis.
Recognition of the behaviors associated with the prodromal phase provides an

opportunity for early intervention with a possibility for improvement in long-term
outcomes. Current treatment guidelines suggest therapeutic interventions that
offer support with identified problems, cognitive therapies to minimize functional
impairment, family interventions to improve coping, and involvement with the
schools to reduce the possibility of failure. Some controversy exists as to the
benefit of using pharmaceutical therapy during the prodromal phase. Can
providing interventions, including pharmacologic treatments, delay (or even
prevent) the onset of psychosis? Minzenberg, Yoon, and Carter (2008) state,
“The use of [antipsychotic] medications to treat symptoms that are below the
threshold of psychosis has to date been poorly studied”
Phase III: Schizophrenia

In the active phase of the disorder, psychotic symptoms are prominent.
Following are the DSM-5 (APA, 2013) diagnostic criteria for schizophrenia:
A. Two (or more) of the following, each present for a significant portion of time
during a 1-month period (or less if successfully treated). At least one of these
must be (1), (2), or (3):
(1) Delusions
(2) Hallucinations
(3) Disorganized speech (e.g., frequent derailment or incoherence).
(4) Grossly disorganized or catatonic behavior
(5) Negative symptoms (i.e., diminished emotional expression or avolition)
B. For a significant portion of the time since the onset of the disturbance, level of
functioning in one or more major areas, such as work, interpersonal relations, or
self-care, is markedly below the level achieved prior to the onset (or when the
onset is in childhood or adolescence, there is failure to achieve expected level of
interpersonal, academic, or occupational functioning).
C. Continuous signs of the disturbance persist for at least 6 months. This 6-

month period must include at least 1 month of symptoms (or less if successfully
treated) that meet Criterion A (i.e., active-phase symptoms) and may include
periods of prodromal or residual symptoms. During these prodromal or residual
periods, the signs of the disturbance may be manifested by only negative
symptoms or by two or more symptoms listed in Criterion A present in an
attenuated form (e.g., odd beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic

features have been ruled out because either (1) no major depressive or manic
episodes have occurred concurrently with the active-phase symptoms; or (2) if
mood episodes have occurred during active-phase symptoms, they have been
present for a minority of the total duration of the active and residual periods of
the illness.
E. The disturbance is not attributable to the physiological effects of a substance

(e.g., a drug of abuse, a medication) or another medical condition.
F. If there is a history of autism spectrum disorder or a communication disorder

of childhood onset, the additional diagnosis of schizophrenia is made only if
prominent delusions or hallucinations, in addition to the other required symptoms
of schizophrenia, are also present for at least 1 month (or less if successfully
treated). Specify if: First episode, currently in acute, partial, or full remission;
Multiple episodes, currently in acute, partial or full remission; Continuous;
Unspecified; With catatonia Specify current severity.
Phase IV: Residual Phase

Schizophrenia is characterized by periods of remission and exacerbation. A
residual phase usually follows an active phase of the illness (symptoms
described in Phase III). During the residual phase, symptoms of the acute stage
are either absent or no longer prominent. Negative symptoms may remain, and
flat affect and impairment in role functioning are common. Residual impairment
often increases between episodes of active psychosis
YW RAH KADAGHAN BA DIAY ANI
Schizoaffective Disorder- diagnosed when the client is severely ill and has a
mixture of psychotic and mood symptoms. The signs and symptoms include
those of both schizophrenia and a mood disorder.
Related Disorders
• Schizophreniform Disorder: The client exhibits an acute, reactive psychosis

for less than the 6 months necessary to meet the diagnostic criteria for
schizophrenia. If symptoms persist over 6 months, the diagnosis is changed to
schizophrenia. Social or occupational functioning may or may not be impaired.
• Catatonia: Catatonia is characterized by marked psychomotor disturbance,
either excessive motor activity or virtual immobility and motionlessness. Motor
immobility may include catalepsy (waxy flexibility) or stupor. Excessive motor
activity is apparently purposeless and not influenced by external stimuli. Other
behaviors include extreme negativism, mutism, peculiar movements, echolalia,
or echopraxia. Catatonia can occur with schizophrenia, mood disorders, or other
psychotic disorders.
• Delusional disorder: The client has one or more non bizarre delusions— that
is, the focus of the delusion is believable. The delusion may be persecutory,
erotomanic, grandiose, jealous, or somatic in content. Psychosocial functioning
is not markedly impaired, and behavior is not obviously odd or bizarre.
• Brief psychotic disorder: The client experiences the sudden onset of at least
one psychotic symptom, such as delusions, hallucinations, or disorganized
speech or behavior, which lasts from 1 day to 1 month. The episode may or may
not have an identifiable stressor or may follow childbirth.
• Shared psychotic disorder (folie à deux): Two people share a similar

delusion. The person with this diagnosis develops this delusion in the context of
a close relationship with someone who has psychotic delusions, most commonly
siblings, parent and child, or husband and wife. The more submissive or
suggestible person may rapidly improve if separated from the dominant person.
• Schizotypal personality disorder: This involves odd, eccentric behaviors,

including transient psychotic symptoms. Approximately 20% of persons with this
personality disorder will eventually be diagnosed with schizophrenia.
ANATOMY & Brain ra man ni diba? IYAKKK T-T

PHYSIOLOGY (only
for the major organ) Neurobiology Of Schizophrenia
Neurotransmitters
A number of neurotransmitters have been implicated in the etiology of
schizophrenia. These include dopamine, norepinephrine, serotonin, glutamate,
and gamma-aminobutyric acid. The dopaminergic system has been most widely
studied and closely linked to the symptoms associated with the disease.
Areas of the Brain Affected

• Four major dopaminergic pathways have been identified:
• Mesolimbic pathway: Originates in the ventral tegmentum area and
projects to areas of the limbic system, including the nucleus accumbens,
amygdala, and hippocampus. The mesolimbic pathway is associated with
functions of memory, emotion, arousal, and pleasure. Excess activity in
the mesolimbic tract has been implicated in the positive symptoms of
schizophrenia (e.g., hallucinations, delusions).
• Mesocortical pathway: Originates in the ventral tegmental area and
has projections into the cortex. The mesocortical pathway is concerned
with cognition, social behavior, planning, problem-solving, motivation,
and reinforcement in learning. Negative symptoms of schizophrenia (e.g.,
flat affect, apathy, lack of motivation, and anhedonia) have been
associated with diminished activity in the mesocortical tract.
• Nigrostriatal pathway: Originates in the substantia nigra and
terminates in the striatum of the basal ganglia. This pathway is
associated with the function of motor control. Degeneration in this
pathway is associated with Parkinson’s disease and involuntary
psychomotor symptoms of schizophrenia.
• Tuberoinfundibular pathway: Originates in the hypothalamus and
projects to the pituitary gland. It is associated with endocrine function,
digestion, metabolism, hunger, thirst, temperature control, and sexual
arousal. Implicated in certain endocrine abnormalities associated with
schizophrenia. The role of dopamine release in the tuberoinfundibular
pathway is to tonically inhibit prolactin release . The main implication of
this is that blockade of D2 receptors by drugs such as antipsychotics
increases prolactin levels.
● Two major groups of dopamine receptors and their highest tissue

locations include the following:
• The D1 family:
D1 receptors: Basal ganglia, nucleus accumbens, and cerebral cortex
D5 receptors: Hippocampus and hypothalamus, with lower
concentrations in the cerebral cortex and basal ganglia
• The D2 family:
D2 receptors: Basal ganglia, anterior pituitary, cerebral cortex, limbic
structures
D3 receptors: Limbic regions, with lower concentrations in basal ganglia
D4 receptors: Frontal cortex, hippocampus, amygdale
ETIOLOGY Predisposing Factors
● Physiological
○ Genetics
○ Histological Changes
○ Biochemical/ Anatomical Abnormalities
Precipitating Factors
● Suffering a loss
● Experiencing Abuse
● Trauma
● Using Illicit Drugs such as Amphetamines, Cannabis, LSD, or
Cocaine.
SYMPTOMATOLOGY Schizophrenia is characterized by positive and negative symptoms that are

(significant features/ present for a significant portion of a 1- month period but with continuous signs of
manifestations) disturbance persisting for at least 6 months. We define positive symptoms as
hallucinations and delusions and negative symptoms as diminished emotional
expression and avolition (lack of interest or motivation in goal-directed behavior,
such as getting dressed, going to work or to school).
Positive or Hard Symptoms

Ambivalence: Holding seemingly contradictory beliefs or feelings about the
same person, event, or situation
Associative looseness: Fragmented or poorly related thoughts and ideas
Delusions: Fixed false beliefs that have no basis in reality
Echopraxia: Imitation of the movements and gestures of another person whom
the client is observing
Flight of ideas: Continuous flow of verbalization in which the person jumps
rapidly from one topic to another
Hallucinations: False sensory perceptions or perceptual experiences that do
not exist in reality
Ideas of reference: False impressions that external events have special
meaning for the person
Perseveration: Persistent adherence to a single idea or topic; verbal repetition
of a sentence, word, or phrase; resisting attempts to change the topic
Bizarre behavior: Outlandish appearance or clothing; repetitive or stereotyped,
seemingly purposeless movements; unusual social or sexual behavior
Negative or Soft Symptoms

Alogia: Tendency to speak little or to convey little substance of meaning
(poverty of content)
Anhedonia: Feeling no joy or pleasure from life or any activities or relationships
Apathy: Feelings of indifference toward people, activities, and events
Asociality: Social withdrawal, few or no relationships, lack of closeness
Blunted affect: Restricted range of emotional feeling, tone, or mood
Catatonia: Psychologically induced immobility occasionally marked by periods
of agitation or excitement; the client seems motionless, as if in a trance
Flat affect: Absence of any facial expression that would indicate emotions or
mood
Avolition or lack of volition: Absence of will, ambition, or drive to take action or
accomplish tasks
Inattention: Inability to concentrate or focus on a topic or activity, regardless of
its importance
GENERAL TABANG
PATHOPHYSIOLOGY
(Simplified) 1. Predisposing and Precipitating
2. Disrupted VTA production of dopamine (ventral tegmental area)
3. Dopamine binds to dopamine receptors
4. Increased dopaminergic transmission in mesolimbic and decreased in
mesocortical
5. Abnormal levels of dopamine
6. SCHIZOPHRENIA
LABORATORY & Laboratory findings

DIAGNOSTIC TESTS
No laboratory tests to specifically diagnose schizophrenia; MRI or CT scans of
the brain or blood tests — to rule out physical illness as the cause of the
symptoms.
Diagnostics Findings
● SCALE FOR THE ASSESSMENT OF NEGATIVE SYMPTOMS (SANS)

● SCALE FOR THE ASSESSMENT OF POSITIVE SYMPTOMS (SAPS)
● POSITIVE AND NEGATIVE SYNDROME SCALE (PANSS)
● ABNORMAL INVOLUNTARY MOVEMENT SCALE (AIMS)
● BRIEF PSYCHIATRIC RATING SCALE (BPRS)- used when
psychiatrists want to check how severe someone’s schizophrenia
is. The test looks at 18 symptoms or behaviors, such as hostility,
disorientation, and hallucination and ranks each on a scale of 1 (not
present) to 7 (extremely severe).
● DYSKINESIA IDENTIFICATION SYSTEM: CONDENSED USER SCALE
(DISCUS)
● SIMPSON–ANGUS RATING SCALE
YW AMBOT UNSA NI WALA GI EXPLAIN SA BOOK TABANG
MEDICAL Cognitive behavioral therapy, behavioral skills training, supported

MANAGEMENT employment, and cognitive remediation interventions may help address the
negative and cognitive symptoms of schizophrenia.
Coordinated specialty care (CSC) - general term used to describe recovery-

oriented treatment programs for people with first episode psychosis, an early
stage of schizophrenia.
PHARMACOLOGIC MANAGEMENT
● First-generation antipsychotics
● Second-generation antipsychotics
● Long-acting injectable antipsychotics
Antipsychotic medications- help reduce the intensity and frequency of

psychotic symptoms (haloperidol and risperidone)
● Conventional (typical) antipsychotics- haloperidol

● Novel (atypical) antipsychotics- risperidone
SURGICAL Surgical Procedures/s (if applicable)

MANAGEMENT N/A
Nursing Interventions (Post-op care)

N/A
NURSING 1. Initiate a nurse–patient relationship by using an accepting,

MANAGEMENT (10) nonjudgmental approach. (Establish rapport)
R: Therapeutic relationship will provide support as the patient begins to
deal with life changes.
2. Be patient.
R: Be patient because their brain is not processing information normally.
3. Administer antipsychotic medications.
R: To help reduce the intensity and frequency of psychotic symptoms
4. Recognize the client’s delusions as the client’s perception of the
environment.
R: Recognizing the client’s perceptions can help you understand the
feelings the patient is experiencing.
5. Interact with the client on the basis of real things; do not dwell on the
delusional material. (Present Reality)
R: Interacting about reality is healthy for the client
6. Recognize and support the client’s accomplishments
R: Recognizing the client’s accomplishments can lessen anxiety and the
need for delusions as a source of self esteem.
7. Show empathy regarding the client’s feelings; reassure the client of your
presence and acceptance.
R: The client’s delusions can be distressing. Empathy conveys your
caring, interest, and acceptance of the client.
8. Do not argue with the client or try to convince the client that the delusions
are false or unreal.
R: Logical argument does not dispel delusional ideas and can interfere
with the development of trust.
9. Establish support systems and care.
R: To provide support and encouragement to the client.
10. Never convey to the client that you accept the delusions as reality.
R: Indicating belief in the delusions reinforces the delusion (and the
client’s illness).
Galing ito kay maam apol (ADDITIONAL NOTES LANG HEHEHE)
Points to Consider When Working with Clients with Schizophrenia

● Remember that although these clients often suffer numerous relapses
and return for repeated hospital stays, they do return to living and
functioning in the community.
✔ Focusing on the amount of time the client is outside the hospital setting
may help decrease the frustration that can result when working with
clients with a chronic illness.
● Visualize the client not at his or her worst, but as he or she gets better,
and symptoms become less severe.
✔ Remember that the client’s remarks are not directed at you personally
but are a byproduct of the disordered and confused thinking that
schizophrenia causes.
○ Remarks are byproducts of the disorder hindi sayo; don't take it
personally
■ “Luoda sa imong pimples maam oy”
✔ Discuss these issues with a more experienced nurse for suggestions on
how to deal with your feelings and actions toward these clients. You are
not expected to have all the answers.
1. Help them get treatment and encourage them to stay in treatment

2. Remember that their beliefs or hallucinations seem very real to them
3. Tell them that you acknowledge that everyone has the right to see things
their way
4. Be respectful, supportive, and kind without tolerating dangerous or
inappropriate behavior
5. Check to see if there are any support groups in your area
PRIORITY NURSING 1. Impaired Verbal Communication r/t Altered Perceptions.

DIAGNOSIS (5) 2. Impaired Social Interaction r/t Difficulty with communication
3. Disturbed Sensory Perception r/t Psychologic stress (pwede ito
auditory or visual depends sa na eexperience niya na hallucination)
4. Defensive Coping r/t Suspicions of the motives of others
5. Disturbed Thought Process r/t Repressed fears
The North American Nursing Diagnosis Association’s (NANDA) nursing

diagnoses commonly 624 established based on the assessment of psychotic
symptoms or positive signs are: • Risk for other-directed violence • Risk for
suicide • Disturbed thought processes • Disturbed sensory perception •
Disturbed personal identity • Impaired verbal communication
The NANDA nursing diagnoses based on the assessment of negative signs and
functional abilities include: • Self-care deficits • Social isolation • Deficient
diversional activity • Ineffective health maintenance • Ineffective
therapeutic regimen management
There are many nursing diagnoses generated from the assessment data. Typical
nursing diagnoses focusing on the physical aspects include self-neglect and
disturbed sleep patterns. During a relapse, imbalanced nutrition: Less than body
requirements, excess fluid volume, and sexual dysfunction are possible
diagnoses. For psychological aspects, acute confusion can be used for
disorganized thinking, hallucinations, or illusions. Other examples of diagnoses
include chronic low self-esteem, ineffective coping, and deficient knowledge. The
nursing diagnoses generated from the assessment of the social domain are
typically impaired social interaction, ineffective role performance, dysfunctional
family process, or interrupted family processes. Outcomes depend on the
specific diagnostic area and the specific symptoms/behaviors displayed by the
individual. Several strength-based nursing diagnoses can be generated from the
assessment data, such as readiness for enhanced coping and readiness for
enhanced hope.
PROGNOSIS Outcomes in schizophrenia are difficult to predict, but a complete return to full
premorbid functioning is not common. However, several factors have been
associated with a more positive outcome. These factors include good premorbid
functioning, later age at onset, female gender, abrupt onset of symptoms with
obvious precipitating factor (as opposed to gradual insidious onset of
symptoms), associated mood disturbance, rapid resolution of active-phase
symptoms, minimal residual symptoms, absence of structural brain
abnormalities, normal neurological functioning, and no family history of
schizophrenia.
REFERENCES
2. Bipolar Disorder -
DEFINITION
Bipolar disorder is characterized by cycles of mania and depression (severe
mood changes) with intervening periods of normalcy.
*Mania - A distinct period of abnormally and persistently elevated, expansive, or irritable

mood and abnormally and persistently increased goal-directed activity or energy, lasting
at least 1 week and present most of the day, nearly every day
*Hypomanic - A distinct period of abnormally and persistently elevated, expansive, or

irritable mood and abnormally and persistently increased activity or energy, lasting at
least 4 consecutive days and present most of the day, nearly every day
Bipolar I – an individual who is experiencing a manic episode or has a history of

one or more manic episodes. The dx is further specified by the current or most
recent behavioral episode experienced.
Bipolar II – recurrent depressive episodes with episodic occurrence of

hypomania.
Cyclothymic – chronic mood disturbance of at least 2-years’ duration involving

numerous period of elevated mood that do not meet the criteria for a hypomanic
episode and numerous periods of depressed mood of insufficient severity or
duration to meet the criteria for a major depressive episode
Substance/Medication-Induced Bipolar and Related Disorder – classified as

mania, hypomania or a major depressive episode directly caused by a
substance/medication that is or has been taken. (Apol, 2022 chos)
ANATOMY & White and Gray Matter

PHYSIOLOGY (only - CNS is made up of 2 tissues: white & gray matter. The gray matter
for the major organ) enables us to control movement, memory, and emotions. It mainly serves
to process info in the brain. In ppl w/ bipolar disorder, studies showed
thinning of gray matter which would lead to decrease in control and
difficulty in motor skills which is why mania seems impulsive or careless.
Hippocampus
- plays a role in learning, consolidating, and memory retrieval. It’s also
involved in verbal memory functions, stress responses, emotions, goal-
directed activity, and sensorimotor integration. Studies have shown that
people w/ bipolar have reduced hippocampus.
○ Serotonin - mood stabilizer; impulsive people apparently have
lower brain serotonin activity
○ Norepinephrine - arousal and alertness/ mood elevation
○ Dopamine - arousal/pleasure; decreased dopamine: depression,
increased dopamine - mania
1. Genetics – there is an average 10-fold increased risk among adult
relatives of indivs w/ bipolar 1 and 2 disorders. Magnitude of risk
increases with kinship.
2. Biogenic Amines - A study revealed an increased density in the anime
releasing cells in the brains of people with bipolar disorder. Just as there
is an indication of lowered levels of norepinephrine and dopamine during
an episode of depression, the opposite appears to be true of an
individual experiencing a manic episode. Thus, the behavioral responses
of elation and euphoria may be caused by an excess of these biogenic
amines in the brain.
*electrolyte imbalances (Na and Ca) may also be related to abnormalities
in cellular membrane function in bipolar.
3. Neuroanatomical Factor - Right-sided lesions in the limbic system,
temporo basal areas, basal ganglia, and thalamus have been shown to
induce secondary mania. Magnetic resonance imaging studies have
revealed enlarged third ventricles and subcortical white matter and
periventricular hyperintensities in clients with bipolar disorder.
1. Sleep/ Chronobiologic Theories - Sleep disturbance is common in
individuals with bipolar disorder, especially mania. Sleep patterns appear
to be regulated by an internal biological clock center in the
hypothalamus. Artificially induced sleep deprivation is known to
precipitate mania in some patients with bipolar disorder
2. Chronic stress – the role of an allostatic load or wear and tear on the
body is thought to contribute to cognitive impairment, comorbidity and
eventual mortality of those with bipolar disorder. As the allostatic load
increases, the number of mood episodes increases, which in turn
increases physical and mental health problems.
3. Medication Side Effects - certain medications used to treat somatic
illnesses have been known to trigger manic episodes. Most common are
steroids used to treat multiple sclerosis or SLE
SYMPTOMATOLOGY Symptoms of mania may be observed on a continuum of three phases, each

(significant features/ identified by the degree of severity: phase I - hypomania; phase II - acute
manifestations) mania; and phase III - delirious mania.
Ito yung sa powerpoint ni maam apol:

DIGFAST
Distractibility/ depression
Irresponsibility
Grandiosity
Flight of Ideas
Increase in goal directed Activities (mania)
Decreased need for Sleep
Talkativeness/pressured sleep
GENERAL
PATHOPHYSIOLOGY
(Simplified)
1. Predisposing and Precipitating

2. Decreased inhibitory control of emotional circuitry
3. Disruption of emotional homeostasis
4. Oscillation between mood states
● Manic episode (minimum of one week)
● Depressive episode (minimum of 2 weeks)
5. BIPOLAR DISORDER
Kani akong simplified if gusto ra ninyo ifollow :> ayoko edi dont

DIAGNOSTIC TESTS
Mood Disorder Questionnaire (MDQ) - The Mood Disorder Questionnaire

(MDQ) is a 13-item checklist developed by Robert M.A. Hirschfeld, M.D. The
MDQ serves as an effective instrument for screening patients who have a history
of a manic episode associated with bipolar disorder. In order to diagnose bipolar
disorder, all 3 criterias should be met:
1. Yes to 7 or more of the 14 items in question 1 and;
2. Yes to question 2 and;
3. “Moderate problem” or “Serious problem” to question 3
MEDICAL 1. Individual Psychotherapy - Interpersonal and social rhythm therapy is

MANAGEMENT tailored to bipolar patients. In addition to focusing on grief, role conflicts,
role transitions, and interpersonal deficiencies, it includes
psychoeducation about bipolar disorder and encourages treatment
adherence.
2. Group Therapy - Once an acute phase of the illness is passed, groups

can provide an atmosphere where they can discuss issues in their lives
that cause, maintain, or arise out of having a serious affective disorder.
The element of peer support may provide a feeling of security, as
troublesome or embarrassing issues are discussed and resolved.
3. Family Therapy - The ultimate objectives in working with families of

clients with mood disorders are to resolve the symptoms and initiate or
restore adaptive family functioning.
4. Cognitive Therapy - the individual is taught to control thought distortions

that are considered to be a factor in the development and maintenance of
mood disorders.The general goals in cognitive therapy are to obtain
symptom relief ASAP, to assist the client in identifying dysfunctional
patterns of thinking and behaving, and to guide the client to evidence and
logic that effectively tests the validity of the dysfunctional thinking.
5. Electroconvulsive Therapy - done when the client does not tolerate or

fails to respond to lithium or other drug treatment or when life is
threatened by dangerous behavior or exhaustion
Pharmacologic Management
1. Antipsychotics (e.g. olanzapine)
- Mechanism of action in the treatment of mania is unknown.
Antipsychotic drugs help regulate the functioning of brain circuits
that control thinking, mood, and perception. The first-generation
antipsychotics work by inhibiting dopaminergic
neurotransmission; their effectiveness is best when they block
about 72% of the D2 dopamine receptors in the brain.
2. Antimanic (e.g. lithium carbonate - DRUG OF CHOICE)

- Not fully understood; May modulate the effects of various
neurotransmitters such as norepinephrine, serotonin, dopamine,
glutamate, and GABA, that are thought to play a role in the
symptomatology of bipolar disorder (may take 1–3 weeks for
symptoms to subside).
3. Anticonvulsants (e.g. valproic acid)

- work by calming hyperactivity in the brain. Specifically, they act by
either: Altering electrical activity in neurons by affecting ion
(sodium, potassium, calcium, chloride) channels in the cell
membrane.
*depakote is valproic acid

*lamictal is anticonvulsant

MANAGEMENT N/A

N/A
NURSING 1. Use empathetic communication

MANAGEMENT (10) R: Acknowledging and empathizing creates a supportive environment
that enhances coping.
2. Provide chances to express concerns, fears, feelings, and expectations.

R: Verbalization of actual or perceived threats can help reduce anxiety
and open doors for ongoing communication.
3. Encourage the patient to recognize his or her own strengths and abilities.
R: During crises, patients may not be able to recognize their strengths.
Fostering awareness can expedite use of these strengths.
4. Do not argue, bargain or try to reason with the pt. Merely state the limits
and expectations
R: Because of the strong influence on client’s behavior, he or she should
receive immediate feedback when behavior is unacceptable. Consistency
is important because inconsistency may cause confusion and
encourages testing of limits
5. Provide positive reinforcements for non manipulative behaviors

R: Positive reinforcement enhances self-esteem and promotes repetition
of desirable behaviors.
6. Help the client identify positive aspects about self, recognize
accomplishments, and feel good about them.
R: As self-esteem is increased, client will feel less need to manipulate
others for own gratification.
7. Reduce environmental stimuli. Assign pt. to private room with simple

decor as possible
R: Client is extremely distractible and responses to even the slightest
stimuli are exaggerated.
8. Remove hazardous objects and substances

R: Rationality is impaired, and client may harm self inadvertently.
9. Provide high-protein, high-calorie nutritious finger foods and drinks that

can be consumed on the run
R: Client has difficulty sitting still long enough to eat a meal. The
likelihood is greater that he or she will eat easy to carry foods
10. Monitor daily record of intake, output, calorie count, and weight
R: These are important nutritional assessment data.
PRIORITY NURSING 1. Ineffective coping r/t neurologic changes in brain OR inadequate level of
DIAGNOSIS (5) perception of control
2. Sleep deprivation r/t altered physiologic status (e.g. bipolar, depression)
3. Impaired social interaction r/t egocentric and narcissistic behavior
4. Imbalanced nutrition: less than body requirements r/t refusal or inability
to sit still long enough to eat
5. Risk for Injury r/t extreme hyperactivity
PROGNOSIS Bipolar 1 disorder usually has a poor prognosis. 50% of patients experience a
second episode within two years of the first episode. Lithium prophylaxis improves
prognosis in about 50% of patients. About 45% of patients have a chronic disorder.
More episodes indicate a poorer prognosis. As discussed, patients with bipolar
affective disorder are at higher risk for suicidal ideation and attempts, which lead
to a poorer prognosis.
REFERENCES
3. Major Depression
DEFINITION Major depressive disorder typically involves 2 weeks or more of a sad mood or
lack of interest in life activities, with at least four other symptoms of depression
such as anhedonia and changes in weight, sleep, energy, concentration,
decision-making, self-esteem, and goals.
a persistently depressed mood and a long-term loss of interest in life
ANATOMY & ● Serotonin

PHYSIOLOGY (only ● Norepinephrine
for the major organ) ○ Usually, presynaptic neurons release these neurotransmitters to
allow them to enter synapses and link with postsynaptic
receptors. Depression results if too few neurotransmitters are
released, if they linger too briefly in synapses, if the releasing
presynaptic neurons reabsorb them too quickly, if conditions in
synapses do not support linkage with postsynaptic receptors, or if
the number of postsynaptic receptors has decreased.
ETIOLOGY Neurobiological →norepinephrine & serotonin

● presynaptic neurons release these neurotransmitters to allow them to
enter synapses and link with postsynaptic receptors.
Psychosocial factors
SYMPTOMATOLOGY Signs and Symptoms/ DSM V

(significant features/
manifestations) ● Sad mood OR loss of interest or pleasure (anhedonia)
● Symptoms are present nearly every day, most of the day, for at least 2
weeks
● Symptoms are distinct and more severe than a normative response to
significant loss
PLUS, four of the following symptoms:

● Sleeping too much or too little
● Psychomotor retardation or agitation
● Poor appetite and weight loss, or increased appetite and weight gain
● Loss of energy
● Feelings of worthlessness or excessive guilt
● Difficulty concentrating, thinking, or making decisions
● Recurrent thoughts of death or suicide
Ruling out: ???

• Episodic • Symptoms tend to dissipate over time • Recurrent • Once depression
occurs, future episodes likely • Average number of episodes is 4 • Subclinical
depression • Sadness plus 3 other symptoms for 10 days • Significant
impairments in functioning even though full diagnostic criteria are not met
Five (or more) of the following symptoms have been present during the same 2-
week period and represent a change from previous functioning; at least one of
the symptoms is either (1) depressed mood or (2) loss of interest or pleasure
(DSM5-TR).
GENERAL SHEKret para bibo HAHHAHHAHHHAHHA

PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS
MEDICAL Pharmacologic Management

MANAGEMENT Antidepressants:
● cyclic antidepressants
● monoamine oxidase inhibitors (MAOIs)
● selective serotonin reuptake inhibitors (SSRIs) and
● atypical antidepressants
Medical Treatments
● Electroconvulsive Therapy
○ Psychiatrists may use electroconvulsive therapy (ECT) to treat
depression in select groups, such as clients who do not respond
to antidepressants or those who experience intolerable side
effects at therapeutic doses (particularly true for older adults).
○ Clients who are actively suicidal may be given ECT if there is
concern for their safety while waiting weeks for the full effects of
antidepressant medication.
○ ECT involves application of electrodes to the head of the client to
deliver an electrical impulse to the brain; this causes a seizure. It
is believed that the shock stimulates brain chemistry to correct the
chemical imbalance of depression.
○ Clients usually receive a series of six to 15 treatments scheduled
three times a week. Generally, a minimum of six treatments are
needed to see sustained improvement in depressive symptoms.
Maximum benefit is achieved in 12 to 15 treatments.
○ Preparation of a client for ECT is similar to preparation for any
outpatient minor surgical procedure: The client receives nothing
by mouth (is NPO) after midnight, removes any fingernail polish,
and voids just before the procedure. An intravenous line is started
for the administration of medication.
Psychotherapy
● A combination of psychotherapy and medications is considered the most
effective treatment for depressive disorders in both children and adults.
● Example:
○ Interpersonal therapy focuses on difficulties in relationships,
such as grief reactions, role disputes, and role transitions. For
example, a person who as a child never learned how to make and
trust a friend outside the family structure has difficulty establishing
friendships as an adult. Interpersonal therapy helps the person
find ways to accomplish this developmental task.
○ Behavior therapy seeks to increase the frequency of the client’s
positively reinforcing interactions with the environment and to
decrease negative interactions. It may also focus on improving
social skills.
○ Cognitive therapy focuses on how the person thinks about the
self, others, and the future and interprets his or her experiences.
This model focuses on the person’s distorted thinking, which, in
turn, influences feelings, behavior, and functional abilities.

MANAGEMENT -N/a

-n/a
NURSING ● Risk for suicide

MANAGEMENT (10) ● Create a safe environment for the client. Remove all potentially
harmful objects from client’s access (sharp objects, straps, belts,
ties, glass items).
○ Client safety is a nursing priority.
● Make rounds at frequent, irregular intervals (especially at night,
toward early morning, at change of shift, or other pre- dictably
busy times for staff).
○ Prevents staff surveillance from becoming predictable. To
be aware of a client's location is important, especially
when staff is busy, unavailable, or less observable.
● COMPLICATED GRIEVING
○ Develop a trusting relationship with the client. Show empathy,
concern, and unconditional positive regard. Be honest and keep
all promises.
■ Trust is the basis for a therapeutic relationship.
○ Teach the normal stages of grief and behaviors associated with
each stage. Help clients to understand that feelings such as guilt
and anger toward the lost entity are appropriate and acceptable
during the grief process and should be expressed rather than held
inside.
■ Knowledge of acceptability of the feelings associated
with normal grieving may help to relieve some of the guilt
that these responses generate.
● LOW SELF-ESTEEM
○ Help clients to recognize and focus on strengths and accom-
plishments. Minimize attention given to past (real or perceived)
failures.
■ Lack of attention may help to eliminate negative
ruminations.
○ Encourage participation in group activities from which clients may
receive positive feedback and support from peers.
● SOCIAL ISOLATION/IMPAIRED SOCIAL INTERACTION

○ Verbally acknowledge client's absence from any group activities.
■ Knowledge that his or her absence was noticed may
reinforce the client’s feelings of self-worth.
○ Provide positive reinforcement for client’s voluntary interactions
with others.
■ Positive reinforcement enhances self-esteem and
encourages repetition of desirable behaviors.
● POWERLESSNESS
○ Help the client set realistic goals.
■ Unrealistic goals set the client up for failure and reinforce
feelings of powerlessness.
○ Help the client identify areas of life situations that are not within
his or her ability to control. Encourage verbalization of feelings
related to this inability
■ in an effort to deal with unresolved issues and accept
what cannot be changed.
PRIORITY NURSING ● Risk for suicide

DIAGNOSIS (5) Grief; hopelessness; social isolation
History of prior suicide attempt
[Has a suicide plan and means to carry it out] Widowed or divorced
Chronic or terminal illness
Psychiatric illness or substance abuse
States desire to die
Threats of killing self
● COMPLICATED GRIEVING
[Real or perceived loss of any entity of value to the individual] [Bereavement
overload (cumulative grief from multiple unresolved
losses)]
[Thwarted grieving response to a loss]
[Absence of anticipatory grieving]
[Feelings of guilt generated by ambivalent relationship with the
lost entity]
● LOW SELF-ESTEEM
[Lack of positive feedback]
[Feelings of abandonment by significant other] [Numerous failures (learned
helplessness)] [Underdeveloped ego and punitive superego] [Impaired cognition
fostering negative view of self]
● SOCIAL ISOLATION/IMPAIRED SOCIAL INTERACTION
Developmental regression]
[Egocentric behaviors (which offend others and discourage
relationships)]
Disturbed thought processes [delusional thinking] [Fear of rejection or failure of
the interaction] [Impaired cognition fostering negative view of self] [Unresolved
grief]
Absence of significant others
● POWERLESSNESS
Lifestyle of helplessness] [Healthcare] environment [Complicated grieving
process] [Lack of positive feedback] [Consistent negative feedback]
PROGNOSIS
REFERENCES
4. Suicide
DEFINITION Suicide
● Act of intentionally ending one's own life
● A sin in many religions
● A crime in some jurisdictions
● Some cultures have viewed it as an honorable way to exit certain
shameful or hopeless situations
● Persons attempting or dying by suicide sometimes leave a suicide note
Suicidal ideation means thinking about killing oneself.

● Active suicidal ideation is when a person thinks about and seeks ways
to commit suicide. People with active suicidal ideation are considered
more potentially lethal.
● Passive suicidal ideation is when a person thinks about wanting to die
or wishes he or she were dead but has no plans to cause his or her
death.
Attempted suicide is a suicidal act that either failed or was incomplete.

In an incomplete suicide attempt, the per son did not finish the act because
1. someone recognized the suicide attempt as a cry for help and responded
or
2. the person was discovered and rescued
ANATOMY & Brain

PHYSIOLOGY (only ● Serotonin
for the major organ) ○ almost exclusively produced in neurons originating in the raphe
nuclei located in the midline of the brainstem
ETIOLOGY PREDISPOSING
● Women are four times more likely than men to attempt suicide
● Men are three times more likely than women to complete suicide
● Men, young women, whites are at increased risk for suicide.
● Over 45 years old
● In the most common pattern, the instability and risk of suicide reach a
peak during young adulthood and then gradually wane with advancing
age
PRECIPITATING
● Separated and divorced people are at increased risk for suicide.
● No religious affiliation
● Living alone
● Environmental factors that increase suicide risk include isolation, recent
loss, lack of social support, unemployment, critical life events, and
family history of depression or suicide.
● Chronic medical illnesses associated with increased risk for suicide
include cancer, HIV or AIDS, diabetes, cerebrovascular accidents, and
head and spinal cord injury.
● Clients with psychiatric disorders, especially major depressive
disorder, bipolar disorder, schizophrenia, substance abuse,
posttraumatic stress disorder, and borderline personality disorder, are at
increased risk for suicide
● A history of previous suicide attempts increases risk for suicide.
● Those with a relative who committed suicide are at increased risk for
suicide: the closer the relationship, the greater the risk.
SYMPTOMATOLOGY Risky Behaviors

(significant features/ ● Some suicidal people in treatment describe placing themselves in risky
manifestations) or dangerous situations such as speeding in a blinding rainstorm or
when intoxicated. This “Russian roulette” approach carries a high risk for
harm to clients and innocent bystanders alike. It allows clients to feel
brave by repeatedly confronting death and surviving.
● Increasing use of alcohol or drugs
Direct Verbal Clues

● I’m going to kill myself
● I wish i were dead
● You’d be better off without me
● I might as well be dead
● If … doesn’t happen, I’m going to end it
● I’m going to commit suicide
Change in affect
● Feeling trapped or hopeless about a situation
● Having mood swings, such as being emotionally high one day and deeply
discouraged the next
● Developing personality changes or being severely anxious or agitated,
particularly when experiencing some of the warning signs listed above
Change in behavior
● Changing normal routine, including eating or sleeping patterns
● Withdrawing from social contact and wanting to be left alone
● Getting the means to take your own life, such as buying a gun or
stockpiling pills
● Giving away belongings or getting affairs in order when there's no other
logical explanation for doing this
● Saying goodbye to people as if they won't be seen again
GENERAL Brain
PATHOPHYSIOLOGY ● Deficits in serotonergic neurotransmission in the brain stem or
(Simplified) serotonergic targets in the forebrain of suicidal individuals
● Serotonin (5-HT) deficits
● Low cerebral spinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA)
● Suicide attempters also exhibit a blunted release of prolactin in response
to administration of fenfluramine, a measure of 5-HT activity
● Influence decision-making and favour suicide.
Childhood adversity increases the risk of suicide

● According to Piaget, children between the ages of 2 and 7 years are in
the preoperational stage of development. They think of death as a
reversible phenomenon and feel that it must have a cause.
● Between the ages of 7 and 11, or during Piaget’s concrete operational
stage, children now understand that death is final and that it is universal.
They understand that a loved one will not return and therefore may
develop a deep sense of sadness and loss upon learning of someone’s
death. Additionally, they learn that all living things do eventually die. They
may inquire as to when their own passing will occur or when a loved one
will die. Nevertheless, they still view death as being caused by external
factors.
● Over the age of 11, children have the ability to understand that death is
intrinsic to life similar to the adult understanding of death. Children now
know death to be a final, universal and inevitable phenomenon. They see
it as inherent to existence and understand that it can be caused by
internal factors like illness.

DIAGNOSTIC TESTS
● Patient Health Questionnaire-9 (PHQ9).
○ This tool is made up of nine questions about suicidal thoughts
and behaviors.
● Ask Suicide-Screening Questions.
○ This includes four questions and is geared toward people aged
10-24.
● SAFE-T.
○ This is a test that focuses on five areas of suicide risk, as well as
suggested treatment options.
● The Columbia-Suicide Severity Rating Scale (C-SSRS).
○ This is a suicide risk assessment scale that measures four
different areas of suicide risk
MEDICAL
MANAGEMENT
● Novel antipsychotics
○ Clozapine
○ Olanzapine
○ Quetiapine
➢ Simultaneous modulation of multiple neurotransmitters (i.e.,
dopamine, norepinephrine, and serotonin), hormones (e.g.,
pregnenolone, cortisol), or intracellular systems (e.g. cyclic
adenosine monophosphate–dependent modulation of N-methyl-
D-aspartate (NMDA) receptor expression, brain-derived
neurotrophic factor upregulation, and regulation of the arachidonic
acid cascade)—mechanisms independent of that which provides
psychotic symptom relief.
● Lithium
➢ Lithium impacts inositol cycling and has some neuroprotective
potential, but it also displays a low therapeutic index.
➢ Doctors do know that lithium targets the central nervous system.
Lithium increases the amount of certain chemicals in your brain
which help to balance mood.
● Antidepressants
● Antiepileptic drugs
○ Levetiracetam
○ Lamotrigine
○ Topiramate

MANAGEMENT N/A

N/A
NURSING 1. Present an attitude that indicates unconditional positive regard not for the
MANAGEMENT (10) act but for the person and his or her desperation.
R: To convey the belief that the person can be helped and can grow and
change.
2. Assess the client with their current plan (specificity of their plan,
availability of means, lethality of method), patient’s previous history (prior
suicide attempts, family history of suicide behaviors), and resources
available.
R: To evaluate major predictors of suicidal behavior.
3. Assume an authoritative role to help clients stay safe by not allowing the
client to be alone in their room to think privately.
R: To let the client know their safety is the primary concern and takes
precedence over other needs or wishes and as this puts the client at
increased risk for suicide.
4. Deny the client’s access to materials on cleaning carts, their own

medications, sharp scissors, and penknives. Remove any item they can
use to commit suicide, such as sharp objects shoelaces, belts, lighters,
matches, pencils, pens, and even clothing with drawstrings.
R: To prevent the client from performing lethal activities while providing a
safe environment.
5. Render close patient supervision by sustaining observation or awareness

of the patient at all times.
R: To prevent suicide as this may be an impulsive act with little or no
warning.
6. Stay with the patient more often.

R: To provide the patient with a sense of security and strengthen self-
worth.
7. Present opportunities for the patient to express thoughts, and feelings in

a nonjudgmental environment.
R: To allow the patient to talk about suicidal thoughts and intentions to
harm themselves as expressing their thoughts and feelings may lessen
their intensity while allowing them to see that staff are open to
discussion.
8. Educate the patient in the appropriate use of medications to facilitate his
or her ability to cope.
R: To provide drug therapy which may benefit the patient endure
underlying health problems such as depression.
9. Contact family members, arrange for individual and/ or family crisis

counseling. Activate links to self-help groups.
R: To reestablishe social ties, diminish sense of isolation, and provide
contact from individuals who care about the suicidal person.
10. Educate the patient cognitive-behavioral self-management responses to

suicidal thoughts.
R: To allow the patient to learn how to identify negative thoughts and
develop positive approaches and positive thinking.
PRIORITY NURSING Risk for suicide R/T

DIAGNOSIS (5) ● Alcohol and substance abuse/use.
● Abuse in childhood.
● Family history of suicide.
● Fits demographic (children, adolescent, young adult male, elderly
male, Native American, Caucasian).
● Grief, bereavement/loss of an important relationship.
● History of prior suicide attempt.
● Hopelessness/helplessness.
● Legal or disciplinary problems.
● Physical illness, chronic pain, terminal illness.
● Psychiatric illness (e.g., bipolar disorder, depression,
schizophrenia).
● Poor support system, loneliness.
AEB
● Statements of despair, helplessness, hopelessness and nothing
left to live for.
● Suicide plan (clear and specific, lethal method and available
means).
● Suicide behavior (attempt, ideation, talk, plan, available means).
● Suicide cues
○ Covert: Making out a will, giving valuables away, writing
forlorn love notes, taking out large life insurance policy.
○ Overt: “No one will miss me”; “No reason to live for”; “I’d
be better off dead”.
Ineffective coping R/T

● Disturbance in pattern of tension release.
● Impulsive use of extreme solutions.
● Inadequate coping skills.
● Inadequate social support created by characteristics of
relationships.
● Inadequate resources available.
● Inadequate opportunity to prepare for a stressor.
● Personal loss or threat of rejection.
● Poorly developed social skills.
● Situational or maturational crises.
AEB
● Abuse of chemical agents.
● Change in usual communication pattern.
● Decreased use of social supports.
● Destructive behavior toward self or others.
● Expression of anxiety, depression, fear, impatience, frustration,
and/or discouragement.
● Inability to meet basic needs.
● Inability to meet role expectations.
● Inability to problem solve.
● Lack of goal-directed behavior.
● Poor problem solving.
● Use of forms of coping that might impede adaptive behavior.
● Verbalization of inability to cope or inability to ask for help.
Hopelessness R/T
● Abandonment.
● Chronic pain.
● Failing or deteriorating physiologic conditions (Cancer, AIDS).
● Long-term stress.
● Lost belief in transcendent values/God.
● Loss of significant support systems.
● Perceived hopelessness, helplessness.
● Perceiving the future as bleak and wasted.
● Prolonged isolation.
● Severe stressful events (financial reversals, relationship turmoil,
loss of job).
AEB
● Decreased affect.
● Decreased judgment.
● Decreased problem solving.
● Impaired decision making.
● Lack of initiative.
● Lack of involvement in care.
● Lack of motivation.
● Loss of interest in life.
● Passivity, decreased verbalization.
● Turning away from the speaker.
Total self-care deficit
PROGNOSIS A significant number of people who attempt suicide and survive eventually
die by their own hands, many within a year of the index attempt. A history of
multiple past attempts further increases risk of eventual suicide. Short-term
intensive treatment, often with psychiatric hospitalization, reduces immediate
risk, but the standard of care often requires more than just a few days of generic
inpatient care. Although for many patients, severe suicide risk is a relatively
transient condition, patients should not be discharged just because they say they
feel better or show superficial signs of lessened risk.
REFERENCES Videbeck, S. L. (2010). Psychiatric-mental health nursing. Lippincott Williams &

Wilkins.
5. Post Traumatic Stress Disorder
DEFINITION Occurs after experiencing a severe physically or psychologically traumatic event
ANATOMY & Hi meg hello

PHYSIOLOGY (only
for the major organ) Brain areas implicated in the stress response include the
● Amygdala
● Hippocampus
● Prefrontal cortex
Norepinephrine
● Norepinephrine is synthesized from dopamine by dopamine β-
hydroxylase. It is released from the adrenal medulla into the blood as a
hormone, and is also a neurotransmitter in the central nervous system
and sympathetic nervous system where it is released from noradrenergic
neurons.
● increases arousal and alertness
● promotes vigilance
● enhances formation and retrieval of memory
● focuses attention
● It also increases restlessness and anxiety.
ETIOLOGY ● Exposure to death, threatened death, serious injury or actual or

threatening sexual violence. Direct exposure (personally witnessed),
repeated exposure, or indirect exposure (i.e. first responders, child victim
advocates, law enforcement, etc.)
● Intrusion or persistently re-experienced stressors in at least one of the
following ways: recurrent memories, traumatic nightmares, flashbacks,
prolonged distress following traumatic reminders, significant physical
symptoms after exposure to stressors
● Avoidance of distressing trauma-related stressors after the event in at
least one way
● Negative alterations in mood and cognitions that began or got worse after
the initial event. Must include 2 of the following: Inability to recall key
features of the event, persistent or negative beliefs, persistent distorted
blame, persistent negative emotions, significant lack of interest, feeling of
alienation, inability to experience positive emotions
● Alterations in reactivity since the traumatic event. Must include 2 of the
following: aggressiveness, self-destructive behavior, hypervigilance,
exaggerated startle response, difficulty concentrating, sleep problems
● Duration of symptoms must be greater than one month
● Functional impairment from symptoms
● Attribution – not related to medication, substance use or other medical
illness
—--------------------------------------------------------------------------------------------------------
Risk and Prognostic Factors Risk (and protective) factors are generally divided
into pre traumatic, peritraumatic, and posttraumatic factors.
Pretraumatic factors
● Temperamental.
○ These include childhood emotional problems by age 6 years (e.g.,
prior traumatic exposure, externalizing or anxiety problems) and
prior mental disorders (e.g., panic disorder, depressive disorder,
PTSD, or obsessive-compulsive disorder [OCD]).
● Environmental.
○ These include lower socioeconomic status; lower education;
exposure to prior trauma (especially during childhood); childhood
adversity (e.g., economic deprivation, family dysfunction, parental
separation or death); cultural characteristics (e.g., fatalistic or self-
blaming coping strategies); lower intelligence; minority
racial/ethnic status; and a family psychiatric history. Social
support prior to event exposure is protective.
● Genetic and physiological.
○ These include female gender and younger age at the time of
trauma exposure (for adults). Certain genotypes may either be
protective or increase risk of PTSD after exposure to traumatic
events.
Peritraumatic factors
● Environmental.
○ These include severity (dose) of the trauma (the greater the
magnitude of trauma, the greater the likelihood of PTSD),
perceived life threat, personal injury, interpersonal violence
(particularly trauma perpetrated by a caregiver or involving a
witnessed threat to a caregiver in children), and, for military
personnel, being a perpetrator, witnessing atrocities, or killing the
enemy. Finally, dissociation that occurs during the trauma and
persists afterward is a risk factor.
Posttraumatic factors
● Temperamental.
○ These include negative appraisals, inappropriate coping
strategies, and development of acute stress disorder.
● Environmental.
○ These include subsequent exposure to repeated upsetting
reminders, subsequent adverse life events, and financial or other
trauma-related losses. Social support (including family stability,
for children) is a protective factor that moderates outcome after
trauma.
SYMPTOMATOLOGY ● Intrusive memories

(significant features/ ○ Unwanted painful recollections of the trauma
manifestations) ○ Having painful flashbacks
■ Recurrent nightmares
■ Lose touch with reality
■ Like actually happening
○ Going over what happened as though it were happening again
● Changes in physical and emotional reactions
○ Prone to being shocked or terrified
○ Always keeping an eye out for potential threats
○ Inability to fall asleep
○ Angry outbursts
○ Irritability
○ Aggressive conduct,
● Avoidance
○ Attempting to keep the terrible experience from coming to mind or
being spoken
○ Evading situations and places that bring up memories of the
traumatizing experience
● Unfavorable changes in thinking and mood
○ Self-doubt or dissatisfaction with own life or others
○ Memory issues, such as forgetting essential details of the
stressful experience
○ Trouble keeping close relationships
Patients with PTSD commonly suffer from different anxiety levels.

Mild anxiety
● minimal to complete absence of physiological symptoms
● The patient comes off as calm and composed but may also detail their
emotional states, such as nervousness or the feeling of having
“butterflies in the stomach .”
● The patient exhibits activeness with energetic facial expressions and
tone for moderate anxiety, with occasional feelings of tension.
● Vital signs
○ normal
○ may partially become elevated.
Severe anxiety
● increased autonomic nervous system function (e.g., increased vital
signs, frequent and urgent urination, diaphoresis, muscle tension, and
dry mouth
● The patient may suffer from chest pain and palpitations during this
stage due to agitation and irritability. He/she may report feelings of
being overwhelmed or overloaded.
Panic level of anxiety

● The patient’s external appearance and demeanor reflect this, such as
changes in behavior from combativeness to isolation and paleness.
● In this stage, the increase in the autonomic nervous system results in the
stimulation of the sympathetic neurotransmitter release.
GENERAL 1. Traumatic stressors such as early trauma can lead to posttraumatic

PATHOPHYSIOLOGY stress disorder (PTSD)
(Simplified) 2. Traumatic stress is associated with increased cortisol and
norepinephrine responses to subsequent stressors.
● Chronic high cortisol causes functional atrophy of the
hypothalamic-pituitary-adrenal axis (HPA), the hippocampus, the
amygdala, and the frontal lobe in the brain.
● Cortisol is generally elevated following trauma exposure (Kotozaki
and Kawashima, 2012).
3. Findings from animal studies have been extended to patients with post-
traumatic stress disorder (PTSD) showing smaller hippocampal and
anterior cingulate volumes, increased amygdala function, and
decreased medial prefrontal/anterior cingulate function.
4. Increases in the quantity or impact of noradrenergic signaling have been
implicated in the pathophysiology of posttraumatic stress disorder
(PTSD). This increased signaling may result from increased
norepinephrine (NE) release, from altered brain responses to NE, or from
a combination of both factors.
1. Studies using magnetic resonance imaging scans have shown that there
is decreased volume of the hippocampus, left amygdala, and
anterior cingulate cortex in patients with PTSD compared with matched
controls.
2. Other reports have demonstrated increased central norepinephrine
levels with down-regulated central adrenergic receptors, chronically
decreased glucocorticoid levels with up-regulation of their
receptors (possibly accounting for the anecdotal finding that there are
more autoimmune diseases in these patients), and hemispheric
lateralization in which there is a relative failure of left hemispheric
function (possibly accounting for confusion related to time sequence of
traumatic events)
3. Researchers suspect that genetics may contribute to an individual's
susceptibility to PTSD through an interaction with environmental
factors. Large-scale genetic studies show that PTSD is a highly
polygenic phenotype that is likely influenced by thousands of loci
across the genome. As an example of a potential gene-environment
interaction, the presence of one of four polymorphisms at the stress-
related gene FKBP5 was associated with an increased risk for PTSD in
patients with a history of child abuse, but not in patients without history of
child abuse.
4. Previous exposure to trauma appears to increase the risk of developing
PTSD with subsequent traumatic events.
5. The mechanism by which this "sensitization" occurs is unclear.

DIAGNOSTIC TESTS N/A
DIAGNOSTICS FINDINGS
● Medical history
○ This is to confirm or identify prior exposure to a traumatic
experience.
● Physiological evaluation
● Physical examination
● Make use of the criteria outlined in the Diagnostic and Statistical Manual
of Mental Disorders (DSM-5) issued by the American Psychiatric
Association.
● MRI
○ decreased volume of the hippocampus, left amygdala, and
anterior cingulate cortex
MEDICAL ● Psychotherapy (often known as "talk" therapy) such as:
MANAGEMENT ○ Cognitive therapy
■ for recognizing problematic cognitive patterns
○ Exposure therapy
■ helps the patient safely confront circumstances and
experiences to acquire appropriate coping
● Eye movement desensitization and reprocessing
PHARMACOLOGIC MANAGEMENT
● SSRI, selective, serotonin reuptake inhibitors and
● SNRI, serotonin norepinephrine reuptake inhibitors are antidepressants
that have proven to be effective for chronic management of symptoms.
○ Antidepressants have effect on the hippocampus that counteract
the effects of stress.

MANAGEMENT N/A

N/A
NURSING 1. Establish trust with the client. Listen to what the client is saying. Behave
MANAGEMENT (10) in a calm manner
R: Especially when a client has a high level of anxiety, establishing trust
can help the client calm down and make treatment more effective
2. Provide extra time for care and allow client extra time to respond to
questions
R: Clients often have difficulty communicating due to racing thoughts or
inability to concentrate. Avoid rushing the client and allow them more
time to answer or respond to promote security and instill a sense of
value.
3. Encourage client to express emotions in a safe environment
R: Allows the client the freedom to acknowledge their feelings and
release any repressed emotions that may be exacerbating their distress.
A safe environment should be free from actual or perceived judgment
and physical or perceived danger.
4. Encourage client to verbally identify current ineffective coping techniques
R: Helps the client understand their current behaviors that may be
preventing effective healing or treatment.
5. Encourage client to write about the traumatic event
R: Allows the provider to better understand the nature of the client’s
condition and anticipate triggers that may cause symptoms. Also allows
client and provider to periodically review evolution of emotions toward the
traumatic event
6. Encourage client to keep a journal of stressors and emotional reactions
to those stressors
R: Helps the client identify triggers that prompt anxiety or symptoms and
evaluate the outcomes of those reactions.
7. Teach visualization and relaxation techniques such as deep breathing
and imagery
R: Helps client learn to manage anxiety that accompanies flashbacks or
environmental stressors and triggers
8. Administer medications appropriately and monitor for side effects or
dependance
R: Selective serotonin reuptake inhibitors (SSRIs) and serotonin-
norepinephrine reuptake inhibitors (SNRIs) are antidepressants that have
proven to be effective for chronic management of symptoms.
9. Provide calming and reassuring environment
R: Clients with PTSD are often fearful. Providing a calm, relaxing
environment can help lessen or relieve anxiety and promote a feeling of
safety.
10. Facilitate access to community resources using Case Manager or Social
Worker
R: Support groups and other community resources such as service
animals, etc., can provide support that the client needs to function in their
daily lives.
PRIORITY NURSING 1. Fear related to perceived threat or danger, secondary to PTSD as

DIAGNOSIS (5) evidenced by verbalization of fearful feelings to a situation or condition,
agitation, alertness, tension, increased heart and respiratory rate.
2. Anxiety related to anticipation of harm, secondary to PTSD as evidenced
by increased blood pressure, heart rate, lack of self-control, irrational or
erratic behavior, and panic attacks.
3. Ineffective Coping related to a sudden change in status, secondary to
PTSD, as evidenced by the inability to cope with reality, incapacity to
perform day-to-day tasks, exhaustion, and self-destructive habits, such
as binge drinking or use of drugs.
4. Insomnia related to difficulty maintaining normal sleep, secondary to
PTSD as evidenced by sleep deprivation, general exhaustion, weakness,
difficulty focusing and recalling information.
5. Hopelessness related to the inability to control the situation, secondary
to PTSD as evidenced by decreased appetite, decreased reactivity to
stimuli, a lack of drive, inability to take the initiative, and lack of
participation in the treatment or care.
PROGNOSIS Without treatment, PTSD can get worse over time. But treatment can help, even
if the traumatic event was many years ago. For some people, treatment can cure
PTSD. For others, it can make symptoms less intense .
REFERENCES
6. General Anxiety Disorder
DEFINITION General Anxiety Disorder
● Persistent and excessive anxiety and worry about various domains,
552 - Varca including work and school performance, that the individual finds difficult
to control
1071 - Kozier ● Experiences physical symptoms (restlessness, feeling keyed up or on
edge, being easily fatigued, difficulty concentrating or mind going blank,
irritability, muscle tension, and sleep disturbance)
● Harrison’s definition: Patients with GAD worry excessively over minor
matters, with life-disrupting effects
----------------------------------------------------------------------------------------------------------
Levels of Anxiety
Mild
● Heightened Perceptual Field
● Focus is flexible & aware of the anxiety
● Physical symptoms may include slight discomfort, restlessness,
irritability, or mild tension-relieving behaviors (e.g., nail biting, foot or
finger tapping, fidgeting).
Moderate
● Narrowed Perceptual Field
● Focuses on the source of anxiety; Less able to pay attention
● The individual may experience tension, pounding heart, increased pulse
and respiratory rate, perspiration, and mild somatic symptoms (e.g.,
gastric discomfort, headache, urinary urgency).
● Voice tremors and shaking may be noticed.
Severe
● Greatly reduced & Distorted Perceptual Field
● Focuses on details or one specific detail; Attention is scattered
● May experience hyperventilation/ sense of impending doom. Trembling
and a pounding heart
Panic
● Unable to attend to the environment
● Focus is lost
● Physical behaviors are erratic, uncoordinated, and impulsive
● The behavior that results may be manifested as pacing, running,
shouting, screaming, or withdrawal.
—-----------------------------------------------------------------------------------------------------
Videbeck’s Levels of Anxiety
Mild Anxiety
● sensation that something is different and warrants special attention
● Often motivates people to make changes or engages in goal-directed
activity
Moderate Anxiety
● disturbing feeling that something is definitely wrong; the person becomes
nervous or agitated.
● has difficulty concentrating independently but can be redirected to the
topic
Severe Anxiety
● more primitive survival skills take over, defensive responses ensue, and
cognitive skills decrease significantly
● Trouble thinking and reasoning
Panic
● emotional–psychomotor realm predominates with accompanying fight,
flight, or freeze responses
● Greatly increase in VS
● cognitive process focuses on the person’s defense
Levels Psychological Responses Physiological Responses
Mild Wide perceptual field Restlessness

Sharpened senses Fidgeting
Increased motivation GI “butterflies”
Effective problem-solving Difficulty sleeping
Increased learning ability Hypersensitivity to noise
Irritability
Moderate Perceptual field narrowed Muscle tension

to immediate task Diaphoresis
Selectively attentive Pounding pulse
Cannot connect thoughts Headache
or events independently Dry mouth
Increased use of High voice pitch
automatisms Faster rate of speech
GI upset
Frequent urination
Severe Perceptual field reduced to Severe headache

one detail or scattered Nausea, vomiting, and diarrhea
details Trembling
Cannot complete tasks Rigid stance
Cannot solve problems or Vertigo
learn effectively Pale
Behavior geared toward Tachycardia
anxiety relief and is Chest pain
usually ineffective
Doesn’t respond to
redirection
Feels awe, dread, or
horror
Cries
Ritualistic behavior
Panic Perceptual field reduced to May bolt and run or totally

focus on self immobile
Cannot process any and mute
environmental stimuli Dilated pupils
Distorted perceptions Increased blood pressure and
Loss of rational thought pulse
Doesn’t recognize Flight, fight, or freeze
potential danger
Can’t communicate
verbally
Possible delusions and
hallucination
May be suicidal
ANATOMY & Autonomic Nervous system - controls body activities automatically; innervates
PHYSIOLOGY (only cardiac muscle, smooth muscle, and glands; also called involuntary nervous
for the major organ) system.
● Sympathetic nervous system: mobilizes the body during extreme
situations; fight-or-flight division
https://www.ncbi.nlm.ni ○ includes adrenergic fibers that release norepinephrine
h.gov/pmc/articles/PMC ○ Increases HR, BP, dilates bronchioles
3684250/ ● Parasympathetic: allows us to “unwind” and conserve energy; Rest-and-
digest system
https://ppp.mhmedical.c Frontal Lobe: regulate impulses, emotions, and behavior

om/content.aspx?booki ● dorsal anterior cingulate cortex (dACC) - amplifies fearful signal coming
d=1793&sectionid=120 from the amygdala
647276 ● ventromedial prefrontal cortex - dampen signals coming from the
amygdala
https://www.ncbi.nlm.ni ● In Anxiety
h.gov/books/NBK44187 ○ GAD is caused by reduced communications between different
0/ parts of the brain, specifically the amygdala, which is responsible
for our "fight or flight" feelings, and the anterior cingulate cortex
https://www.youtube.co (ACC), the part of the brain that controls emotional response.
m/watch?v=gmwiJ6ghL ○ Implications and suggestions show that it results in the brain's
IM “anxiety button” remaining switched on rather than turning off
○ Furthermore, anxiety was associated with a negative connectivity
https://doctorlib.info/the between amygdala and ventral medial prefrontal cortex (mPFC),
rapy/pharmacotherapy- suggesting disrupted emotion regulation.
principles-
practice/43.html Region: Diencephalon
● Thalamus - where sensory data
from environmental threats are
https://anxietynetwork.c first processed
om/reduced-brain- ● Hypothalamus - part of the
connections limbic system
● Limbic System: a collection of
https://bmcpsychiatry.bi emotional-processing brain
omedcentral.com/articl structures
es/10.1186/s12888- ● Hypothalamus - most
016-0904-8 basic function is to
maintain homeostasis;
has a role in controlling the body’s response to stress & regulating
behavior
● Hippocampus - major role in learning and memory. It is the part
that encodes threatening events into memory.
○ Emotional learning (learning the value of stimuli or
contexts) is central to the causative mechanisms of
anxiety disorders.
● Cingulate Gyrus - believed to be helpful in regulating
emotions, behavior, and pain, responsible for controlling
autonomic motor function;
● Amygdala - regulate emotions, such as fear, anxiety, and
aggression; also involved in tying emotional meaning to
memories;
○ Patients w/ anxiety disorders show heightened amygadala
response
Region: Brain Stem - Reticular Activating System (RAS)

● Helps the amygdala regulate arousal, vigilance, and fear
● The connection is mediated by Serotonin and Norephinephrine
○ Locus Coeruleus or LC (in the pons) - contains noradrenergic
cells that produces norephinephrine
➢ Increase activity in this area is associated with increase in
arousal, anxiety, and panic
○ Raphe nuclei (throughout the brain stem)- produces serotonin
➢ Activity of serotonin cells inhibits firing of noradrenergic
cells in the LC
● Theory: Elevated noradrenergic system activity and low serotonin
system activity are responsible for the development of anxiety
Neurotransmitters
Norepinephrine
● Source: Brain Stem, Hypothalamus
● Neurotransmitter that excites cellular function
Gamma-aminobutyric acid (GABA) - amino acid neurotransmitter

● Source: Spinal cord, cerebellum, basal ganglia
● Inhibitory neurotransmitter
● Functions as the body’s natural antianxiety agent by reducing cell
excitability, thus decreasing the rate of neuronal firing
● Found in ⅓ of the nerve synapses, especially those in the limbic system
& locus coeruleus
● Increased by norepinephrine
Serotonin
● Source: Brain stem, hypothalamus, dorsal horn of the spinal cord
● An indolamine neurotransmitter
● Has Many subtypes
○ 5-Hydroxytryptamine type 1a plays a role in anxiety, and affects
aggression and mood
------------------------------------------------------------------------------------------------------
SIMPLER VERSION FROM NURSING BOOK (HALTER/VARCAROLIS)
An imbalance of certain neurotransmitters are thought to disrupt specific brain
regions that contribute to various anxiety disorders
Frontal Cortex: cognitive interpretations (e.g. potential threat)
Hypothalamus: activation of stress response (fight-or-flight response)
Hippocampus: associated with memory r/t fear responses
Amygdala: regulate emotions, such as fear, anxiety, and aggression;
Serotonin
● Helps regulate mood, sleep, sexual desire, appetitie, and inhibits pain
● Anxiety disorders: Reduced levels of serotonin transmission.
● Low levels of serotonin believed to play a role in anxiety disorders &
depression
Gamma-aminobutyric acid (GABA)

● Slows neuron activity which plays a role in lowering anxiety and also
affects memory
Norepinephrine:
● Plays a role in sensitization, fear conditioning, stress response
● Excessive and unregulated norepinephrine thought to be r/t to anxiety
disorders

● Sex: Women are twice as likely to be diagnosed with GAD, though
difference may be the result of the underdiagnosis of men
Fryers T, Brugha T. ● Family History: Studies have shown that first degree relatives of
Childhood determinants someone with GAD are more likely to develop mood and anxiety
of adult psychiatric disorders in general, with a specific increased risk for developing GAD. A
disorder. Clin Pract person can have a genetic vulnerability to developing GAD if certain
Epidemiol Ment Health. genetic markers have been passed onto them. (RBFOX1 gene)
2013;9:1-50. ● Race: Individuals of European descent tend to experience generalized
doi:10.2174/174501790 anxiety disorder more frequently than do individuals of non-European
1309010001 descent (i.e., Asian, African, Native American and Pacific Islander).
● Substance abuse: Smoking, alcohol, and drug use can increase the risk
of GAD. Using everyday addictive substances like caffeine can heighten
feelings of worry or nervousness, contributing to the development of
anxiety.
● Societal Factors: Researchers are finding that the use of social media,
particularly in excess, can greatly impact mental health, sometimes
resulting in anxiety
● Environmental Factors: childhood adversities or trauma. Mental health
researchers have found that trauma in childhood can increase a person's
risk of developing GAD. Difficult experiences such as physical and
mental abuse, neglect, the death of a loved one, abandonment, divorce,
or isolation can all be contributing factors.
Accdg to DSM 5
Temperamental. Behavioral inhibition, negative affectivity (neuroticism), and

harm avoidance
Environmental. TL/DR: None. Although childhood adversities and parental

overprotection have been associated with GAD, no environmental factors haave
been identified as specific to generalized anxiety disorder or necessary or
sufficient for making the diagnosis.
Genetic and psychological. ⅓ of the risk of experiencing GAD is genetic, and

these genetic factors overlap with the risk of neuroticism and are shared with
other anxiety and mood disorders, particularly major depressive disorder.
------------------------------------------------------------------------------------------------------
Age. Median age at onset for GAD is 30 years old.
SYMPTOMATOLOGY 1. Restlessness or feeling keyed up or on edge

(significant features/ 2. Being easily fatigued
manifestations) 3. Difficulty concentrating or mind going blank
4. Irritability
5. Muscle tension
6. Sleep disturbance (difficulty falling or staying asleep, or restless,
unsatisfying sleep)
GENERAL
PATHOPHYSIOLOGY POTANGINA SEND HELP PLEASE
(Simplified)
1. Predisposing and Precipitating factors
2. Hippocampus and cingulate gyrus abnormally process threat
3. Increase in cortisol release and epinephrine release
4. Stress hormones interact with brain and body
5. ANXIETY DISORDER

DIAGNOSTIC TESTS
To rule out organic causes:
1. Thyroid function tests
● Hyperthyroidism
2. Blood glucose level
● DM can cause fatigue(?)
3. Echocardiography
● MI
4. Toxicology Screen
● Substance abuse
Diagnostic Criteria
A. Excessive anxiety & worry, occurring more days than not for at least 6
months, about a number of events or activities (such as work or school
performance)
B. The individual finds it difficult to control the worry
C. The anxiety and worry are associated with three (or more) of the
following six symptoms (with at least some symptoms having been
present for more days than not for the past 6 months).
Note: Only one item is required in children
1. Restlessness or feeling keyed up or on edge
2. Being easily fatigued
3. Difficulty concentrating or mind going blank
4. Irritability
5. Muscle tension
6. Sleep disturbance (difficulty falling or staying asleep, or
restless, unsatisfying sleep)
D. The anxiety, worry, or physical symptoms cause clinically significant
distress or impairment in social, occupational, or other important areas of
functioning
E. The disturbance is not attributable to the physiological effects of a
substance (e.g. drug of abuse, medication) or another medication (e.g.,
hyperthyroidism)
F. The disturbance is not better explained by another mental disorder (e.g.,
anxiety or worry about having panic attacks in panic disorder, negative
evaluation in social anxiety disorder [social phobia], contamination or
other obsessions in obsessive-compulsive disorder, separation from
attachment figures in separation anxiety disorder, reminders of traumatic
events in posttraumatic stress disorder, gaining weight in anorexia
nervosa, physical complaints in somatic symptom disorder, perceived
appearance flaws in body dysmorphic disorder, having a serious illness
in illness anxiety disorder, or the content of delusional beliefs in
schizophrenia or delusional disorder).
Other Diagnostic Features

1. Excessive anxiety and worry (apprehensive expectation) about a number
of events or activities
2. Finds it difficult to control the worry and to keep worrisome thoughts from
interfering with attention to tasks at hand
3. Adults often worry about everyday, routine life circumstances, such as
possible job responsibilities, health and finances, the health of family
members, misfortune to their children, or minor matters (e.g., doing
household chores or being late for appointments)
4. Children tend to worry excessively about their competence or the quality
of their performance
5. Focus of worry may shift from one concern to another
Associated Features Supporting Diagnosis

1. Assoc w/ Muscle tension there may be trembling, twitching, feeling
shaky, and muscle aches or soreness
2. Somatic symptoms (e.g., sweating, nausea, diarrhea) & exaggerated
startle response
3. Autonomic hyperarousal (e.g., accelerated heart rate, SOB, dizziness)
are less prominent in GAD than in other anxiety disorder (i.e. panic
disorder)
4. Conditions assoc w/ stress (e.g., irritable bowel syndrome, headaches)
MEDICAL Psychotherapy
MANAGEMENT
Cognitive-behavioral Therapy (CBT) - techniques useful in changing patterns
533 of thinking by helping clients to recognize negative thoughts and to replace them
with different patterns of thinking
https://www.verywell ● Positive self-talk - client changes thinking about the self from negative
mind.com/what-is- to positive
thought-stopping- ● Decatastrophizing - involves the therapist’s use of questions to more
and-how-does-it- realistically appraise the situation; To view life events more realistically
work-2584122 and not as catastrophes
○ Therapist: ““What is the worst thing that could happen? Is that
likely? Could you survive that? Is that as bad as you imagine?”
https://www.aafp.org/ ● Positive reframing - turning negative messages into positive messages
afp/2015/0501/p617.ht ○ Negative: My heart is pounding. I think I’m going to die
ml#sec-4 ○ Positive: I can stand this. This is just anxiety. It will go away
● Thought Stopping - client stops negative thought patterns; to alter the
process of negative or self-critical thought patterns
○ Splashing the face with cold water
○ snapping a rubber band worn on the wrist
○ firmly saying, “Stop!” either out loud or in your head
Agents Examples How it Works
SSRIs Paroxetine (Paxil) Regulate the serotonin

levels in the brain & help
elevate mood
Benzodiazepines Diazepam (Valium) Binds to benzodiazepine

receipts, facilitates action of
GABA, slowing neural
transmission thus lowering
anxiety
Nonbenzodiazepine Buspirone (Buspar) Treat the worry associated
anxiolytic with GAD rather than the
muscle tension.
Functions as a serotonin
receptorl partial agonist
resulting in anxiolytic
Noradrenergic Drugs Propanolol (Inderal) Blocks adrenergic receptor;

Reduces physical signs of
anxiety (e.g. decreases HR
and BP)

MANAGEMENT N/A

N/A
NURSING 1. Remain with the client at all times when levels of anxiety are high
MANAGEMENT (10) a. The client’s safety is a priority. A highly anxious client should not
be left alone; his or her anxiety will escalate. Conveys acceptance
Videbeck - 527 and ability to give help
2. Move the client to a quiet area with minimal or decreased stimuli
Halter - 564 such as a small room or seclusion area
a. Anxious behavior can be escalated by external stimuli. In a large
area, the client can feel lost and panicky, but a smaller room can
enhance a sense of security.
3. Remain calm in your approach to the client.
a. The client will feel more secure if you are calm and if the client
feels you are in control of the situation.
4. Encourage the patient to talk about his/feeling and concerns
a. When concerns are stated aloud, problems can be discussed and
feelings of isolation decreased
5. Use short, simple, and clear statements.
a. The client’s ability to deal with abstractions or complexity is
impaired. Promotes comprehension
6. Assure client that you are in control and can assist him or her
a. Counters feeling of loss of control that accompanies severe
anxiety
7. Give brief directions
a. Reduces indecision. Conveys belief that patient can respond in a
healthy manner
8. Encourage patient to discuss preceding events
a. Promotes future change through identification of stressors
9. Identify what has provided relief in the past
a. Provides awareness of self as individual with some ability to cope
10. Encourage the client’s participation in relaxation exercises such as
deep breathing, progressive muscle relaxation, meditation, and
imagining being in a quiet, peaceful place.
a. Relaxation exercises are effective, nonchemical ways to reduce
anxiety.
11. Encourage the client to identify and pursue relationships, personal
interests, hobbies, or recreational activities that may appeal to the
client
a. The client’s anxiety may have prevented him or her from
engaging in relationships or activities recently, but these can be
helpful in building confidence and having a focus on something
other than anxiety.
12. Provide outlets for working off excess energy (e.g., walking, playing
ping-pong, dancing, exercising)
a. Physical activity can provide relief of built-up tension, increase
muscle tone, and increase endorphin levels.
PRIORITY NURSING 1. Anxiety

DIAGNOSIS (5) ➢ r/t situational event or psychological stress
➢ r/t perception of a severe threat
Swearingen - 702 ➢ Unconscious conflict about essential values and goals of life
2. Ineffective coping
➢ r/t persistent anxiety, fatigue, difficulty concentrating
➢ r/t situational/maturational crisis
3. Powerlessness
➢ r/t fear of disapproval from others
4. Social Isolation
➢ r/t repressed fears
5. Self-care deficit
➢ r/t disabling anxiety
Other Diagnosis
6. Chronic Low self-esteem
7. Deficient Knowledge
➢ r/t unfamiliarity with the prescribed medications and therapy
sessions
8. Risk for Suicide
9. Impaired Sleeping pattern
10. Fatigue
11. Hopelessness
PROGNOSIS The prognosis for patients with generalized anxiety disorder is guarded. Many
https://www.ncbi.nlm. patients are not compliant with medications because of cost and adverse effects.
nih.gov/books/NBK44 Relapses are common, and patients often search for physicians who comply
1870/ with their needs. Because of the lack of conventional medicine to cure the
disorder, many opt for alternative therapies without much success. Overall, the
quality of life of these patients is poor.
WTF IS A GUARDED PROGNOSIS

-------------------------------------------------------------------------------------------------------
Simplified
● recurrence is common
● patients with anxiety disorders are more likely to develop a medical
illness like CAD, stroke, DM, HTN
OTHER NOTES Fear

● Feeling afraid or threatened by a clearly identifiable external stimulus that
represents danger to the person
Anxiety
● the anticipation of future threat
● Associated with muscle tension & vigilance in preparation for future
danger and cautious or avoidant behaviors
● Vague feeling of dread or apprehension; it is a response to external or
internal stimuli that can have behavioral, emotional, cognitive, and
physical symptoms.
● normal when it is appropriate to the situation and dissipates when the
situation has been resolved
Anxiety disorder
● Excessive or persisting beyond developmentally appropriate periods
● Persistent (lasting 6 months or more)
Generalized anxiety disorder VS Nonpathological anxiety

1. GAD are excessive and typically interfere w/ psychosocial functioning;
While worries of everyday life are not excessive & are perceived as more
manageable and may be put off when more pressing matters arise
2. GAD: Worries are more pervasive, pronounced, and distressing; have
longer duration; and frequently occur without precipitants
3. GAD: people with this report subjective distress due to constant worry
and related impairment in social, occupational, or other important areas
of functioning
Frontal Cortex
● Prefrontal Cortex (PFC) - responsible for executive functions such as
planning, decision making, predicting consequences for potential
behaviors, and understanding & moderating social behavior
● Orbitofrontal cortex (OFC) - codes information, controls impulses, and
regulates mood.
● Ventromedial PFC - is involved in reward processing and visceral
response to emotions
● Summary: This frontal cortical regions regulate impulses, emotions, and
behavior
Temperament refers to the biologic processes of sensation, association, and

motivation that underlie the integration of skills and habits based on emotion
1. Harm Avoidance
○ High - exhibit fear of uncertainty, social inhibition, shyness with
strangers, rapid fatigability, and pessimistic worry in anticipation
of problems
■ May result in excessive anxiety
○ Low - carefree, energetic, outgoing, and optimistic
2. Novelty Seeking
○ High - quick tempered, curious, easily bored, impulsive,
extravagant, and disorderly
○ Low - slow-tempered, stoic, reflective, frugal, reserved, orderly,
and tolerant of monotony; he or she may adhere to a routine of
activities.
3. Reward Dependence: defines how a person responds to social cues.
○ High - tenderhearted, sensitive, sociable, and socially dependent
○ Low - practical, toughminded, cold, socially insensitive, irresolute,
and indifferent to being alone. Social withdrawal, detachment,
aloofness, and disinterest in others can result.
4. Persistence
○ High - hardworking and ambitious overachievers who respond to
fatigue or frustration as a personal challenge
○ Low - inactive, indolent, unstable, and erratic. They tend to give
up easily when frustrated and rarely strive for higher
accomplishments.
● Each of these four genetically trait affects a person’s automatic
responses to certain situations. These responses patterns are ingrained
by 2 to 3 years of age
Behavioral Inhibition - Behavioral inhibition is a personality type that shows a

tendency toward distress and nervousness in new situations. Behavioral
inhibition in children includes shyness around unfamiliar people and withdrawal
from new places.
Neuroticism is the trait disposition to experience negative affects, including

anger, anxiety, self‐consciousness, irritability, emotional instability, and
depression
REFERENCES DSM 5 - p. 222

Videbeck
● Anxiety and Anxiety Disorder (516)
Harrison - 3263
7. Autism Spectrum Disorder
DEFINITION Autism spectrum disorder (ASD) is a complex neurobehavioral and developmental
disorder characterized by deficits in three domains: impaired social interaction;
impaired communication; and restricted, stereotypical behavioral patterns.
Note: The term “spectrum” is used because patients can have a wide range of
symptoms that begin in early childhood and may last through adulthood.
ANATOMY &
PHYSIOLOGY (only
for the major organ)
1. Physiological
a) Genetics:
® 1 child with ASD has > risk for having more than one child with
the disorder
® both monozygotic and dizygotic twins have also provided
evidence of a genetic involvement
b) Neurological: Abnormalities in brain structures or functions have

been correlated with ASD.
® Total brain volume, the size of the amygdala, and the size of
the striatum have all been identified as enlarged in about 9%
to16% of children <4y/o with ASD.
® Certain developmental problems (postnatal neurological
infections, congenital rubella, phenylketonuria, and fragile X
syndrome) also have been implicated.
c) Gender
® More prevalent in girls
2. Environmental
The DSM-5 reports that “a variety of nonspecific risk factors, such as advanced
parental age, low birth weight, or fetal exposure to valproate, may contribute
to risk of ASD”
SYMPTOMATOLOGY 1. Failure to form interpersonal relationships.

(significant features/ ● unresponsiveness to people, lack of eye contact and facial
manifestations) responsiveness, indifference or aversion to affection and physical
contact.
● In early childhood, there is a failure to develop cooperative play and
friendships.
2. Impairment in communication and imaginative activity.

● Language may be totally absent or immature grammatical
structure, incorrect use of words, echolalia, or inability to use
abstract terms. Accompanying nonverbal expressions may be
inappropriate or absent.
3. Bizarre responses to the environment.

● resistance or extreme behavioral reactions to minor occurrences;
abnormal, obsessive attachment to peculiar objects; ritualistic
behaviors.
4. Extreme fascination for objects that move (e.g., fans, trains).

● Special interest in music, playing with water, buttons, or parts of
the body.
5. Unreasonable insistence on following routines in precise detail

● e.g., insisting that exactly the same route always be followed when
shopping
6. Marked distress over changes in trivial aspects of environment

● e.g., when a vase is moved from its usual position
7. Stereotyped body movements

● e.g., hand flicking or clapping, rocking, or whole-body swaying
8. Behaviors that are self-injurious.
● head banging or biting the hands or arms, may be evident .
GENERAL Shet a u q na sa werld gowdnayt

PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS
● There are no reliable biomarkers or specific diagnostic tests for ASD;

therefore, the diagnosis must be made based on the person's behavior.
● usually identified by 18 months and no later than 3 years of age
MEDICAL NO CURE for ASD. Treatment can be effective in managing symptoms,

MANAGEMENT including difficulty communicating with others and repetitive behaviors.
1. Comprehensive and individualized treatment (SPED and language

therapy)
2. Cognitive behavioral therapy (for anxiety and agitation)
3. Pharmacologic
○ antipsychotics (haloperidol - Haldol)
○ combined antipsychotics (for tantrums, stereotyped behaviors)
○ naltrexone (ReVia), clomipramine (Anafranil), clonidine
(Catapres), and stimulants to diminish self-injury and hyperactive
behaviors

MANAGEMENT N/A

N/A
NURSING Risk for self-mutilation r/t hysterical reactions to changes in the environment
MANAGEMENT (10)
® Prepare helmet, hand mitts, and appropriate padding.
R: A helmet may be used to protect against head banging, hand mitts to
prevent hair pulling, and appropriate padding to protect extremities from
injury during hysterical movements.
® Offer self to child during times of increasing anxiety

R: To decrease need for self-mutilative behaviors and provide feelings of
security
Impaired social interaction r/t neurological alterations or unfulfilled trust vs.

mistrust
® Ensure that warmth, acceptance, and availability are conveyed, along
with consistency in terms of presence.
R: Warmth, acceptance, and availability, along with consistency of staff
assignment, enhance the establishment and maintenance of a trusting
relationship.
® Provide child with familiar objects (favorite toys, blanket).

R: These items will offer security during times when the child feels
distressed. Go slowly. Do not force interactions. Begin with positive
reinforcement for eye contact.
Impaired verbal communication r/t withdrawal into self or inability to trust

® Use the techniques of consensual validation and seeking clarification
to decode communication patterns. (Examples: “I think you must have
meant ...” or “Did you mean to say that ... ?”
R: These techniques work to verify the accuracy of the message received
or to clarify any hidden meanings within the message. Take caution not to
“put words into the client’s mouth.”
® Give positive reinforcement when eye contact is used to convey

nonverbal expressions.
R: Positive reinforcement increases self-esteem and encourages
repetition of the behavior.
Disturbed personal identity r/t neurological alteration or unfulfilled trust vs.

mistrust
® Assist child to recognize separateness during self-care activities,
such as dressing and feeding.
R: These activities increase child’s awareness of self as separate from
others.
® Point out and assist child in naming own body parts.

R: This activity may increase the child’s awareness of self as separate
from others.
Risk for injury r/t hysterical reactions

® Place infants or toddlers in the crib, raise rails on the bed. Remove
objects in the room that may cause injury in case of hyperactivity or
anxiety.
R: To ensure safety and avoid injury. Many children with ASD also have
seizure disorders while objects littering around
® Try to determine why self-mutilative behaviors occur.

R: Injury from mutilative behaviors may be averted if the cause can be
determined.
PRIORITY NURSING 1. Risk for self-mutilation r/t hysterical reactions to changes In the environment
DIAGNOSIS (5) 2. Impaired social interaction r/t neurological alterations or unfulfilled trust vs.
mistrust
3. Impaired verbal communication r/t withdrawal into self or inability to trust
4. Disturbed personal identity r/t neurological alteration or unfulfilled trust vs.
mistrust
5. Risk for injury r/t hysterical reactions
PROGNOSIS Current research estimates that 20% of adults with ASD achieve most
independent living outcomes, while 46% require substantial levels of support in
most independent living outcomes (Farley et al., 2018).
If behavior deteriorates in adolescence, it may reflect the effects of hormonal

changes or the difficulty meeting increasingly complex social demands.
REFERENCES
8. Personality Disorders
DEFINITION General: A group of disorders characterized by rigid, maladaptive traits that
cause great distress or an inability to get along with others
CLUSTER A CLUSTER B CLUSTER C

Odd & Eccentric Dramatic & Erratic Anxious & Fearful
● PARANOID: a ● ANTISOCIAL: a ● AVOIDANT: a

pattern of distrust pattern of pattern of social
and disregard for, inhibition,
suspiciousness and violation of, feelings of
such that others' the rights of inadequacy, and
motives are others hypersensitivity
interpreted as ● BORDERLINE: to negative
malevolent. a pattern of evaluation
● SCHIZOID: a instability in ● DEPENDENT: a
pattern of interpersonal pattern of
detachment from relationships, submissive and
social self-image, and clinging behavior
relationships and affects, and related to an
a restricted range marked excessive need
of emotional impulsivity to be taken care
expression. ● HISTRIONIC: a of
● SCHIZOTYPAL: pattern of ● OBSESSIVE-
a pattern of acute excessive COMPULSIVE:
discomfort in emotionality and a pattern of
close attention-seeking preoccupation
relationships, ● NARCISSISTIC: with orderliness,
cognitive or a pattern of perfectionism,
perceptual grandiosity, need and control
distortions, and for admiration,
eccentricities of and lack of
behavior. empathy
ANATOMY &
PHYSIOLOGY (only
Brain
● Interprets information
● Regulates all organs
● Controls body movement
● Regulates thinking, memory & speech
Cerebral Cortex: outer gray layer of the brain which contains neurons (grey
matter) and is divided into four lobes
1. Frontal lobe
➢ Personality, behavior, emotions
➢ Judgment, planning, problem solving
➢ Speech: speaking and writing (Broca’s area)
➢ Body movement (motor strip)
➢ Intelligence, concentration, self awareness
2. Parietal lobe
➢ Interprets language, words
➢ Sense of touch, pain, temperature (sensory strip)
➢ Interprets signals from vision, hearing, motor, sensory and
memory
➢ Spatial and visual perception
3. Occipital lobe
➢ Interprets vision (color, light, movement)
4. Temporal lobe
➢ Understanding language (Wernicke’s area)
➢ Memory
➢ Hearing
➢ Sequencing and organization
Limbic system: a collection of structures involved in processing emotion and

memory; located within the cerebrum of the brain, immediately below the temporal
lobes
Substructures of the Limbic

System:
➢ Hippocampus- located
in the medial temporal
lobe and connected
with the amygdala that
controls emotional
memory recalling and
regulation
➢ Amygdala- regulate
emotions, such as fear and aggression; also involved in tying
emotional meaning to memories; reward processing, &
decision-making.
➢ Cingulate Gyrus- believed to be helpful in regulating emotions,
behavior, and pain, responsible for controlling autonomic motor
function; involved in fear and the prediction and avoidance of
negative stimuli, through monitoring the body’s response to
unpleasant experiences
➢ Hypothalamus- most basic function is to maintain homeostasis;
has a role in controlling the body’s response to stress &
regulating behavior
➢ Basal Ganglia- situated at the base of the forebrain and top of the
midbrain; involved in cognitive and emotional behaviors, and
with having a role in rewards and reinforcements. Because of
this, it can be linked with addictive behaviors and the formation of
habits.
● Genetics - linked to a family history of mental illness; Note: the tendency to

develop a personality disorder might be inherited, not the disorder itself.
● Gender - Most personality disorders affect more men
According to Statistics:
CLUSTER A CLUSTER B CLUSTER C

● Paranoid: M>F ● Antisocial: M>F ● Avoidant: M>F
● Schizoid: M>F ● Borderline: F>M ● Dependent: F=M
● Schizotypal: M>F ● Histrionic: F=M ● Obsessive -
● Narcissistic: M>F Compulsive: M>F
PRECIPITATING
● Childhood experiences (parental rewarding of temper tantrums, rigid
upbringing, parental fostering of dependency)
● Increased stress or external pressures (e.g., caused by work, family,
or a new relationship)
SYMPTOMATOLOGY General Signs & Symptoms:

(significant features/ ● Changes in cognition
manifestations) ● Fluctuation in emotional response (affect)
● Changes in interpersonal functioning
● Fluctuating impulse control
CLUSTER A
● PARANOID:
“GET FACT”
➔ Grudges held for long periods
➔ Exploitation expected (without a sufficient basis)
➔ Trustworthiness of others doubted
➔ Fidelity of sexual partner questioned
➔ Attack on character are perceived
➔ Confides in others rarely
➔ Threatening meanings read into events
● SCHIZOID
“SIR SAFE”
➔ Solitary Lifestyle
➔ Indifferent to praise or criticism
➔ Relationships of no interest
➔ Sexual expereinces not of interest
➔ Activities not enjoyed
➔ Friends lacking
➔ Emotionally cold and detached
● SCHIZOTYPAL
“UFO AIDER”
➔ Unusual perceptions
➔ Friendless except for family
➔ Odd beliefs, thinking, and speech
➔ Affect – inappropriate, constricted

➔ Ideas of reference
➔ Doubts others – suspicious
➔ Eccentric – appearance/behavior
➔ Reluctant in social situations, anxious
“FLAT EARTH”
➔ Fantastic, and magical thinking, odd beliefs
➔ Lack of close friends
➔ Appearance that is eccentric or peculiar
➔ Tendency to withdraw socially
➔ Excessive paranoid ideas or suspiciousness

➔ Abnormal perceptual experiences
➔ Ritualistic behavior
➔ Tendency to conspiratorial explanation
➔ Hostility
CLUSTER B
➔ ANTISOCIAL
“4 B’s DSM”
➔ Be physically aggressive
➔ Behave recklessly
➔ Blame others for their problems
➔ Break the law
➔ Destroy property
➔ Manipulate or deceive others
➔ Show no remorse for hurtful actions
● BORDERLINE
“I RAISED A PAIN”
➔ Identify disturbance
➔ Relationships are unstable

➔ Abandonment frantically avoided (whether real or imagine)
➔ Impulsivity
➔ Suicidal gestures (threats, self-mutilation, etc.)
➔ Emptiness
➔ Dissociative symptoms
➔ Affective instability
➔ Paranoid ideation (stress-related and transient)

➔ Anger is poorly controlled
➔ Idealization followed by devaluation
➔ Negativistic (undermine themselves with self-defeating behaviour)
● HISTRIONIC
“I CRAVE SIN”
➔ Inappropriate behavior - seductive or provocative
➔ Center of attention
➔ Relationships are seen as closer than they really are
➔ Appearance is most important
➔ Vulnerable to others’ suggestions
➔ Emotional expression is exaggerated
➔ Shifting emotions, Shallow
➔ Impressionistic manner of speaking (lacks detail)
➔ Novelty is craved
● NARCISSISTIC
“A FAM GAME”
➔ Admiration required in excessive amounts
➔ Fantasizes about unlimited success, brilliance, etc.
➔ Arrogant
➔ Manipulative
➔ Envious of others
➔ Associates with special people
➔ Me first attitude
➔ Empathy lacking for others
➔
CLUSTER C
➔ AVOIDANT
“RIDICULE”
➔ Restrained within relationships
➔ Inhibited in interpersonal situations
➔ Disapproval expected at work
➔ Inadequate (view of self)
➔ Criticism is expected in social situations
➔ Unwilling for attachment to others
➔ Embarrassment is the feared emotion
● DEPENDENT
“DARN HURT”
➔ Disagreement is difficult to express
➔ Advice – needs excessive input
➔ Responsibility for major areas delegated to others
➔ Nurturance – seeks excessive degree from others
➔ Helpless when alone

➔ Unrealistically preoccupied with being left to care for self
➔ Relationship are desperately sought (when an established one ends)
➔ Tasks – has difficulty initiating projects
● OBSESSIVE-COMPULSIVE
“LOW MIRTH”
➔ Leisure activity is minimal
➔ Organizational focus
➔ Work and productivity predominate
➔ Miserly spending habits
➔ Inflexible arounds morals, values, etc.
➔ Rigidity and stubbornness
➔ Task completion impared (by perfectionism)
➔ Hoards items – cannot discard them
GENERAL
PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS
According to the DMS-5, a person must meet the following criteria to be
diagnosed with a personality disorder:
● A persistent, inflexible, pervasive pattern of maladaptive traits involving ≥
2 of the following: cognition (thoughts & emotions / ways or perceiving
and interpreting self, others, and events), affectivity, interpersonal
functioning, and impulse control
● Significant distress or impaired functioning resulting from the
maladaptive pattern
● Onset of patterns of behavior that can be traced back to adolescence or
early adulthood
● Patterns of behaviors that cannot be explained by any other mental
disorders, substance use, or medical conditions
MEDICAL ● Psychotherapy - aims to improve perceptions of and responses to

MANAGEMENT social and environmental stressors.
○ Focuses on the unconscious motivation for seeking total
satisfaction from others and for being unable to commit oneself to
a stable, meaningful relationship
○ Tx of choice for histrionic personality disorders
● Group Therapy - allows interpersonal psychopathology to display itself
among peer patients, whose feedback is used by the therapist to identify
and correct maladaptive ideas, communication, and behavior.
○ Indicated for antisocial personality disorder but can also be
utilized for individuals with avoidant personality disorder
● Cognitive Therapy - identifies the distortions and engages the patient in
efforts to reformulate perceptions and behaviors.
○ Offer reinforcement for positive change
○ To help the client recognize and correct inaccurate internal
mental schemata
○ Indications: obsessive-compulsive, antisocial, and avoidant
● Behavioral Therapy - development of coping skills to improve affective
stability and impulse control and on reducing self-harmful behavior.
● Interpersonal Therapy
○ To establish an empathic therapist-client relationship based on
collaboration and guided discovery in which the therapist
functions as a role model for the client.
○ Suggested for all types of personality disorders except histrionic,
antisocial, and avoidant.
PSYCHOPHARMACOLOGY
● Antipsychotics
○ For paranoia, psychosis, aggression, and posttraumatic stress
○ Ex: haloperidol, olanzapine, risperidone
● Anticonvulsants
○ For aggression, impulsivity, mood disorders, and suicidality
○ Ex: carbamazepine, valproate
● Antidepressants
○ For depression, anxiety, panic attacks
○ Ex: fluoxetine, venlafaxine
● Anxiolytics/Antianxiety drugs
○ Ex: clomipramine, clonazepam
NURSING 1. Observe and identify behaviors and set clear limits with consequences.
MANAGEMENT (10) R: Helps to set and maintain structure and limits that develop feelings of
security and safety.
2. Provide a safe environment and ensure precautionary safety measures.
R: Removing potentially harmful objects prevents the patient from acting
on sudden self-destructive impulses.
3. Be consistent when interacting with the client and in routine care.
R: Changes in consistency threaten the structure of care and open up the
opportunity for the client to use manipulative behaviors or tactics. The
client may be resistant to change, so consistency helps encourage new
thought processes.
4. Approach and interact with a calm, respectful, supportive and stable
attitude.
R: Personal insecurities or emotions can cause tension or power struggles
with the client. Professionalism helps improve the client’s treatment and
therapy and avoid negative behaviors.
5. Discuss with the client their plans and goals; help distinguish between
positive, realistic goals and unrealistic goals.
R: Help the client regain control of reality and become more focused.
Helps the client understand their capabilities. Set realistic, short term
goals for the client and offer recognition for attaining those goals; Helps
the client realize their abilities and limitations. Encouragement improves
self-esteem and cooperation.
6. Provide realistic feedback and evaluations.
R: Manipulative behavior may ensue without honest, realistic
interpretations of behavior or therapy progress and may negatively impact
the treatment. Helps discern areas of improvement and areas that still
need work.
7. Enforce limits and consequences, and discourage hostile or aggressive
behaviors.
R: Helps reinforce the structure and discourage inappropriate behaviors.
Maintains the safety of clients and others.
8. Discuss alternative ideas or ways of thinking.
R: Helps the client develop coping skills for emotions or feelings.
9. Monitor and encourage positive social interaction with others in a safe
environment.
R: Help clients develop positive social skills and healthy interactions.
Offers an opportunity to learn new ways of dealing with social situations.
10. Teach clients relaxation techniques and deep breathing exercises.
R: Help clients control anxiety and manage situations independently to
reduce symptoms.
PRIORITY NURSING 1. Ineffective coping r/t lack of impulse control

DIAGNOSIS (5) ○ Encourage client to recognize and verbalize feelings of
inadequacy and need for acceptance from others, and how these
feelings provoke defensive behaviors, such as blaming others for
own behaviors.
R: Recognition of the problem is the first step in the change process
toward resolution.
○ Help the client gain insight into own behavior. Often, these
individuals rationalize to such an extent that they deny that their
behavior is inappropriate.
R: Client must come to understand that certain behaviors will not
be tolerated within the society and that severe consequences will
be imposed on those individuals who refuse to comply.
2. Chronic Low Self Esteem r/t retarded ego development

○ Help client identify positive aspects of the self and develop ways
to change the characteristics that are socially unacceptable.
R: Individuals with low self-esteem often have difficulty recognizing their
positive attributes. They may also lack problem-solving ability and require
assistance to formulate a plan for implementing the desired changes.
○ Discuss with client his or her plans for the future. Work with client
to set realistic short-term goals. Identify skills to be learned to
help client reach his or her goals.
R: Looking toward the future minimizes dwelling on the past and
negative self-rumination. When realistic short-term goals are met, client
can gain a sense of accomplishment, direction, and purpose in life.
Accomplishing goals can bolster a sense of control and enhance self-
perception.
3. Impaired Social Interaction r/t
○ Provide immediate, matter-of-fact, non threatening feedback for
unacceptable behaviors. Client may lack knowledge about how he
or she is being perceived by others.
R: Providing this information in a non-threatening manner may help to
eliminate these undesirable behaviors.
○ Problem solve and role play with client acceptable social skills
that will help obtain needs effectively and appropriately.
R: Over time, alternative ways of experiencing interpersonal relationships
might emerge. Take one small skill that client is willing to work on, break
it down into small parts, and work on it with the client.
4. Disturbed Personal Identity r/t underdeveloped ego
○ Encourage client to discuss thoughts and feelings. Help client to
recognize ownership of these feelings rather than projecting them
onto others in the environment.
R: Verbalization of feelings in a nonthreatening environment may help
client come to terms with unresolved issues.
○ Always call client by his or her name. If client experiences feelings
of depersonalization or derealization, orientation to the
environment and correction of misperceptions may be helpful.
R: These interventions help to preserve client’s feelings of dignity and
self-worth.
5. Risk for self-mutilation r/t impulsive behavior.
○ Assess history of self-mutilation.
R: Identifying patterns and circumstances surrounding self-injury can
help the nurse plan interventions and teaching strategies suitable to the
client.
○ Provide a safe environment & ensure precautionary safety
measures.
R: Removing potentially harmful objects prevents the patient from acting
on sudden self-destructive impulses.
PROGNOSIS Personality disorders are lifelong conditions, although attributes of cluster A and
B disorders tend to become less severe and intense in middle age and late life.
Cluster C characteristics tend to become exaggerated in later life.
Individuals with a personality disorder (especially cluster B) are at risk for the
following:
● Suicide
● Substance abuse
● Accidental injury
● Depression
● Homicide - A potential complication, particularly in paranoid and
antisocial personality disorders
Personality disorders are not only distressing for the individual, but also a burden
to society. Studies have revealed that personality disorders have strong
correlations with disability benefits. Because they lack insight, and will not seek
proper medical attention, the overall prognosis is grim. Symptomatology tends to
wax and wane over time.
REFERENCES Bienenfeld, D. (2021, November 22). Personality Disorders: Background,
Pathophysiology, Etiology. Medscape.com; Medscape.
https://emedicine.medscape.com/article/294307-overview#a2
9. Neurologic-Dementia and Alzheimer’s
DEFINITION Dementia - Dementia is a set of symptoms, an umbrella term, for a set of
symptoms caused by physical disorders affecting the brain. It is the decrease in
cognitive ability and memory with fully intact consciousness. Alzheimer’s is the
most common cause of dementia accounting (60% to 80%).
ANATOMY & Neurons :)

PHYSIOLOGY (only ● Send and receive messages to the brain
for the major organ) ● Dendrites
○ Bring information to the neuron
● Axon
○ Sends information to other neurons
○
● Cell body or soma
○ spherical part of the neuron that contains the nucleus.
○ The cell body connects to the dendrites and the axon
Parts of the Brain that are affected

● Entorhinal cortex – involved in memory
● Hippocampus – involved in memory
● Cerebral cortex – involved in language, reasoning, and social behavior
ETIOLOGY PREDISPOSING FACTORS:

● Age: Biological Senescence causes degradation of vessels and makes it
more prone for neurological damage.
● Amyloid Precursor Protein: Enables more production of Senile Plaques
● Presenilin Gene Mutation: Aggregates mutation of Beta-Amyloids
which promotes build up of it.
● Senile Plaques (Beta-amyloids): Natural protein found in the protein
and is cleaned by enzymes - but if its not cleaned it will form a toxic
plaque that will damage the brain.
● Tau protein (neurofibrillary tangles): Dead neurons that died and
tangled up with themselves which causes a build up and more damage to
the neurons nearby.
PRECIPITATING FACTORS:
● Head Injury/Brain Injury: Direct damage to brain can cause
deterioration of its function and neurological damage that leads to
dementia
● Atherosclerosis: Buildup of plaques in the neurovascular vessels
causes damage.
SYMPTOMATOLOGY
Mild Moderate Severe
manifestations)
● Memory loss ● Increased memory ● Inability to
● Poor judgment loss communicate
● Repeating ● Confusion ● Weight loss
questions ● Inability to learn ● Seizures (Neuron
● Wandering and new things damage)
getting lost ● Difficulty with ● Dysphagia (difficulty
● Losing things or language, problems swallowing)
misplacing in odd with reading, ● Loss of bowel and
places writing, and working bladder control
● Mood and with numbers.
personality changes ● Difficulty organizing
● Increased anxiety thoughts and
and/or aggression thinking logically
● Shortened attention
span
● Problems coping
with new situations
● Difficulty carrying
out multi step tasks
(LIKE GETTING
DRESSED)
● Hallucinations,
delusions, and
paranoia
● Repetitive
statements or
movement,
occasional muscle
twitches
GENERAL
PATHOPHYSIOLOGY The pathophysiology of dementia is not understood completely (Emmady & Tadi,
(Simplified) 2021).
1. Precipitating and Predisposing factors
2. Accumulation of native proteins in the brain
3. Alzheimer disease is characterized by widespread atrophy of the
cortex and deposition of amyloid plaques and tangles of
hyperphosphorylated tau protein in the neurons which contribute to
their degeneration.
LABORATORY & Laboratory and Diagnostic findings

DIAGNOSTIC TESTS ● MSE
○ Problem solving skills
○ Attention span
○ Counting Skills
○ Memory
● CT SCAN/MRI
○ Looks for plaque build ups and brain structure.
● Precivity AD Test
○ Looks at the amount of proteins such as B-amyloid in blood
(Since increased ang B-amyloid)
MEDICAL
MANAGEMENT
Cholinesterase Inhibitors: (Inhibits breakdown of Acetylcholine; Since low and
acetylcholine sa alzheimer’s)
● Donepezil (Aricept)
● Galantamine (Razadyne)
● Rivastigmine (Exelon)
NMDA (N-methyl D-aspartate) receptor antagonist
- Memantine

MANAGEMENT N/A

N/A
NURSING 1. Establish rapport

MANAGEMENT (10) R: To establish an effective communication between the patient
Disturbed thought process
2. Assess patient’s ability for thought processing
R: To know how severe the alteration of thought process is.
3. Limit decisions that the patient makes
R: Will enable the patient to avoid the feeling of being frustrated and
increase the feeling of security.
Self-care deficit
4. Assist with as much activity as needed in terms of self-care
R: Promotes independence and self-esteem while helping the patient
perform the activities.
5. Instruct patient to do a short step-by-step method in performing self care
R: Rushing can make the patient lost and frustrated.
Disturbed sleep pattern
6. Adjust the patient’s sleeping environment to be quiet, relaxing, and
comfortable
R: External stressors can cause interference with the patient going to
sleep.
7. Provide relaxation techniques; such as listening to music.
R: Helps in relaxation and helps patients go to sleep.
Anxiety
8. Keep patient’s daily routine consistent as possible
R: Sudden diversion from the patient’s daily routine could cause tension
and anxiety to the patient
9. Instruct patients to have adequate rest periods throughout the day.
R: Fatigue contributes to anxiety and lowers the ability to tolerate stress.
Risk for injury
10. Adjust patient’s environment to have less hazards
R: Avoiding a confrontation of objects that could cause injury for the
patient would minimize the chances of the patient getting injured.
PRIORITY NURSING 1. Disturbed thought process r/t impaired cognitive ability

DIAGNOSIS (5) 2. Self-care deficit r/t impaired cognitive ability
3. Disturbed sleep pattern r/t chemical imbalance in the brain
4. Anxiety r/t medical condition
5. Risk for injury r/t impaired cognitive ability
PROGNOSIS Patients with Alzheimer's disease often live on an average of 4 to 8 years but
can survive up to 20 years or more with strict discipline of medication and
support system.
10. Eating Disorders
DEFINITION ● Characterized by a persistent disturbance of eating or eating-related

behavior that results in the altered consumption or absorption of food and
that significantly impairs physical health or psychosocial functioning.
● Diagnostic criteria are provided for pica, rumination disorder,
avoidant/restrictive food intake disorder, anorexia nervosa, bulimia
nervosa, and binge-eating disorder.
Pica
- Individual persistently and compulsively eating nonfood substances that
are non-nutritious
Rumination Disorder
- Repeated regurgitation and rechewing of food for a period of at least 1
month
Avoidant/ Restrictive Intake Disorder

- disturbance in eating or feeding pattern without fear of weight gain or a
drive for thinness or body dysmorphia
Anorexia Nervosa
- Intense fear of gaining weight or becoming fat (even though underweight)
Bulimia Nervosa
- Recurrent episodes of binge eating. A sense of lack of control over eating
during the episode (e.g., a feeling that one cannot stop eating or control
what or how much one is eating)
Binge Eating Disorder

- Eating a large amount of food, rapidly and discreetly, in a given time (2
hrs)
ANATOMY & Same lang anaphy sa tanan siguro sa psych (nvm lobe nalang siguro) - ben10
PHYSIOLOGY (only
for the major organ) Sige sige

● Age
○ A - 14 to 18 YO
○ B - 18 or 19 YO
● Sex (F>M)
● Genetics
● Diet
● Anxiety disorders (e.g.,obsessive–compulsive disorder)
● Disruptions of the nuclei of the hypothalamus
○ lateral hypothalamus - decreased eating and decreased
responses to sensory stimuli that are important to eating
○ ventromedial hypothalamus - leads to excessive eating, weight
gain, and decreased responsiveness to the satiety effects of
glucose, which are behaviors seen in bulimia.
● Abuse laxatives
○ higher risk for medical complications
● Environmental
SYMPTOMATOLOGY Anorexia
(significant features/ ● Amenorrhea
manifestations) ● Constipation
● Overly sensitive to cold, lanugo hair on body
● Loss of body fat
● Muscle atrophy
● Hair loss
● Dry skin
● Dental caries
● Pedal edema
● Bradycardia, arrhythmias
● Orthostasis
● Enlarged parotid glands and hypothermia
● Electrolyte imbalance (i.e., hyponatremia, hypokalemia)
Bulimia
● Binge-purge cycle
● Usual onset: 15-24 YO
● Laxative, diet pills, & diuretics abuse
● Ipecac abuse
● Menses irregular
● Increased peristalsis, rectal bleeding, & constipation
● Afraid of losing control over eating
●
● Normal weight (common) or overweight
● Episodes: 2x/wk in 3 mons
● Russell’s sign (reddened knuckles)
● Vomiting (self-induced)
● Overly concerned with body shape & weight
● Salivary glands, enlarged (parotid)
● Afraid of becoming fat
PSYCHODYNAMIC Helpppp mamaaaaa

THEORY
GENERAL
PATHOPHYSIOLOGY
(Simplified)
LABORATORY & Anorexia Nervosa
DIAGNOSTIC TESTS ● Hematology. Leukopenia is common, with the loss of all cell types but
usually with apparent lympho<^ytosis. Mild anemia can occur, as well as
thrombocytopenia and, rarely, bleeding problems.
● Serum chemistry. Dehydration may be reflected by an elevated blood
urea nitrogen level. Hypercholesterolemia is common. Hepatic enzyme
levels may be elevated. Hypomagnesemia, hypozincemia,
hypophosphatemia, and hyperamylasemia are occasionally observed.
Self-induced vomiting may lead to metabolic alkalosis (elevated serum
bicarbonate), hypochloremia, and hypokalemia; laxative abuse may
cause a mild metabolic acidosis.
● Endocrine (T3 & T4 level tests). Serum thyroxine (T4) levels are usually
in the low-normal range; triiodothyronine (T3) levels are decreased, while
reverse T3 levels are elevated. Females have low serum estrogen levels,
whereas males have low levels of serum testosterone.
● Electrocardiography. Sinus bradycardia is common, and, rarely,
arrhythmias are noted. Significant prolongation of the QTc interval is
observed in some individuals.
● Bone mass. Low bone mineral density, with specific areas of osteopenia
or osteoporosis, is often seen. The risk of fracture is significantly
elevated.
● Electroencephalography. Diffuse abnormalities, reflecting a metabolic
encephalopathy, may result from significant fluid and electrolyte
disturbances.
● Resting energy expenditure. There is often a significant reduction in
resting energy expenditure.
● Physical signs and symptoms. Many of the physical signs and
symptoms of anorexia nervosa are attributable to starvation. Amenorrhea
is commonly present and appears to be an indicator of physiological
dysfunction. If present, amenorrhea is usually a consequence of the
weight loss, but in a minority of individuals it may actually precede the
weight loss. In prepubertal females, menarche maybe delayed. In
addition to amenorrhea, there may be complaints of constipation,
abdominal pain, cold intolerance, lethargy, and excess energy.
● Physical examination. The most remarkable finding on physical
examination is emaciation. Commonly, there is also significant
hypotension, hypothermia, and bradycardia. Some individuals develop
lanugo, a fine downy body hair. Some develop peripheral edema,
especially during weight restoration or upon cessation of laxative and
diuretic abuse. Rarely, petechiae or ecchymoses, usually on the
extremities, may indicate a bleeding diathesis. Some individuals
evidence a yellowing of the skin associated with hypercarotenemia. As
may be seen in individuals with bulimia nervosa, individuals with anorexia
nervosa who self-induce vomiting may have hypertrophy of the salivary
glands, particularly the parotid glands, as well as dental enamel erosion.
Some individuals may have scars or calluses on the dorsal surface of the
hand from repeated contact with the teeth while inducing vomiting.
Bulimia Nervosa
●
MEDICAL Anorexia Nervosa

MANAGEMENT 1. Weight restoration
2. Nutritional rehabilitation
3. Rehydration
4. Correction of electrolyte imbalances
Clients receive nutritionally balanced meals and snacks that gradually increase
caloric intake to a normal level for size, age, and activity. Severely malnourished
clients may require total parenteral nutrition, tube feedings, or hyperalimentation
to receive adequate nutritional intake. Generally, access to a bathroom is
supervised to prevent purging as clients begin to eat more food. Weight gain and
adequate food intake are most often the criteria for determining the effectiveness
of treatment.
Psychopharmacology
Anorexia
1. Amitriptyline (Elavil) and the antihistamine cyproheptadine (Periactin) in
high doses (up to 28 mg/day)
a. can promote weight gain in inpatients with anorexia nervosa
2. Olanzapine (Zyprexa)
a. has been used with success because of its antipsychotic effect
(on bizarre body image distortions) and associated weight gain
3. Fluoxetine (Prozac)
a. has some effectiveness in preventing relapse in clients whose
weight has been partially or completely restored
4. Clomipramine(Anafranil)
5. Cyproheptadine (Periactin)
6. Chlorpromazine (Thorazine)
Bulimia
1. Antidepressants - to treat bulimia
a. desipramine (Norpramin), imipramine (Tofranil), amitriptyline
(Elavil), nortriptyline (Pamelor), phenelzine (Nardil), and fluoxetine
(Prozac)
b. prescribed in the same dosages used to treat depression more
effective than were the placebos in reducing binge eating
c. improved mood and reduced preoccupation with shape and
weight; however, most of the positive results were short term.
Psychotherapy

MANAGEMENT

MANAGEMENT (10) 2. Provide a pleasant, calm atmosphere at mealtimes
a. Mealtimes become episodes of high anxiety, and knowledge of
regulations decreases tension, particularly when patient has given
up so much control entering treatment
3. Encourage the client to eat with other clients when tolerated.
a. Eating with other people will discourage secrecy about eating,
though initially the client’s anxiety may be too high to join others
at mealtime.
4. Encourage the client to express feelings, such as anxiety and guilt about
having eaten.
a. Expressing feelings can help decrease the client’s anxiety and the
urge to engage in purging behaviors.
5. Encourage the client to incorporate fattening (or “bad”) foods into the diet
as he or she tolerates.
a. This will enhance the client’s sense of control of overeating.
6. Encourage the client to use a diary to write types and amounts of foods
eaten and feelings that occur before, during, and after eating, especially
related to urges to engage in binge or purge behaviors.
a. A diary can help the client explore food intake, feelings, and
relationships among these feelings and behaviors. Initially, the
client may be able to write about these feelings and behaviors
more easily than talk about them.
7. Discuss the types of foods that are soothing to the client and that relieve
anxiety.
a. You may be able to help the client see how he or she has used
food to deal with feelings.
8. Maintain a nonjudgmental approach when discussing the client’s
feelings.
a. Being nonjudgmental gives the client permission to discuss
feelings that may be negative or unacceptable to him or her
without fear of rejection or reprisal.
9. Help the client explore ways to relieve anxiety, express feelings, and
experience pleasure that are not related to food or eating.
a. It is important to help the client separate emotional issues from
food and eating behaviors.
10. Encourage pwatient to apply the knowledge,skills, and gains made from
the various individual, family, and group therapy sessions
a. Patient has been receiving intensive therapy and education,
which have provided tools and techniques that are useful in
maintaining healthy behaviors.
PRIORITY NURSING 1. Imbalanced nutrition: less than body requirements r/t electrolyte
DIAGNOSIS (5) imbalances
2. Ineffective Coping r/tunmet dependency needs
3. Disturbed body image r/t alteration in self-perception
4. Anxiety r/t low self-esteem
5. Ineffective denial r/t unable to admit impact of disease on life pattern
PROGNOSIS Clients with anorexia nervosa can be difficult to treat because they are often
resistant, appear uninterested, and deny their problems.
REFERENCES Videbeck - p 862

Shives - p 343
https://medlineplus.gov/eatingdisorders.html
https://www.psychiatry.org/patients-families/eating-disorders/what-are-eating-
disorders
11. Substance abuse - marijuana and shabu use
DEFINITION ● Substance abuse is the use of drugs in excessive amounts which leads to
a cluster of cognitive, behavioral, and physiological symptoms indicating
that the individual continues using the substance despite significant
substance-related problems.
● Marijuana (depressant): Delta 9 tetrahydrocannabinol (THC)- main
psychoactive ingredient of mj which has the highest concentration found
in the bud of the plant
● Shabu: man-made drug; made from easy to produce chemicals
Stages in Addiction Cycle

1. Intoxication: it is the use of substances that results in maladaptive
behavior.
2. Withdrawal Syndrome: this refers to the adverse psychological and
physical effects associated with the cessation or significant reduction of a
substance's use.
3. Detoxification: is a term that refers to the process of safely abstaining
from a substance.
2 groups of substance-related disorders:

- Substance-use disorders are patterns of symptoms resulting from the use
of a substance that you continue to take, despite experiencing problems
as a result
- Substance-induced disorders including intoxication, withdrawal, and other
substance/medication-induced mental disorders, are detailed alongside
substance use disorders.
● Cannabis use disorder

○ Using cannabis for a min. of 1 year with the presence of at least 2
symptoms
○ Having cravings for cannabis
● Cannabis intoxication
○ Side effects seen as a result of the ingredient THC
● Cannabis withdrawal
○ Symptoms may include dysphoria (anxiety, irritability, depression,
restlessness), disturbed sleep, gastrointestinal symptoms, and
decreased appetite
○ Often paired with rhythmic movement disorder
○ Most symptoms begin during the 1st week of abstinence and
resolve after a few weeks.
ANATOMY &
PHYSIOLOGY (only
ETIOLOGY Predisposing factors:

● Physical
○ Genetic factors (Researchers found few biochemical or metabolic
differences between people who do and do not develop substance
use disorder)
● Personal
○ Low levels of self-control (impulsivity)
○ High levels of risk-taking
○ Novelty-seeking (strong desire to explore new things)
● Circumstances and disorders
○ Sad, depressed, emotionally distressed, socially alienated
● Cultural and social factors
○ Influenced by family members/peers
○ Abusive family
○ Low socio-economic status
○ Drug- tolerant culture
SYMPTOMATOLOGY ● Euphoria
(significant features/ ● Eye twitching
manifestations) ● Body odor
● Weight loss
● Pinpoint pupils
● Paranoia
● Skin irritations
● Loss of teeth
● Impaired motor coordination
● Social withdrawal/impairment
● Tachycardia
● Increased appetite
SEVERITY:
Mild- presence of 2-3 symptoms

Moderate- presence of 4-5 symptoms
Severe- presence of 6 or more symptoms
GENERAL
PATHOPHYSIOLOGY
(Simplified)
LABORATORY & Meth test

DIAGNOSTIC TESTS ● Blood: 24-48 hrs after use
● Urine: 1-4 days after use
● Hair: 30 days after use
MEDICAL
MANAGEMENT
PSYCHOTHERAPY

MANAGEMENT N/A

N/A

MANAGEMENT (10) R: To establish an effective communication with the pt
2. Convey attitude of acceptance, separating individual from unacceptable
behavior.
R: Promotes feelings of dignity and self-worth
3. Educate regarding effects of addiction on mood and personality.
R: Individuals often mistake effects of addiction and use this to justify or
excuse drug use.
4. Be alert to changes in behavior, (restlessness, increased tension).
R: Confrontation can lead to increased agitation, which may compromise
safety of patient and staff.
5. Maintain firm expectation that the patient attends recovery support and
therapy groups regularly.
R: Attendance is related to admitting need for help, to working with
denial, and for maintenance of a long-term drug-free existence.
6. Encourage and support patient’s taking responsibility for own recovery
(development of alternative behaviors to drug urge and use). Assist
patient to learn own responsibility for recovering.
R:Denial can be replaced with positive action when the patient accepts
the reality of own responsibility.
7. Encourage family members to seek help whether or not the abuser seeks
it.
R: To assist the patient deal appropriately with the situation.
PRIORITY NURSING 1. Denial r/t delays in seeking assistance

DIAGNOSIS (5) 2. Ineffective individual coping r/t inadequate support systems
3. Imbalanced nutrition: less than body requirements r/t to taking drugs
instead of eating
4. Altered social interaction r/t addictive behavior
5. Deficient knowledge r/t denial of problems with substance use
PROGNOSIS - Addiction is a lifelong disease. But people can recover from addiction and
lead full lives. Getting help is essential to recovery. Different tools work for
different people, but ongoing therapy and self-help groups such as
Narcotics Anonymous help many.
- Substance use disorder is a “relapsing disease.” People who are in
recovery from this disease have a higher chance of using drugs again.
Recurrence can happen even years after you last took drugs.
REFERENCES
MEDSURG
1. Liver Cirrhosis
DEFINITION A chronic disease characterized by the development of scar tissues (fibrosis)
due to chronic damage to the liver. (e.g Alcohol or Toxins)
ANATOMY & - LIVER

PHYSIOLOGY (only - SMALL AND LARGE INTESTINES
for the major organ) - SPLEEN
- KIDNEYS
- MEN ARE MORE LIKELY TO HAVE LIVER DISEASES DUE TO BEING
MORE SUSCEPTIBLE TO HCC DEVELOPMENT. ESTROGEN PLAYS
A VITAL ROLE IN ANTI-INFLAMMATION (INFLAMMATION IS ONE OF
THE MAJOR CAUSES OF FIBROSIS).
- AGE (BIOLOGICAL SENESCENCE)
- GENETICS (ALPHA-1-ANTITRYPSIN DEFICIENCY)
PRECIPITATING
- ALCOHOL CONSUMPTION
- HEPATITIS B AND C
- NUTRITIONAL DEFICIENCY (PROTEIN DEFICIT)
SYMPTOMATOLOGY - ASCITES
(significant features/ - JAUNDICE
manifestations) - PERIPHERAL EDEMA
- PORTAL HYPERTENSION
- DEHYDRATION
GENERAL PREDISPOSING/PRECIPITATING FACTORS → DAMAGE TO HEPATOCYTES

PATHOPHYSIOLOGY
(Simplified) → STELLATE CELLS ACTIVATION AND ATTRACTION OF KUPFFER CELLS →
RELEASE OF CYTOKINES AND TGFs → INFLAMMATION AND STIMULATION
OF STELLATE CELLS TO TRANSFORM INTO MYOFIBROBLAST WHICH
PRODUCES COLLAGEN → COLLAGEN FORMATION CAUSES SCARRING
OF LIVER TISSUE → DX: HEPATIC CIRRHOSIS

DIAGNOSTIC TESTS
-ALT/SGPT AND AST/SGOT
-ALP (ALKALINE PHOSPHATASE)
-CBC (Pancytopenia)
-CXR
-UA (Increased Bilirubin levels)
MEDICAL
MANAGEMENT
- CORTICOSTEROIDS → PREDNISOLONE, PREDNISONE, AND CORTISONE

- DIURETICS FOR PERIPHERAL EDEMA → FUROSEMIDE [LOOP DIURETIC]
(LASIX)
- ANTIHYPERTENSIVES → DIURETICS PARIN (HYDROCHLOROTHIAZIDE,
CHLORTHALIDONE, AND FUROSEMIDE)
NSAIDS ARE AVOIDED DUE TO HOW THEY UNDERGO LIVER
METABOLISM WHICH DAMAGES THE LIVER WHILE BEING METABOLIZED
(HEPATOTOXICITY)

MANAGEMENT -LIVER TRANSPLANT

1. Provide oxygen ventilation
R: Renal support and neurological therapy
2. Assess bleeding in access site or elsewhere
R: Bleeding in the surgical wound often depicts serious complications
due to surgical error.
3. Assess and monitor vital signs
R: Indicator for beneficial or adverse effects of the procedure.
4. Assess urine color and output
R: Can be an indicator of renal damage.
5. Provide sterile dressing changes
R: To prevent infection and promote wound healing.
NURSING 1. Establish Rapport

MANAGEMENT (10) R: Explainable
2. Monitor and record vital signs
R: Attain baseline data for reference of treatment
3. Elevate head of the bed to semi-fowler position
R: Promote better lung expansion and facilitate better gas exchange
4. Render O2 inhalation
R: To maintain oxygen balance
5. Demonstrate and assist patient in performing deep-breathing exercises
R: Aids in better lung expansion
6. Maintain a quiet and comfortable environment
R: To avoid stressor that could potentiate exacerbation of health
condition.
7. Monitor temperature; Note presence of chills, or changes in sputum
discharge.
R: A rapid changes or presence of these can be an indicative of infection
8. Provide a nonpharmacologic pain management
R: Promote alternative non-medication pain management.
9. Adjust patient bed to avoid any bruising or any chances of getting a cut
R: To avoid risk of bleeding since pt has a decrease in coagulation
factors.
10. Administer medication as timely as ordered by the Attending Physician.
R: To prevent overdose and to promote betterment of health condition(s).
PRIORITY NURSING 1. Ineffective Breathing Pattern r/t collection of fluid in the peritoneal space
DIAGNOSIS (5) 2. Excess fluid volume r/t high interstitial pressure
3. Acute pain r/t inflammation of liver tissue
4. Risk for bleeding r/t thrombocytopenia
5. Risk for infection r/t decreased WBC count
PROGNOSIS Early detection of liver damage could indicate a higher chance of good
prognosis; the later the detection - the higher the MELD score - the more
chances of having a bad prognosis.
2. Pancreatitis -
DEFINITION Inflammation of the pancreas; commonly described as autodigestion of the
pancreas
ADDITIONAL INFO
Interstitial edematous pancreatitis
● lack of pancreatic or peripancreatic parenchymal necrosis with diffuse
enlargement of the gland due to inflammatory edema
● edema and inflammation in interstitial pancreatitis is confined to the
pancreas itself
● Minimal organ dysfunction is present, and return to normal function
usually occurs within 6 months.
Necrotizing pancreatitis
● tissue necrosis in either the pancreatic parenchyma or in the tissue
surrounding the gland.
● Can be sterile or infected
● if the parenchyma is involved this is a marker for more severe disease
● Enzymes damage the local blood vessels, and bleeding and thrombosis
can occur
● The tissue may become necrotic, with damage extending into the
retroperitoneal tissues
● Local complications include pancreatic cysts or abscesses and acute
fluid collections in or near the pancreas
ANATOMY &
PHYSIOLOGY (only
The Pancreas
● Located in the upper abdomen
Exocrine Function (secreting externally; hormonal secretion from excretory

ducts)
1. Secretions are produced by acinar cells
2. Secretions collect in the pancreatic duct, which joins the common bile
duct & enters the duodenum at the ampulla of Vater
3. Sphincter of Oddi: Surrounding the ampulla; partially controls the rate at
which secretions from the pancreas & the gallbladder enter the
duodenum
Secretions:
● Digestive enzymes high in protein content & an electrolyte-rich fluid
● Secretion, which are very alkaline bc of their high concentration of
sodium bicarbonate , are capable of neutralizing the highly acid gastric
juice that enters the duodenum
● Enzymes:
a. Amylase - digestion of carbohydrates
b. Trypsin - digestion of proteins; a protease
c. Lipase - digestion of fats
Things that stimulate these secretion

● Secretin (hormone): major stimulus for increased bicarbonate secretion
from the pancreas
● CCK (hormone): major stimulus for digestive enzyme secretion
● Vagus nerve: influences exocrine pancreatic secretion
Endocrine Function (secreting internally; hormonal secretion of a ductless

gland)
● Islets of Langerhans: collection of cells embedded in the pancreatic
tissue
○ Composed of alpha, beta, and delta cells
Insulin (Beta cells)

● Lower blood glucose by permitting entry of glucose into the cells of the
liver, muscle, and other tissues, where it is either stored as glycogen or
used for energy
● Promotes the storage of fat in adipose tissue & synthesis of proteins in
various body tissues DOYY STUDY WELL DOYY
● w/o insulin, glucose is excreted in the urine
● Level of glucose in the blood normally regulate the rate of insulin
secretion from the pancreas
Glucagon (Alpha Cells)

● Raise the blood glucose by converting glycogen to glucose in the liver
● Secreted in response to a decrease in the level of blood glucose
Somatostatin (Delta cells)

● Exerts a hypoglycemic effect by interfering w/ release of growth hormone
from the pituitary & glucagon from the pancreas, both of which tend to
raise blood glucose levels
ETIOLOGY Predisposing
1. Advancing Age
a. Progressive decrease in physiologic function of major organs
2. Genes
a. Hereditary pancreatitis - small incidence
b. PRSS1 gene mutation - elevated trypsin activity
3. Race
a. More common in blacks than whites
Precipitating
1. Gallstones / Cholelithiasis
a. pancreatic duct obstruction that leads to biliary reflux is believed
to activate the enzymes in the pancreatic duct system.
2. Alcohol consumption
a. Transiently increases pancreatic exocrine secretions and
contraction of the sphincter of Oddi
b. Has direct toxic effects on acinar cells (induction of oxidative
stress).
c. Alcohol-induced pancreatitis likely results from alcohol causing
increased, viscous secretions that block small pancreatic ducts
and by premature activation of digestive and lysosomal enzymes
within acinar cells
3. Use of tobacco products
a. Nicotine induces damage through signal transduction pathways in
pancreatic acinar cells, leading to elevated levels of intracellular
calcium release and/or impaired pancreatic blood flow.
b. It was suggested that smoking induces an inflammatory process
in pancreatic tissue, as it stimulates expression of pancreatic
procollagen 1 gene, interleukin-1ß and TGF-ß in acinar cells
4. Infections
a. Direct Tissue injury
b. E.g. mumps viral infection causes pancreatitis
5. Hypertriglyceridemia
a. increase plasma viscosity, which may induce ischemia in
pancreatic tissue and trigger organ inflammation
6. Drugs
a. Corticosteroids, thiazide, diuretics, oral contraceptives, and other
meds
b. Causes pancreatic duct constriction, cytotoxic and metabolic
effects, accumulation of a toxic metabolite or intermediary, and
hypersensitivity reactions
c. Some drugs may cause high triglyceride levels
7. Blunt Abdominal Trauma
a. Pancreatic Tissue Damage
8. Surgery on/near the pancreas or after instrumentation of the
pancreatic duct
a. Postoperative complications; Cell-injury
b. The increased pressure while injecting the contrast media can
cause the activation of digestive enzymes which then trigger
pancreatic autodigestion and the initiation of local inflammation
SYMPTOMATOLOGY Major Symptoms

(significant features/ 1. Severe Abdominal Pain
manifestations) 2. Abdominal Tenderness and Guarding
3. Nausea and Vomiting
4. Absent / Decreased Bowel Sound
5. Turner’s sign
6. Cullen’s sign
7. ARDS
—-----------------------------------------------------------------------------------------------------
1. Severe abdominal pain: major symptom
➢ Typically in the midepigastrium or in LUQ
➢ Radiate to the back, chest, or flank areas
➢ Acute in onset
➢ 24-84 hrs after a very heavy meal or alcohol ingestion
➢ Dissue & difficult to localize
➢ Unrelieved by antacids
➢ Pain can be accompanied by
2. Abdominal Distention
3. Poorly defined, palpable abdominal mass
4. Decreased peristalsis
➢ caused by peripancreatic spread of the inflammatory process
that produces a generalized ileus
5. Vomiting that fails to relieve the pain or nausea
➢ Emsesis is usually gastric in origin but may also be bile stained
6. Abdominal Tenderness and Guarding
7. Rigid or Boardlike abdomen
➢ May indicate peritonitis
8. Turner’s sign / Cullen’s sign
➢ Indicate severe pancreatitis
➢ Necrosis induced hemorrhaging spreads to the soft tissues of the
body areas
9. Fever
➢ Due to inflammatory proces
10. Mental Confusion / Agitation
11. Hypovolemia - due to loss of large amounts of protein-rich fluid into the
tissues and peritoneal cavity; increased microvascular permeability;
endotoxemia (from breakdown of the barriers b/t GI flora and the
bloodstream)
➢ Hypotension
➢ Tachycardia
➢ Cyanosis
➢ Cold, Clammy Skin
12. AKI
13. ARDS
➢ Pancreatic inflammation leads to leaky blood vessels throughout
the body, which makes it hard to breath
➢ Alveolar damage
14. Myocardial depression
15. Hypocalcemia
➢ when there is a lot of fat necrosis because that process tends to
consume calcium.
16. Hypoglycemia
17. DIC
➢ Due to systemic activation of blood coagulation factors
➢ Blood clots form throughout the body; uses up clotting factor
making it easier to bleed
➢ Causes imbalance in clotting homeostasis and damaging other
vital organs
Note:
● Pain & tenderness are caused by irritation & edema of the inflamed
pancreas
● Increased tension on the pancreatic capsule & obstruction of the
pancreatic ducts also contribute to the pain.
GENERAL Screenshot from Porth’s

PATHOPHYSIOLOGY
(Simplified)
NEED HELP SEND

HELP 🏳
-------------------------------------------------------------------------------------------------------
Brunner’s Pathophysiology
1. Self-digestion of the pancreas by its own proteolytic enzymes, principally
trypsin, causes acute pancreatitis
2. Gallstones enter the common bile duct & lodge at the ampulla of Vater
3. Obstructs the flow of pancreatic juice or causing a reflux of bile from the
common bile duct into the pancreatic duct.
4. Thus, activating the powerful enzymes within the pancreas
a. Normally these remain in an inactive form until pancreatic
secretions reach the lumen of the duodenum
5. Activation of the enzymes can lead to vasodilation, increased vascular
permeability, necrosis, erosion, and hemorrhage
Other explanation
The pancreatic duct becomes temporarily obstructed, accompanied by
hypersecretion of the exocrine enzymes of the pancreas. These enzymes enter
the bile duct, where they are activated and, together with bile, back up (reflux)
into the pancreatic duct, causing pancreatitis.

DIAGNOSTIC TESTS
Serum amylase and lipase levels
● Used in dx but can be attributed to many other cases
● Elevated w/in 24 hrs of onset of the symptoms
● Returns to normal within 48-72 hrs, but lipase may remain elevated for a
longer period, often days longer than amylase
● They are grater than 3 times the upper limit of normal values
Urinary amylase levels

● Elevated; elevated longer than serum amylase lvls
WBC
● Elevated
Hypocalcemia
● Correlates w/ severity of pancreatitis
● Signs of hypocalcemia may develop, probably as a result of the
precipitation of serum calcium in the areas of fat necrosis
●
In some patients
● Transient hyperglycemia, glucosuria, and elevated serum bilirubin
HCT or HGB
● Monitor the patient for bleeding
X-ray of the abdomen and chest

● To differentiate pancreatitis from other disorders that can cause similar
symptoms and to detect pleural effusions
Ultrasound studies, contrast-enhanced CT scans, and MRI
● To identify an increase in the diameter of the pancreas
● To detect pancreatic cysts, abscesses, or pseudocysts
Paracentesis or Peritoneal lavage
● Obtain peritoneal fluid and may contain increased levels of pancreatic
enzymes
ERCP
● Rarely used in diagnostic evaluation because the patient is acutely ill but
is valuable in the treatment of gallstone pancreatitis
● Identify stones, tumors, or narrowing in the biliary and pancreatic ducts.
● Contrast agent is injected through the ducts
MEDICAL 1. NPO
MANAGEMENT a. To inhibit stimulation of the pancreas and its secretion of
enzymes
2. Enteral Feeding
a. Whenever possible
b. To meet nutritional needs
c. To pervent infectious complications safely and cost-effectively
3. Parenteral Nutrition
a. For those with severe acute pancreatitis, particularly in those who
are unable to tolerate enteral nutrition
4. Nasogastric Suction
a. To relieve N/V
b. To decrease painful abdominal distention and paralytic ileus
5. Biliary Drains and Stents
a. Placement of biliary drains (for external drainage) and stents
(indwelling tubes) in the pancreatic duct through endoscopy has
been performed to reestablish drainage of the pancreas. As a
result, decreases pain
6. Respiratory Care
a. ABG, humidified O2, intubation/mech vent
b. Biliary Drainage
H2 antagonists
● E.g.: cimetidine (Tagamet) & ranitidine (Zantac)
● Decrease pancreatic activity by inhibiting secretion of gastric acid
PPI
●pantoprazole (Protonix)
●For those who don’t tolerate H2 antagnosits or for whom this therapy is
ineffective
Parenteral opioids
● E.g.: morphine, fentanyl (Sublimaze), or hydromorphone (Dilaudid)
● Accdg to Maam Bee, we dont give morphine only Dilaudid / Demerol
● Pain relief and to minimize restlessness, which may stimulate pancreatic
secretion further
● Via Pt-controlled analgesia / bolus / continuous infusion
Antiemetic agents
● To prevent vomiting
Intensive Care
Antibiotics
● If infection is present
Insulin
● If hyperglycemia occurs

MANAGEMENT
1. Endoscopic retrograde cholangiopancreatography (ERCP)
a. Remove gallstones if gallstones are the cause of pancreatitis
b. May also used to treat strictures
2. Debridement and Drainage
a. to remove infected pancreatic tissue or necrosis
b. To drain fluid from the pancreas that has accumulated as a result
of an infection
1. Assess & monitor VS

a. To check for signs of infection & if there is hemorrhage
2. Assess incision or operative site
a. To check for any signs of infection, and to check if the dressing is
dry and intact and needs replacement
3. Assess and record the amount and characteristics of drainage
a. Purulent wound drainage can be a sign of infection. It has a foul
odor and has a thick & milky discharge
4. Perform hand hygiene before and after dressing changes and any
contact with the surgical site
a. To prevent transmission of microorganisms
5. Provide sterile dressing changes.
a. To prevent infection and promote wound healing
-----------------------------------------------------------------------------------------------------------
- Pt has multiple drains
- Surgical incision left open for irrigation and repacking every 2 to 3 days to
remove necrotic debris
NURSING Please refer to Nursing Diagnosis

MANAGEMENT (10) —------------------------------------------------------------------------------------------------------
1. Promote bed rest
a. to decrease the metabolic rate and reduce the secretion of
pancreatic and gastric enzymes.
2. Change position frequently
a. To prevent atelectasis and pooling of respiratory secretions.
b. To prevent skin breakdown
3. Monitor Daily Weights
a. Provide a baseline and a means to measure weight gain or
weight loss
PRIORITY NURSING 1. Acute Pain r/t irritation and edema of the inflamed pancreas and
DIAGNOSIS (5) excess stimulation of pancreatic secretions
a. Assess pain with pain scale / PQRST method
Ⓡ When there is an increasing severity of pain the Pt may be
experiencing hemorrhage of the pancreas / dose of
analgesic med may be inadequate
b. Educate Pt about nonpharmacologic pain management (proper
positioning, music, distraction, and imagery)
Ⓡ Use of nonpharmacologic methods will enhance the
effects of analgesic medications; Much better intervention
for those who are prone to chemical dependence
2. Impaired comfort r/t nasogastric tube
a. Provide frequent oral hygiene and care
Ⓡ decrease discomfort from the nasogastric tube and relieve
dryness of the mouth.
b. Apply water-soluble lubricant around external nares
Ⓡ Prevents irritation of nares
3. Imbalanced nutrition: less than body requirements r/t impaired
pancreatic secretions and increased metabolic needs
a. Monitor blood glucose level q 4-6 hrs if administering parenteral
nutrition
Ⓡ Impairment of endocrine function of the pancreas leads to
increased serum glucose levels; Blood glucose needs to
be monitored with parenteral nutrition due to the high
glucose level in the fluids.
b. Provide high-carbohydrate, low-protein, low-fat diet when
tolerated
Ⓡ These food increase caloric intake without stimulating
pancreatic secretions beyond the ability of the pancreas to
respond
4. Ineffective breathing pattern r/t splinting from severe pain,
pulmonary infiltrates and pleural effusion
a. Maintain Semi-Fowler Position
Ⓡ to decrease pressure on the diaphragm by a distended
abdomen and to increase respiratory expansion.
b. Administer oxygen as prescribed. Monitor oxygen delivery system
at regular intervals
Ⓡ Hypoxia is an early sign of impending respiratory failure
and necessitates oxygen delivery. Oxygen therapy
decreases the workload of the respiratory system and the
tissue utilization of oxygen
5. Risk for defficient Fluid Volume r/t vomiting and gastric suctioning
a. Assess VS
Ⓡ This assessment enables detection of a falling BP and
increasing HR (100- 140 bpm), which can occur with
moderate to severe fluid loss.
b. Measure intake and output (I&O), including vomiting or gastric
aspirate and diarrhea. Calculate 24- hour fluid balance.
Ⓡ Indicators of replacement needs and effectiveness of
therapy.
PROGNOSIS May result in complete recovery, may recur without permanent damage, or may
progress to chronic pancreatitis. The severity of acute pancreatitis and its
outcomes can be predicted based on clinical and laboratory data
REFERENCES Brunner - 3806

Porth -773
Robbins - 676
Harrison - 2439
3. Hyperthyroidism-
DEFINITION ● Hyperthyroidism is a collective term for a condition marked by increased
thyroid activity and overproduction of thyroid hormones thyroxine (T4)
and triiodothyronine (T3).
● Hyperthyroidism is a disorder caused by excessive delivery of Thyroid
Hormone to the tissues.
ANATOMY & ● Thyroid gland → The thyroid gland is a butterfly-shaped organ located in
PHYSIOLOGY (only
for the major organ) the lower neck, anterior to the trachea. It produces three hormones:
thyroxine (T4), triiodothyronine (T3), and calcitonin.
○ Both amino acids contain iodine molecules that are bound to the
amino acid structure. The primary function of thyroid hormone is
to control cellular metabolic activity.
■ Triiodothyronine (T3) → 5 times more than T4, has a more
rapid metabolic action.
■ Thyroxine (T4) → maintains body metabolism in a steady
state.
ETIOLOGY
Predisposing Precipitating
Age Stress
Gender Smoking
Family History Infection
Iodine Exposure
Postpartum
HAART d/t immune reconstitution
SYMPTOMATOLOGY ● Nervousness → this is more likely to be the presenting symptom.

● Unusual perspiration
manifestations)
● Exophthalmos
● Progressive weight loss
● Abnormal muscular fatigability
● Weakness
● Goiter/ enlarged thyroid gland
GENERAL
PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS ● Serum TA
● Serum TSH (sensitive assay)
● Serum T4
● Serum T3
● T3 uptake (T3RU)
● Thyroid suppression
●
MEDICAL Treatment of hyperthyroidism is directed toward reducing thyroid hyperactivity

MANAGEMENT to relieve symptoms and preventing complications. Use of radioactive iodine is
the most common form of treatment for Graves’ disease in North America. Beta-
adrenergic blocking agents (eg, propranolol [Inderal]) are used as adjunctive
therapy for symptomatic relief, particularly in transient thyroiditis (Cooper,
2005).
● Antithyroid medications
○ Must ask if the patient is taking amiodarone hydrochloride (Cordarone), a
dysrhythmic, because it contains large amounts of iodine
MANAGEMENT ● Thyroidectomy→ A thyroidectomy may also be done for respiratory
obstruction by a goiter or thyroid cancer. If a partial thyroidectomy
is done, the remaining thyroid tissue should provide adequate
amounts of thyroid hormones. If a complete thyroidectomy is
done, the client will require thyroid hormone replacement for life.
○ Clients usually take propylthiouracil (PTU) for 4 to 6 weeks before
surgery and iodine preparations may be prescribed 10 to 14 days
before surgery to decrease thyroid vascularity and decrease
bleeding.
● Ensure gag, cough, and swallowing reflexes are present before offering
oral fluids.
R: Decreases risk of aspiration.
● Maintain a client in Fowler’s position when drinking or eating.
R: Use of 90-degree angle for consumption of food and fluids will decrease risk
of aspiration.
● Encourage the client to drink slowly and chew thoroughly.
R: Adequate chewing of food produces a bolus that is easier to swallow and
drinking slowly helps to decrease the risk of aspiration.
● Keep intubation and tracheostomy kits readily available. Keep suctioning
equipment ready.
R: Emergency resuscitation equipment should be readily available for
emergency intubation or tracheostomy if needed.
● Complete respiratory assessment frequently and monitor for respiratory
distress and laryngeal spasms, tetany.
R: Provides a baseline assessment and monitors for changes that may indicate
the need for prompt treatment. Hypocalcemia is accompanied by laryngeal
spasms and tetany if accidental removal or injury has occurred to parathyroid
glands.
NURSING ● Monitor weight daily. Use the same scale, same amount of clothing, at
MANAGEMENT (10) the same time daily.
R: Weight is compared with baseline to determine the need for an increase or
decrease in caloric intake.
● Encourage six meals per day with adequate protein, carbohydrate, and
caloric intake.
R: Adequate nutritional intake is needed with elevated metabolic state.
● Arrange a consultation with the dietitian to assist in determining the
client’s increased nutritional needs. Encourage the client to eat a well-
balanced diet.
R: Dietitian has special training in the area of nutrition and can determine client
caloric needs and provide education about nutritional needs.
● Provide snacks throughout the day.
R: Snacking can increase caloric needs to meet metabolic demands.
● Complete prealbumin test to determine protein reserve.
R: There is an increased need for protein in a client with hyperthyroidism.
● Administer isotonic solutions or eye lubricants to keep the eyes moist. At
night, elevate the head of the bed, which may assist in keeping the
eyelids closed, or cover the eyes with eye guards to prevent drying.
R: Abnormal positioning of the eye prevents adequate lid closure and permits
drying of eyes, which could result in corneal ulceration and discomfort.
Lubricating solutions and eye guards will protect cornea from injury
● Suggest to client that dark or tinted wraparound glasses may protect the
eyes from wind and airborne particles.
R: Inability to adequately close the eye permits entry of airborne particles and
increases risk for injury to the eye.
● Provide a well-ventilated room with temperature control.
R: Promotes comfort if heat intolerant.
● Provide frequent bathing and changes in linens or clothing.
R: Promotes comfort if diaphoretic
● Monitor the amount of food ingested and caloric intake.
R: Provides data to determine if diet is adequate to prevent weight loss.
PRIORITY NURSING ● Hyperthermia related to increased metabolic rate
DIAGNOSIS (5) ● Imbalanced Nutrition: Less than Body Requirements related to increased
metabolism
● Risk for Injury related to exophthalmos
● Impaired Swallowing related to mechanical obstruction (edema)
● Ineffective Airway Clearance related to hemorrhage, edema, laryngeal spasm
PROGNOSIS
REFERENCES
4. Addison’s Disease -
DEFINITION Chronic adrenocortical insufficiency due to inadequate adrenal cortex function,
cannot produce sufficient cortical hormones; Also known as Primary Adrenal
Insufficiency
ANATOMY & Hypothalamus - Regulates body temperature, food intake, water balance, and
PHYSIOLOGY (only thirst - Also regulates hormonal output of anterior pituitary gland and acts as an
for the major organ) endocrine organ.
Secretes hormone called Corticotropic releasing hormone which stimulate the

anterior pituitary gland to release adenocorticotropic hormone (ACTH)
Adrenal Gland - Produces corticosteroids, mineralocorticoids, glucocorticoids,

and sex hormones.
Cortex (Glandular) - Produces sex hormones (Androgens and estrogen), salt

balance hormone (Aldosterone), and sugar balance hormone (cortisol).
Outer Layer of Adrenal Cortex (Zona Glomerulosa): Produces Aldosterone
Middle Layer of Adrenal Cortex (Zona Fasciculata): Produces Cortisol
Inner Layer of Adrenal Cortex (Zona Reticularis): Produces sex hormones
Medulla (Neural Tissue) - Produces hormones involved in flight-or-fight

response (catecholamines, epinephrine, and norepinephrine)
● Genetics - (Human Leukocyte Antigen) [causes an inappropriate
immune response which attacks the adrenal cortex]
● Amyloidosis - Abnormality of plasma cells in the bone marrow which
causes build up and infiltrate the adrenal gland which causes damage.
● Cancer - Cancer cells infiltrate the adrenal gland and cause damage.
Precipitating
● Tuberculosis - Can cause a shift of Th1/Th2 balance towards Th2; T-
cell dysfunction which causes immunologically-mediated tissue damage
of the adrenal gland.
SYMPTOMATOLOGY - Tiredness
(significant features/ - Dizziness
manifestations) - Nausea
- Weight Loss
- Pigmentation (Generalized)
- Vomiting
- Diarrhea
- Arthralgia
- Myalgia
GENERAL Predisposing and Precipitating Factors → Damage to Adrenal Gland → Inability to

PATHOPHYSIOLOGY
(Simplified) secrete hormones properly → DX: Addison’s Disease
LABORATORY & Aldosterone Test - Check aldosterone levels

DIAGNOSTIC TESTS Serum Cortisol - Check cortisol levels
Serum ACTH - Elevated normally due to the insufficiency
Adrenal autoantibodies - Antibodies to 21-hydroxylase and 17-hydroxylase
(proteins sa adrenal gland and if naay defect kay mag cause if immunologically-
mediated tissue damage)
CT Scan - visualize adrenal gland
MEDICAL
MANAGEMENT
Glucocorticoid hormone supplement replacement - (Hydrocortisone,
dexamethasone, and prednisone)
Mineralocorticoid hormone supplement replacement- Fludrocortisone (9-
flurohydrocortisone)

MANAGEMENT N/A

N/A
NURSING 1. Monitor and record vital signs

MANAGEMENT (10) R: Attain baseline data for reference of treatment
2. Assess skin turgor
R: Indicator of dehydration
3. Elevate head of the bed to semi-fowler position
R: Promote better lung expansion and facilitate better gas exchange
4. Render O2 inhalation
R: To maintain oxygen balance
5. Demonstrate and assist patient in performing deep-breathing exercises
R: Aids in better lung expansion
6. Emphasize the need to eat given meals.
R: To avoid further exacerbation of imbalance in nutrition and to
replenish the lost nutrition.
7. Promote intake of at least 2L of water per day
R: To promote rehydration of loss fluid.
8. Adjust patient bed and environment to avoid any injury
R: To avoid risk of bone fracture due to the weakening of bones of the pt.
9. Adjust patient bed to avoid any bruising or any chances of getting a cut
R: To avoid risk of bleeding since pt is vulnerable to infection
10. Administer medication as timely as ordered by the Attending Physician.
R: To prevent overdose and to promote betterment of health condition(s).
PRIORITY NURSING 1. Fluid Volume Deficit r/t sodium body imbalance

DIAGNOSIS (5) 2. Decreased Cardiac Output r/t sodium body imbalance
3. Imbalanced Nutrition: less than body requirements r/t insufficient dietary
intake
4. Risk for Infection r/t immunosuppression
5. Risk for Injury r/t increase in osteoclast activity
PROGNOSIS Unattended management of Addison’s disease can lead to death but with
medical management and strict discipline to follow it, people with addison
disease can live a normal life.
5. Diabetes Mellitus
DEFINITION
Diabetes mellitus (DM)
● Chronic metabolic disorder characterized by persistent hyperglycemia.

● Group of diseases that affect how your body uses blood sugar (glucose).
It may be due to impaired insulin secretion, resistance to peripheral
actions of insulin, or both.
● Metabolic disorder caused by inadequate insulin production or insulin
action or both leading to elevated levels of blood glucose
Types of Diabetes Mellitus
● Gestational Diabetes Mellitus- High blood glucose levels during

pregnancy are linked to difficulties for both the mother and the child.
GDM normally goes away after pregnancy, but women who have it and
their children are more likely to develop type 2 diabetes later in life.
● Type 1 Diabetes Mellitus- can occur at any age, but it is most common
in children and adolescents. In type 1 diabetes, the body generates
very little or no insulin, requiring daily insulin injections to keep blood
sugar levels in control.
● Type 2 Diabetes Mellitus- most common, accounting for roughly 90% of
all diabetes cases. When you have type 2 diabetes, your body does not
use the insulin it generates effectively. A healthy lifestyle, which
includes increased physical activity and a balanced diet, is the
cornerstone of type 2 diabetes management. Most persons with type 2
diabetes, however, will eventually need oral medications and/or insulin to
keep their blood glucose levels under control.
ANATOMY &
PHYSIOLOGY (only
The pancreas consists of islet cells (islets of Langerhans) that create and
release important hormones directly into the bloodstream. Two of the main
pancreatic hormones are insulin, which acts to lower blood sugar, and
glucagon, which acts to raise blood sugar. Maintaining proper blood sugar
levels is crucial to the functioning of key organs including the brain, liver, and
kidneys.
ETIOLOGY
Type 2 Diabetes
Predisposing Factors (Non-modifiable)
● Age- Age equal to or greater than 45 years

● Hereditary(Genetics)- Family history of diabetes (e.g., parents or
siblings with diabetes)
● Race- African American, Hispanic/Latino American, American Indian, or
Alaska Native (some Pacific Islanders and Asian Americans are also at
higher risk
Precipitating Factors (Modifiable)
● Prediabetes- Insulin resistance develops in your cells, and your

pancreas is unable to produce enough insulin to overcome this
resistance. Sugar accumulates up in your bloodstream instead of going
into your cells, where it is needed for energy.
● Previously identified impaired fasting glucose or impaired glucose
tolerance
● Weight/Obesity (i.e., ≥20% over desired body weight or body mass
index ≥30 kg/m2) - Excessive weight or obesity, which induces insulin
resistance, is one of the variables that contribute to type 2 diabetes.
● Inactivity or sedentary lifestyle- Lack of exercise can also cause
insulin resistance and impaired insulin secretion.
● Hypertension (≥140/90 mm Hg)
● History of gestational diabetes or delivery of a baby over 9 lbs
SYMPTOMATOLOGY
(significant features/ 3 main signs and symptoms (3 P’s)
manifestations)
● Polyuria (Frequent urination)
● Polydipsia (Increased thirst)
● Polyphagia (Extreme hunger)
Additional S&S
● Unexplained weight loss

● Presence of ketones in the urine (ketones are a byproduct of the
breakdown of muscle and fat that happens when there's not enough
available insulin)
● Delayed wound healing
● Fatigue and weakness
GENERAL
PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS
● Glycated Hemoglobin (A1c) Test- This blood test indicates your
average blood sugar level for the past two to three months. It measures
the percentage of blood sugar attached to hemoglobin, the oxygen-
carrying protein in red blood cells.
● Random Blood Sugar Test - A blood sample will be taken at a random
time. Regardless of when the patient last ate.
● Fasting Blood Sugar Test- A blood sample will be taken after an
overnight fast.
● Oral Glucose Tolerance Test - For this test, the patient fast overnight,
and the fasting blood sugar level is measured. Then the patient will drink
a sugary liquid, and blood sugar levels are tested periodically for the next
two hours.
N/A
MEDICAL Nutritional Management

MANAGEMENT
● Diet Meal Plan (focuses on the percentages of calories that come from
carbohydrates, proteins, and fats)
○ bread/starch, vegetable, milk, meat, fruit, and fat. Foods within
one group (in the portion amounts specified) contain equal
numbers of calories and are approximately equal in grams of
protein, fat, and carbohydrate.
● Exercise- lower blood glucose and reducing cardiovascular risk factors
● Insulin
o Rapid-acting (taking effect within a few minutes and lasting 2-4

hours)
o Regular or short-acting (taking effect within 30 minutes and lasting

3-6 hours)
o Intermediate-acting (taking effect in 1-2 hours and lasting up to 18

hours)
o Long acting (taking effect in 1-2 hours and lasting beyond 24

hours)
o Ultra-long-acting (taking effect in 1-2 hours and lasting 48 hours
Note: Absorption occurs most quickly in the abdomen, followed by the arms,
thighs, hips, and subscapular regions. (sites for insulin administration)
● Oral antidiabetic Agents (metformin)- suppressed gluconeogenesis
gluconeogenesis - conversion of non-carbohydrate substrates into

glucose

MANAGEMENT
N/A
Pero sabi ng isang book for TYPE 1 Diabetes (additional notes…)
Pancreas transplantations have been performed and have successfully

eliminated the need for exogenous insulin in some clients. At present, pancreas
transplants are being performed primarily on clients with type 1 diabetes who
also need kidney or other organ transplants because the serious side effects of
the antirejection medications do not justify a pancreas transplant alone.
Pancreatic islet cell transplants are also being done experimentally with
limited success but hold much promise for the future.
N/A
NURSING 1. Monitor vital signs and mental status.

MANAGEMENT (10) Rationale: To provide a baseline from which to compare abnormal
findings.
2. Advise patient about the importance of an individualized meal plan in
meeting weekly weight loss goals and assist with compliance.
Rationale: To help maintain blood glucose levels as close to normal as
possible, and maintain or lose weight.
3. Monitor for signs of hypoglycemia.
Rationale: Severe hypoglycemia can cause accidents, injuries, coma,
and may even prove fatal.
4. Instruct patient to take oral hypoglycemic medications as directed.
Rationale: To help in controlling the blood glucose level.
5. Teach the patient to treat hypoglycemia with crackers, or a snack.
Rationale: Hypoglycemia should be treated with a carbohydrate snack
(15g from a fast-acting source). Examples include fruit juice, soda, hard
candies, teaspoons of sugar, or commercially prepared glucose tablets.
6. Stress the importance of achieving blood glucose control.
Rationale: Control of blood glucose levels within the nondiabetic range
can significantly reduce the development and progression of
complications.
7. Teach the patient to rotate insulin injection sites.
Rationale: Systematic rotation of injection sites has traditionally been
recommended to prevent lipodystrophy (atrophy or hypertrophy in the
subcutaneous fat that decreases the absorption of insulin)
8. Teach the patient how to perform home glucose monitoring.
Rationale: Blood glucose is monitored before meals and at bedtime.
Glucose values are used to adjust insulin doses.
9. Explain the importance of exercise in maintaining or reducing weight.
Rationale: Exercise plays a role in lowering blood glucose and reducing
cardiovascular risk factors for patients with diabetes. Exercise lowers
blood glucose levels by increasing the uptake of glucose and improving
the utilization of insulin.
10. Provide written information about diabetes management for the patient to
refer to.
Rationale: To reinforce learning and convey the maximum amount of
information
PRIORITY NURSING 1. Risk for Unstable Blood Glucose r/t medication management.
DIAGNOSIS (5) 2. Imbalanced Nutrition Less Than Body Requirements r/t reduction of
carbohydrate metabolism due to insulin deficiency, inadequate intake
due to nausea and vomiting.
3. Fluid Volume Deficit r/t osmotic diuresis from hyperglycemia, polyuria,
decreased fluid intake.
4. Impaired Skin Integrity r/t decreased sensory sensation, impaired
circulation, decreased activity / mobilization, lack of knowledge of skin
care.
5. Activity Intolerance r/t weakness due to decreased energy production.
PROGNOSIS
Good Prognosis when diabetic management is strictly followed.
When compared to the entire population, the average life expectancy is around
70 percent. After manifestation, the average survival time is more than 18 years.
Diabetic coma is no longer a leading cause of death. Today, approximately 75%
of diabetics die as a result of vascular problems, the most common of which is
coronary heart disease.
REFERENCES Brunner - p. 3842

Harrison - p. 2842
Sir Roy yassss sakalam
Diagnostics books nasa drive
Med surg Nursing book - p. 624 maganda ito na book skl
6. Myasthenia Gravis (MG) -
DEFINITION ● It is a chronic autoimmune neuromuscular disorder characterized by
fatigue and severe weakness of skeletal muscles.
ANATOMY &
PHYSIOLOGY (only Neuromuscular System
for the major organ) ● nervous system and muscles works together to control, direct and allow
movement of the body
Neuromuscular junction (NMJ)
● a highly specialized synapse between a motor neuron nerve terminal and

its muscle fiber that are responsible for converting electrical impulses
generated by the motor neuron into electrical activity in the muscle fibers.
Synaptic end bulb
● located towards the end of the axon terminal, closest to the muscle fiber
● Site of communication between neurons or between neuron and target
cell/ organ
Synaptic Cleft
● a space that separates two neurons
● helps to decode the message
Axon
● Long projections carrying electrochemical impulses away from the body
of the neuron
Axon Terminal
● After the signal leaves the axon in a healthy neuron it goes to the axon
terminal (the end of the axon) where it synapses (where a nerve signal
passes) with another neuron, muscle or glands to cause an action of
some type.
Thymus Gland
● Located in the upper chest beneath the sternum
● May trigger or maintain the production of antibodies that result in the
muscle weakness
1. Age
a. ( 20 to 40 years of age for Female and 60 to 70 years for men)
2. Sex
a. (F > M)
3. Autoimmune disorders
a. Own body produces circulating antibodies, blocking acetylcholine
receptors at the postsynaptic myoneural junction. Individuals with
conditions such as autoimmune thyroid disorders, rheumatoid
arthritis, and SLE frequently have MG.
Precipitating
1. Infection
2. Medication (aminoglycosides, anti-arrhythmic drug, quinolones)
SYMPTOMATOLOGY Most commonly affected - Muscle of the face

(significant features/ ● Weakness of ocular muscles
manifestations) ○ Ptosis
○ Diplopia
○ Strabismus
● Weakness of facial muscles
○ Bland, mask-like expression
● Weakness of lip muscle (orbicularis oris muscle)
○ Myasthenic sneer
● Weakness of tongue
○ Dysarthria
● Weakness of throat muscles
○ Dysphagia
○ Drooling
○ Risk for aspiration
● Weakness of jaw muscles
○ Drooping of jaw
● Weakness of neck muscles
○ Head bobbing
● Weakness of diaphragm and intercostal muscles
○ Respiratory difficulty
Myasthenic crisis
● Severe form of MG.
● The classic symptoms of MG become more severe therefore immediate
action is needed.
● Occurs when Pt w/ MG are undermedicated with tensilon.
Cholinergic crisis
● Happens when the myoneural or neuromuscular junction is
overstimulated due to excessive acetylcholine.
● Respiratory difficulty and bradycardia are manifestations of this crisis
● Occurs when Pt w/ MG are overmedicated with tensilon.
GENERAL
PATHOPHYSIOLOGY
(Simplified)
1. Antibodies at acetylcholine receptors

2. Impaired transmission of impulses
3. Voluntary muscle weakness

DIAGNOSTIC TESTS N/A
1. Anticholinesterase (tensilon) test
a. the patient is injected with edrophonium chloride (Tensilon), a
short-acting anticholinesterase. Patients with MG show a
significant improvement in muscle strength that lasts
approximately 5 minutes. This test is also used to differentiate
myasthenic crisis (caused by insufficient medication, so the
patient shows improvement with the drug) from cholinergic crisis
(caused by overmedication, so the patient does not show
improvement).
b. Immediate improvement in muscle strength after administration of
this agent represents a positive test and usually confirms the
diagnosis.
2. Repetitive nerve stimulation (RNS)
a. demonstrates a decrease in successive action potentials
3. Single-fiber electromyography
a. can detect delayed or failed neuromuscular transmission in
muscle fibers supplied by a single nerve fiber. Serum assay of
circulating acetylcholine receptor antibodies, if increased, is
strongly diagnostic of MG.
b. detects a delay or failure of neuromuscular transmission and is
about 99% sensitive in confirming the diagnosis of myasthenia
gravis
4. Ice test
a. indicated in patients who have cardiac conditions or asthma. With
this test, an ice pack is held over the patient’s eyes for 1 minute;
the ptosis should temporarily resolve in a patient with myasthenia
gravis
b. improvement in ptosis is due to the cold decreasing the
acetylcholinesterase break-down of acetylcholine at the
neuromuscular junction
MEDICAL 1. Administration of anticholinesterase medications

MANAGEMENT 2. Immunosuppressive therapy
a. to reduce production of the antibody.
b. Corticosteroids suppress the patient’s immune response,
decreasing the amount of antibody production, and this correlates
with clinical improvement.
3. Intravenous immune globulin (IV IG)
a. used to treat exacerbations; however, in selected patients, it is
used on a long-term adjunctive basis.
b. Involves the administration of pooled human gammaglobulin and
improvement occurs in a few days
c. The effects of IVIG typically last only about 28 days after infusion,
and complications include headache, migraine exacerbation,
aseptic meningitis, and flulike symptoms
4. Therapeutic plasma exchange (TPE)
a. formerly referred to as plasmapheresis
b. used to treat exacerbations.
c. The patient’s plasma and plasma components are removed
through a centrally placed large-bore double-lumen catheter.
d. The blood cells and antibody-containing plasma are separated,
after which the cells and a plasma substitute are reinfused.
e. Temporary reduction in the level of circulating antibodies is
provided with TPE.
f. A typical course consists of daily or alternate-day treatment, and
the number of treatments is determined by the patient’s response.
g. Symptoms improve in 75% of patients undergoing TPE; however,
improvement lasts only a few weeks after treatment is completed
● Anticholinesterases/ cholinesterase inhibitors
○ Stops breakdown of acetylcholine
○ Increases concentration of acetylcholine around the muscle cells
and helps counteract the effects of acetylcholine receptor
antibodies
○ Pyridostigmine bromide (Mestinon)
■ first line of therapy
■ It provides symptomatic relief by inhibiting the breakdown
of acetylcholine and increasing the relative concentration
of available acetylcholine at the neuromuscular junction.
■ to prevent muscular manifestations during the
perioperative period
■ Cholinesterase inhibitors are used in MG to enhance the
effects of acetylcholine at the remaining skeletal muscle
receptors. Cholinesterase inhibitors do not cure or change
the underlying pathophysiologic processes, but they can
provide effective, lifelong improvement of symptoms.
Because the cholinesterase inhibitors are nonselective,
the neuromuscular, muscarinic, and ganglionic junctions
are each affected
■ Cholinesterase inhibitors should not be administered to
patients experiencing obstruction of the intestinal or
urinary tract. Caution is advised when administering these
drugs to patients with asthma, hyperthyroidism,
bradycardia, or peptic ulcer disease. Cholinesterase
inhibitors can cross the placenta; reproductive counseling
is indicated.
○ Neostigmine (Prostigmin)
■ used only when pyridostigmine is unavailable
● Immunosuppressive drugs
○ Prednisone -
■ Reduce production of autoantibodies
■ given daily and maintained for 1 to 2 months; as
symptoms improve, the medication is tapered
■ most important immunosuppressant and provides short-
and long-term benefit.
● Cytotoxic medications
○ used to treat myasthenia gravis if there is an inadequate
response to steroids.
○ Azathioprine (Imuran)
■ inhibits T lymphocytes and B cell proliferation and reduces
acetylcholine receptor antibody levels.
● Antidote for tensilon test: Atropine

○ blocks the ACh receptors on nerve cells
○ to control potential side effects of this medication, which include
bradycardia, asystole, bronchoconstriction, sweating, and
cramping.

MANAGEMENT 1. Thymectomy - recommended for patients younger than 60
- Reduces muscle weakness
a. Transcervical approach and transsternal approach
i. considered less invasive
b. Latter approach
i. allows a more extensive removal of the gland; however, it
also poses more potential complications because it
involves splitting the sternum.
2. Tracheostomy
a. required when the diaphragm or intercostal muscles are involved
1. Assess & monitor VS

a. To check for signs of infection & if there is hemorrhage
2. Assess incision or operative site
a. To check for any signs of infection, and to check if the dressing is
dry and intact and needs replacement
3. Perform hand hygiene before and after dressing changes and any
contact with the surgical site
a. To prevent transmission of microorganisms
4. Provide sterile dressing changes.
a. To prevent infection and promote wound healing
5. Provide meticulous pulmonary hygiene: turning, deep breathing, and
coughing at least every 2 hours; use an incentive spirometer.
a. Regardless of surgical approach, measures are aimed at
preventing pulmonary complications of atelectasis and
pneumonia.
NURSING 1. Establish rapport.

MANAGEMENT (10) a. To facilitate patient’s cooperation and trust.
2. Assess Pt’s level of knowledge and ability to learn.
a. to obtain necessary information in creating a plan of care.
3. Determine degree of perceptual or cognitive impairment and ability to
follow directions.
a. Impairments related to age, chronic or acute disease condition,
trauma, surgery, or medications require alternative interventions
or changes in the care plan.
4. Assist with turning, deep breathing, and coughing at least every 2 hours.
Teach proper coughing techniques; use an incentive spirometer every 2
hours while the patient is awake.
a. Position changes promote lung expansion; coughing helps clear
secretions from the tracheobronchial tree.
5. Place in a semi-Fowler’s position.
a. This position expands the lungs and alleviates pressure from the
diaphragm, especially important if the patient is obese.
6. Plan meals to promote medication effectiveness.
a. Pyridostigmine should be given 30 minutes before the meal to
provide optimal muscle strength for swallowing and chewing.
7. Incorporate Pt’s eating style and pace when feeding
a. To avoid fatigue and frustrations with process
8. Provide environmental stimuli as needed
a. To maintain contact with reality, or reduce stimuli to lessen
anxiety that may worsen problem.
9. Teach caregivers the Heimlich maneuver and how to suction.
a. Knowing specific measures to take in case of aspiration
decreases both the patient’s and family’s anxiety and promotes
confidence in managing potential problems.
10. Teach clients to take medications at regularly scheduled times to
maintain appropriate level.
a. Maintains desired level of medication to manage the effects of
MG.
11. Encourage client to wear a Medic Alert bracelet indicating the name and
dosage of medications being taken.
a. Promotes safety and provides important information in an
emergency. If client experiences a myasthenia crisis and is
unable to talk, a Medic Alert bracelet notifies others of medical
condition and the need for medication.
12. Encourage continuation of facial exercise program
a. To maintain or improve muscle strength
PRIORITY NURSING 1. Ineffective breathing pattern/ ineffective airway clearance r/t

DIAGNOSIS (5) neuromuscular weakness and decreased energy, fatigue
2. Impaired verbal communication r/t neuromuscular weakness, fatigue,
and physical barrier (intubation)
3. Impaired swallowing r/t neuromuscular impairment (laryngeal and
pharyngeal) and muscular fatigue
4. Deficient Knowledge r/t disease process and understanding of methods
used to control disease and prevent complications
5. Risk for aspiration r/t impaired swallowing
PROGNOSIS There is NO CURE for myasthenia gravis; treatments do not stop the production
of the acetylcholine receptor antibodies.
The prognosis has improved strikingly as a result of advances in treatment.

Nearly all myasthenic patients can be returned to full for MG include
anticholinesterase medications, immunosuppressive agents, thymectomy,
plasmapheresis, and intravenous immunoglobulin (IVIg) - harrison
REFERENCES Balita - p150

Brunner - p. 5448 - 5456
Harrison - p. 3237
Lewis - p.1437 - 1439 and 1558
LeMone - p. 1538 - 1542
Lois - p. 1036
7. Peptic Ulcer Disease
DEFINITION A Peptic Ulcer is an ulceration in the mucosal wall of the stomach, pylorus,
duodenum, or esophagus in portions accessible to gastric secretions; erosion may
extend through the muscle. vc
ANATOMY &
PHYSIOLOGY (only
STOMACH
Stomach Lining:
● Mucosa (innermost) - top layer releases mucous rich in bicarbonate
which protects lining from acid & has gastric pits that contains:
- Parietal cells: HCL
- Chief Cells: pepsinogen
- G cells: gastrin
● Epithelial Layer: absorbs & secretes mucus and digestive

enzymes
● Lamina Propria: contains blood and lymph vessels
● Muscularis Mucosa: contains smooth muscle which contract
during digestion
● Submucosa - contains con. Tissue, nerves & vessels

● Muscularis externa - 3 layers of muscles; aids in peristalsis
● Serosa (outermost) -
connective tissue which connects to
the organs
Regions of the Stomach

- Cardia: contains foveolar
cells-secretes mucus
- Fundus & Body: contains
Parietal cells (secretes HCL) & chief
Cells (secretes Pepsinogen)
- Pyloric Antrum: contains g-
cells (secretes Gastrin)
DUODENUM: contains Brunner

Gland (secretes mucus rich in
bicarb ion)
ETIOLOGY PREDISPOSING:
● Genetics / Family History
● History of Gastritis
- Gastritis can cause erosion of the stomach lining which may also
affect the duodenum. = weakened protective lining.
● Zollinger-Ellison Syndrome
- Tumor formation located in the duodenum & pancreas causes
over secretion of gastrin = increased stomach acid
PRECIPITATING:
● Helicobacter Pylori (H. Pylori)
- Produces urease which breaks urea = production of ammonia &
CO2 that neutralizes acid & breaks down mucosa
- Transmission: Oral-oral / fecal-oral
● Usage of NSAIDs
- Dec. production of prostaglandin which is important in the health of the
stomach lining
● Substance Abuse (Smoking & Alcohol)
- Smoking interferes with the GI’s protective mechanisms;
increases stomach acid production over time, and it reduces
bicarbonate production.
- Alcohol is known to cause gastric mucosal irritation and
nonspecific gastritis
● Other risk factors: Stress, caffeine, use of corticosteroids
SYMPTOMATOLOGY General S&Sx:

(significant features/ ● severe, sharp epigastric pain, may be referred to the shoulder;
manifestations) ● abdominal tenderness;
● N&V
● constipation/diarrhea
● burning sensation in the midepigastrium or the back/pyrosis
GASTRIC DUODENAL (more common)
● Food makes pain WORSE ● Food makes pain BETTER /

(1-2 hrs ac) relieves
● Gnawing, sharp pain (3-4 hrs pc)
● Weight loss ● Burning pain in the mid-
● Severe vomit blood: “coffee epigastric area 1 ½ to 3 hrs
ground” or bright after meal
red(hematemesis) ● Walk in middle of night w/ pain
● Normal weight
● Severe, tarry, dark stool
(melena)
GENERAL
PATHOPHYSIOLOGY
(Simplified)
1. Risk Factors
2. Increased enzymatic activity
3. Decreased mucosal resistance to digestive enzymes
4. Damage to gastroduodenal mucosal lining
5. Peptic Ulcer Disease

DIAGNOSTIC TESTS ● H. Pylori Tests
○ Stool Test
○ Blood Test
○ Urea Breath test: pt ingests urea tablet ( if h.pylori is present there
will be breakdown of urea into amonia & CO2 ); used to measure
CO2 levels
● Barium Swallow
○ Visualizes esophagus, stomach, duodenum & jejunum
○ NPO 6-8 hrs
○ BaSu4 per orem
○ X-ray taken standing up or lying down
○ After procedure: give laxative; instruct pt to increase OFI; inform
stool will be white for 24-72 hrs; observe for constipation &
abdominal distention
● Esophagogastroduodenoscopy (EGD) or UGI Endoscopy
○ Direct visualization of esophagus, stomach & duodenum
○ NPO 6-8 hrs
○ Give anticholinergics to reduce mucus secretion
○ After procedure: place pt on side-lying to prevent aspiration;
NPO until gag reflex returns (2-4 hrs after)
● Gastric Analysis
○ Measures secretion of HCL & pepsin
○ NPO 12 hrs
○ Insert NGT - connected to suction
○ Gastric contents collected q15 mins to 1 hr
● CT Scan abd. w/ contrast
MEDICAL
MANAGEMENT
Ulcer Healing:
● H2 Receptor Antagonist(e.g. Ranitidine/Famotidine)
○ blocks histamine which causes parietal cell dec. secretion of HCL
○ Do NOT give @ same time as antacids ; wait 30-45 mins); ulcer
healing
● Proton Pump Inhibitor (e.g. Omeprazole)
○ attaches to the “protein-pump” on the parietal cells which is
(H+/K+) & blocks the release of hydrogen ions (which would have
mixed w/ chlorid ions = HCL = dec. acid) ; ulcer healing
Initial H. Pylori Therapy
● Antibiotics (e.g. Metronidazole, Clarithromycin): used to kill H. Pylori
Decrease Acid Production:

● Antacids (e.g. Al Hydroxide, Mg Hydroxide, Calcium Carbonate):
neutralizes stomach acid and prevents production of pepsin
○ Interferes w/ many drugs: antibiotics, mucosal healing, h2 blockers
○ Give 1-2 hr/s ac
● Prostaglandin E1 Analogue: reduces gastric acid & enhances mucosal
resistance to injury
Mucosal Barrier Fortifiers (e.g. Carafate, Sucralfate): forms a protective coat;

lines the stomach & adheres to ulcer site & protects it from acids
○ Give on empty stomach 1-2 hrs ac
○ Do NOT give w/ antacids/ H2 blockers

MANAGEMENT ● Vagotomy: cut parts of vagus nerve to prevent stimulation of HCL
● Pyloroplasty: open the pylorus that has narrowed due to scarring
● Gastric Resection: remove diseased parts of the stomach (pyloric valve
& duodenum)
○ Billroth I (Gastroduodenostomy) : creation of an anastomosis
between the duodenum and the gastric remnant
○ Billroth II (Gastrojejunostomy) : constructed by sewing a loop
of jejunum to the gastric remnant ; prone to dumping syndrome

1) Monitor VS.
® To establish baseline data and to monitor for complications.
2) Assess incision or operative site
® To check for any signs of infection, and to check if the dressing
is dry and intact and needs replacement.
3) Assess bowel sounds.
® To check for bowel movement.
a) Maintain NPO status as prescribed for 1-3 days until
peristalsis returns.
b) Progress the diet from NPO to sips of clear water to 6
small bland meals a day.
4) Elevate HOB to semi-fowler’s position.
® Since the pt’s stomach surface area has been reduced, semi-
fowler’s position will help prevent reflux.
5) Watch out for Dumping Syndrome, hemorrhage, diarrhea,
hypoglycemia, & vitamin B12 deficiency.
® Since the stomach has been reduced, there is increased
chance for rapid emptying or dumping syndrome. Hypoglycemia
may occur due to inadequate nutrient absorption. The stomach is
responsible for the Vit B12 absorption and conversion.
NURSING 1. Assess VS.
MANAGEMENT (10) ® To establish baseline data.
2. Assess bowel sounds (Check tenderness of abdomen, stools, vomit).
® To check if there is bowel obstruction @ pylorus from chronic ulceration
(fibrosis is present).
3. Assess pain (Onset, Location, Duration, Characteristics, Aggravating
factors, Relieving factors).
® Clients with gastric ulcer typically demonstrate pain 1 to 2 hours after
eating. The client with duodenal ulcers demonstrate pain 2 to 4 hours
after eating or in the middle of the night. With both gastric and duodenal
ulcers, the pain is located in the upper abdomen and is intermittent.
4. Weigh pt.
® Weight loss is an indication of inadequate nutritional intake. Gastric
ulcers are more likely to be associated with vomiting, loss of appetite and
weight loss than duodenal ulcers.
5. Monitor for signs of GI bleeding.
® This may require prompt or emergent intervention.
6. Provide therapeutic environment for adequate rest and provide non-
pharmacological measures for pain such as deep breathing, and guided
imagery.
® Nonpharmacological relaxation techniques will decrease the production
of gastric acid, which in turn will reduce pain.
7. Provide Pt. Education regarding dietary modifications.
a. Eat bland diet freq. small meals.
b. Provide for adequate rest.
c. Lie down for 30 mins pc eating.
d. Don’t drink fluids w/ meals but pc.
e. Avoid sugary foods/drinks or very hot or cold.
f. Eat high protein, fiber & low carb meals.
g. Avoid spicy & acidic ( tomato/citric or fruits/juices; caffeine,
chocolate, alcohol, fried food.
® Caffeine stimulates the secretion of gastric acid. Coffee, even if
decaffeinated, contains a peptide that stimulates the release of gastrin and
increases acid production. Alcohol causes gastric irritation and increases
gastric pain.
8. Encourage cessation of smoking.
® Smoking decreases the secretion of bicarbonate from the pancreas into
the duodenum, resulting in increased acidity of the duodenum.
9. Instruct the client to avoid the use of aspirin, corticosteroids, and
NSAIDs.
® These medications may cause irritation of the gastric mucosa.
10. Administer medications as prescribed.
® To treat pain/ promote ulcer healing/ kill H.Pylori.
PRIORITY NURSING ● Acute pain related to effect of gastric acid secretion on damaged
DIAGNOSIS (5) tissue
○ Assess pain (Onset, Location, Duration, Characteristics,
Aggravating factors, Relieving factors).
® Clients with gastric ulcer typically demonstrate pain 1 to 2 hours
after eating. The client with duodenal ulcers demonstrate pain 2 to
4 hours after eating or in the middle of the night. With both gastric
and duodenal ulcers, the pain is located in the upper abdomen and
is intermittent.
○ Provide therapeutic environment for adequate rest and provide
non-pharmacological measures for pain such as deep breathing,
and guided imagery.
® Nonpharmacological relaxation techniques will aid in the
decrease of the production of gastric acid, which in turn will reduce
pain.
● Anxiety related to an acute illness
○ Establish rapport with the patient.
○ Inform the patient regarding the procedures and why it is being
performed.
○ Inform the patient of the medications that need to be administered
and why it is being given.
● Imbalanced nutrition: Less than Body Requirements related to
changes in the diet (anorexia, abdominal pain)
○ Weigh pt.
® Weight loss is an indication of inadequate nutritional intake.
Gastric ulcers are more likely to be associated with vomiting, loss
of appetite and weight loss than duodenal ulcers.
○ Provide Pt. Education regarding dietary modifications.
■ Eat bland diet freq. small meals.
■ Provide for adequate rest.
■ Lie down for 30 mins pc eating.
■ Don’t drink fluids w/ meals but pc.
■ Avoid sugary foods/drinks or very hot or cold.
■ Eat high protein, fiber & low carb meals.
■ Avoid spicy & acidic ( tomato/citric or fruits/juices; caffeine,
chocolate, alcohol, fried food.
® Caffeine stimulates the secretion of gastric acid. Coffee, even if
decaffeinated, contains a peptide that stimulates the release of
gastrin and increases acid production. Alcohol causes gastric
irritation and increases gastric pain.
● Deficient knowledge r/t prevention of symptoms and management of
the condition
○ Encourage cessation of smoking.
® Smoking decreases the secretion of bicarbonate from the
pancreas into the duodenum, resulting in increased acidity of the
duodenum.
○ Instruct the client to avoid the use of aspirin, corticosteroids, and
NSAIDs.
® These medications may cause irritation of the gastric mucosa.
● Risk for Deficient Fluid Volume r/t GI bleeding and/or N&V
○ Assess bowel sounds (Check tenderness of abdomen, stools,
vomit).
® To check if there is bowel obstruction @ pylorus from chronic
ulceration (fibrosis is present).
○ Monitor for signs of GI bleeding.
® This may require prompt or emergent intervention.
PROGNOSIS When the underlying cause of peptic ulcer disease is addressed, the
prognosis is excellent. Most patients are treated successfully with the
eradication of H pylori infection, avoidance of nonsteroidal anti-inflammatory
agents (NSAIDs), and the appropriate use of antisecretory therapy.
If untreated:
Complications may occur such as bleeding, perforation & obstruction
REFERENCES
8. Multiple Sclerosis
DEFINITION An autoimmune disease that affects the myelin sheath of the neurons in the
CNS. It affects the neurons in the brain and spinal cord, and this leads to many
sensory and motor problems.
ANATOMY &
PHYSIOLOGY (only
Glial cells - responsible for producing myelin in the CNS

Neurons (nerve cells) – cells in the nervous system that send and receive signals
from the brain.
➔ Dendrites - receive the signal needed
➔ Soma (body) - helps pass on the signal it just received from the dendrites
to the rest of the neuron
➔ The signal goes down and passes where the soma of the neuron and axon
connect at the axon hillock
➔ Signal goes down to axon. For the axon to be able to deliver this signal
properly to either another neuron, muscle, or gland, it must be nicely be
insulated and protected by the myelin sheath
➔ Myelin Sheath- made up of schwann cells (fats and protein); surrounds
the axon
➔ Axon terminal – After the signal leaves the axon in a healthy neuron it
goes to the axon terminal (the end of the axon) where it synapses (where
a nerve signal passes) with another neuron, muscle or glands to cause
an action of some type.
ETIOLOGY EXACT CAUSE IS UNKWOWN!
More prone: 20-40 y/o, women, those with genetic predisposition

● Genetic predisposition – presence of a specific cluster (haplotype) of
human leukocyte antigens on the cell wall. Its presence may increase
susceptibility to factors, such as viruses, that trigger the autoimmune
response activated in MS.
Risk factors: AVATAN

● Autoimmune activity – immune system attacks own body; results in
demyelination (destruction of myelin) in brain and spinal cord
● Vascular Lesions — lesions in the brain or spinal cord may result to
scarring which may disrupt normal electrical transmission between
impulses.
● Allergic Response, Viral Infection, Toxins — allergens in the
environment, viruses and toxins may also be triggering agents in MS,
causing demyelination.
● Trauma — trauma may cause damage to the cells that produce myelin or
to the myelin sheath itself.
● Anoxia — When the brain is insufficiently oxygenated, anoxia and
ischemia may occur. Ischemia causes rapid energy depletion which may
lead to demyelination.
● Nutritional Deficiencies and Anorexia Nervosa— research found out
that deficiency in vitamins that help electrical impulse transmission (B
complex vitamins and vitamin D) may contribute to the occurrence of MS.
SYMPTOMATOLOGY The signs and symptoms of MS are varied and multiple, reflecting the location of
(significant features/ the lesion. Symptoms some and go — relapsing-remitting multiple sclerosis
manifestations) (RRMS).
● Ataxic gait, scanning speech, intention tremors (if in CEREBELLUM)

● Nystagmus, diplopia, vision loss and/or scotoma (if in OPTIC NERVE)
● Bladder incontinence or retention; increased DTR, muscle spasms,
muscle fatigue; pain, paresthesia, proprioception loss, heat and temp
sensitivity (in SPINAL CORD)
GENERAL
PATHOPHYSIOLOGY
(Simplified)
Explanation:
The clinical presentation of MS starts from the destruction of Glial cells in
the central nervous system (CNS) which includes the brain and spinal cord. Glial
cells are responsible for producing myelin in the CNS. Myelin is a substance that
insulates the speed at which impulses are transmitted. In MS, the myelin is
damaged. The process in which the myelin is destroyed is called demyelination.
In order to compensate, neuroglial tissue proliferate to form myelin. Instead
of myelin, hard yellow plaques of scar tissue forms. This scar tissue disrupts the
nerve conduction and the axon begins to degenerate. Demyelination results to
impaired transmission of nerve impulses (slowed or blocked).
In the cerebellum, impaired transmission causes ataxic gait, scanning
speech (speaking with abnormally long pauses between words or individual
syllables of words) and intention tremors (tremors when person is in motion).
In the optic nerves, impaired transmission causes nystagmus (dancing
eyes), diplopia, vision loss and/or scotoma (blind spot).
In the brain's cells and frontal lobe, impaired transmission causes emotional
lability and even some degree of memory loss.
In the spinal cord, impaired transmission leads to bowel and bladder
incontinence or retention. The corticospinal tract will also be affected, resulting to
increased deep tendon reflexes, muscle spasms and muscle fatigue. The sensory
pathways will also be impaired causing pain, paresthesia, proprioception loss and
heat & temperature sensitivity.

DIAGNOSTIC TESTS ● Bladder dysfunction
● MRI: lesions, plaques in brain/spinal cord
● Lumbar puncture: assesses spinal fluid for specific proteins called
oligoclonal bands (which are immunoglobulins). If these are present it
shows there is inflammation in the CNS.
● Assess pt’s symptoms
MEDICAL NO CURE exists for MS. Treatment focuses on relieving symptoms, delay
MANAGEMENT progression of disease.
· Disease-Modifying Therapies (to reduce relapse)
o Beta interferon (Rebif, Betaferon): decreases the number of
relapses of symptoms by decreasing inflammation and the
immune system response
o Corticosteroids (prednisone): decrease inflammation
o mitoxantrone (Novantrone) – those with secondary progressive
RRMS
· Symptom Management
o Baclofen (skeletal muscle relaxant; for spasms)
o Beta-adrenergic blockers – propranolol; Anticonvulsant –
gabapentin (ataxia)
o Anticholinergic agents (Oxybutynin) – relaxes bladder; for
overactive
o Cholinergic (Bethanechol) – helps with completely emptying the
bladder by helping bladder contract fully

MANAGEMENT
NURSING 1. Promote physical mobility (walking, daily exercise for muscle

MANAGEMENT (10) stretching).
R: Walking improves the gait while muscle stretching improves or stops muscle
spasm.
2. Instruct patient to avoid very strenuous activity.

R: Very strenuous physical exercise is not advisable, because it raises the body
temperature and may aggravate symptoms.
3. Minimize effects of immobility (perform coughing and deep breathing

exercises)
R: Effective coughing and deep breathing technique is helpful when it comes to
clearing secretions which may have accumulated in the bronchi as a complication
of decreased physical activity and immobility.
4. If ataxia is present, instruct pt to walk with feet apart or use assistive

device (walker, cane).
R: Walking with feet apart widen the base of support and increase walking stability,
while assistive device aids pt in supporting his/her gait and prevent injury.
5. Advise pt to wear wrist cuffs or weighted bracelets if experiencing

intentional tremors.
R: This assistive device is designed to help reduce symptoms in individuals with
persistent tremors.
6. Make accessibility to bathroom or urinal/bedpan easy if there is overactive

bladder.
R: To avoid peeing in undies or in bed.
7. Instruct pt to increase OFI.

R: To prevent stasis of urine and to keep it from becoming too concentrated.
8. Instruct pt to consume high fiber foods (beans, broccoli) if constipation is

present.
R: It helps add bulk and weight to stools, soften them, and stimulate bowel
movements
9. Coordinate with SLP (speech-language pathologist) if dysphagia,

dysarthria are noted, and reinforce instructions.
R: SLP evaluates speech and swallowing, and instruct strategies to compensate
for speech and swallowing problems.
10. Help pt in improving cognitive function (Vision: eye patch for diplopia;
Emotional responses: emotional support).
R: An eye patch or a covered eyeglass lens may be used to block the visual
impulses of one eye if the patient has diplopia, while emotional support assists
patients to adapt to the changes and uncertainties associated with MS and to cope
with the disruption in their lives.
PRIORITY NURSING 1. Impaired bed and physical mobility related to weakness, muscle paresis,
DIAGNOSIS (5) spasticity, increased weight
2. Risk for injury related to sensory and visual impairment
3. Impaired urinary elimination (urgency, frequency, incontinence), constipation,
and bowel incontinence related to nervous system dysfunction
4. Impaired verbal communication and risk for aspiration related to cranial nerve
involvement
5. Chronic confusion related to cerebral dysfunction
PROGNOSIS MS itself is rarely fatal, but complications may arise from severe MS, such as chest
or bladder infections, or swallowing difficulties.
It is estimated that for all MS patients the chance of walking unaided in 15 years
following disease onset is 50%. 1/2 of the patients will need assistance in walking
or will be wheelchair bound; another 1/2 of the patients will be able to ambulate
unaided.
The average longevity in the population of patients with MS is very difficult to

estimate because it varies widely from patient to patient. Average life span of 25
to 35 years after the diagnosis of MS is made are often stated.
REFERENCES Hinkle, J. & Cheever, K. (2018). Brunner & Suddarths Textbook of Medical
Surgical Nursing. (14th ed.). Lippincott Williams & Wilkins.
Registered Nurse RN. (2018). Multiple Sclerosis Nursing | Multiple Sclerosis

Treatment, Symptoms, NCLEX Review. Retrieved from
https://www.registerednursern.com/multiple-sclerosis-ms-nclex-review/
9. Cerebrovascular Disease
DEFINITION Cerebrovascular disease is an umbrella term that refers to a functional
abnormality to the central nervous system (CNS) that occurs when the normal
blood supply to the brain is disrupted.
2 MAJOR TYPES:
1. Ischemic stroke
- formerly referred as “brain attack”
- “thrombotic/ embolic”
- a sudden loss of function resulting from the occurrence of
vascular occlusion and hypoperfusion
Classifications:
● Large artery thrombosis- caused by atherosclerotic plaques in the large
blood vessels of the brain. Thrombus formation and occlusion at the site
of the atherosclerosis result in ischemia and infarction.
● Small penetrating artery thrombosis- a common type of ischemic stroke
that affects one or more vessels; also called lacunar strokes due to the
build up of cavity after the death of infarcted brain tissue.
● Cardiogenic embolic strokes - associated with cardiac dysrhythmias,
usually atrial fibrillation, valvular heart disease and thrombi in the left
ventricle. Emboli originate from the heart and circulate to the cerebral
vasculature, most commonly the left middle cerebral artery, resulting in a
stroke. Embolic strokes may be prevented by the use of anticoagulation
therapy in patients with atrial fibrillation.
● Cryptogenic strokes- no known cause, and strokes from other causes,
such as illicit drug use (cocaine), coagulopathies, migraine/vasospasm,
and spontaneous dissection of the carotid or vertebral arteries.
2. Hemorrhagic stroke
- Extravasation of blood into the brain or subarachnoid
space
Strokes using the time course are commonly classified in the ff:
- Transient ischemic attack (TIA) : sudden loss of motor, sensory, or visual
function which may last a few seconds or minutes but not longer than
24hrs (“mini strokes” ; same pathology w/ stroke but no cerebral
infarction occurs)
- Reversible ischemic neurologic deficit: signs and symptoms are
consistent with but more pronounced than a TIA and last more than 24
hrs.
- Stroke in evolution: worsening or neurologic signs and symptoms over
several minutes/hours (a progressing stroke)
- Completed stroke: stabilization of the neurologic signs and symptoms.
No further progression of the hypoxic insult to the brain.
ANATOMY &
PHYSIOLOGY (only
The brain is also divided into several lobes:
● Frontal lobe- responsible for problem solving and judgment and motor
function.
● Parietal lobe- manages sensation, handwriting, and body position.
● Temporal lobe- involved with memory and hearing.
● Occipital lobe- contains the brain's visual processing system.
The brain is surrounded by a layer of tissue called the meninges. The skull
(cranium) helps protect the brain from injury.
ETIOLOGY Predisposing:
● Age
○ high risk groups of people over the age of 55
● Male gender
● African-Americans
Precipitating:
● Hypertension
● Cardiovascular diseases
○ Atrial fibrillation
○ CAD
○ Heart failure
○ Left ventricular hypertrophy
○ Myocardial infarction (especially anterior)
○ Rheumatic heart disease
● High cholesterol levels
● Obesity
● Elevated hematocrit
○ Increases the risk of cerebral infarction
● Smoking
● Diabetes mellitus
○ Associated with accelerated atherogenesis
● Drug abuse (cocaine)
● Excessive alcohol consumption
● Oral contraceptive use
○ Increases risk, especially with coexisting HTN, smoking, and high
estrogen levels
SYMPTOMATOLOGY BEFAST!! (ISCHEMIC STROKE)

manifestations) B- Loss of balance
E - Eyes (blurred vision)
F - Face drooping
A- Arm/leg weakness
S- Speech difficulty
T- Time to call 911
HEMORRHAGIC STROKE
- Severe headache
- Sudden decrease in LOC
- Possible focal seizures
GENERAL
PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS - CBC, platelet and clotting studies
- CT scan
- 12-lead electrocardiogram
- Carotid ultrasound
- Cerebral angiography
- Transcranial doppler (TCD)
- Electroencephalogram (EEG)
- Positive emission tomography (PET) scanning
- Transthoracic or transesophageal echocardiography
- MRI
- Magnetic resonance angiography (MRA)
MEDICAL
MANAGEMENT
● Thrombolytic therapy
○ Tissue plasminogen activator (t-PA) (3hrs)
● Antiplatelets
○ Aspirin
○ Dipyridamole
○ Clopidogrel
○ Ticlopidine
● Anticoagulants (blood thinners)
○ Warfarin
● Antihypertensives
● Neuroprotective agents

MANAGEMENT ● Carotid endarterectomy (for TIA or mild stroke)
● Hemicraniectomy - performed to reduce ICP from brain edema
1. Monitor BP and observe for s/sx of hypotension

2. Monitor neurologic status and report any changes in mental status/
neurologic function.
3. Assess and document the characteristics of the incision site.
4. Keep the incision site clean and dry.
5. Assist the physician in dressing.
NURSING 1. Monitor VS noting: hypertension or hypotension; compare BP

MANAGEMENT (10) readings in both arms.
R: Fluctuations in pressure may occur because of cerebral pressure or
injury in the vasomotor area of the brain.
2. Maintain patent airway and respiratory pattern.
R: Neurologic deficits of a stroke may include loss of gag reflex or cough
reflex; thus, airway patency and breathing pattern must be part of the
initial assessment.
3. Monitor and document neurological status and compare with
baseline.
R: Assesses trends in LOC and potential for increased ICP and is useful
in determining the location, extent, and progression or resolution of CNS
damage.
4. Closely monitor for bleeding
R: Intracranial bleeding is a major complication for stroke patients
5. Elevate the head of the bed
R: To decrease ICP
6. Maintain correct positioning by applying posterior splint to the
affected extremity.
R: Correct positioning is important to prevent contractures, maintain good
body alignment, and prevent compressive neuropathies, especially of the
ulnar and peroneal nerves.
a. Place a pillow in the axilla to prevent shoulder adduction.
R: This helps prevent edema and the resultant joint fibrosis that will
limit range of motion if the patient regains control of the arm.
b. Positioning the hand and fingers in slight supination.
R: To prevent hand edema
7. Turn the patient from side to side every 2 hours.

R: To promote venous return and prevent edema
8. Encourage the patient to engage in a passive ROM exercise
program.
R: The affected extremities are exercised passively 4 to 5 times a day to
maintain joint mobility, regain motor control, and prevent further
deterioration of the muscular system.
9. Administer supplemental oxygen as indicated.
R: Hypoxemia can cause cerebral vasodilation and edema formation.
10. Ensure safety by raising the side rails of the bed.
R: To reduce the risk of falling from the bed and assist in repositioning
the patient on the bed.
11. Assist with safe feeding
R: Decreases the risk for aspiration
12. Analyze voiding pattern and offer urinal or bedpan on patient’s

voiding schedule
PRIORITY NURSING 1. Impaired physical mobility r/t loss of balance and coordination
DIAGNOSIS (5) 2. Acute pain (shoulder) r/t hemiplegia
3. Self- care deficits r/t stroke sequelae
4. Disturbed sensory perception r/t altered sensory reception, transmission
or integration
5. Risk for impaired skin integrity r/t hemiparesis
PROGNOSIS - Strokes are generally more severe in patients with hemorrhagic stroke
(HS). Within the first 3 months after stroke, HS is associated with a
considerable increase of mortality, which is specifically associated with the
hemorrhagic nature of the lesion.
- The patient prognosis after an ischemic stroke is much more positive than
after a hemorrhagic stroke. In addition to killing off brain cells, hemorrhagic
stroke increases the risk of dangerous complications such as increased
intracranial pressure or spasms in the brain vasculature.
REFERENCES Hinkle, J. & Cheever, K. (2018). Brunner & Suddarths Textbook of Medical
Surgical Nursing. (14th ed.). Lippincott Williams & Wilkins.
10. Glaucoma -
DEFINITION Glaucoma is used to refer to a group of ocular conditions characterized by
elevated IOP (intraocular pressure) with a pressure > 21 mmHg/2.8 KPa which
damages the optic nerve.
1. Wide-Angle Glaucoma (Open Angle) – angle between the cornea and iris is
“open” or wide. This is because drainage system slowly gets clogged.
2. Narrow-Angle Glaucoma (Closed Angle) – angle between the cornea and iris
is too narrow for the aqueous humor to pass through because the lens is
pushing against the iris. Drainage system is blocked which leads to rapid
increase in pressure.
ANATOMY & Eyes

PHYSIOLOGY (only
Ito na lang draw niyo guys mas dali
● Cornea
● Iris
● Lens
● Optic Nerve
● Ciliary body - produces aqueous humor
● Lamina Cribrosa
● Aqueous fluid outflow system (Trabecular meshwork, schlemm’s canal
and aqueous veins
● African American Race – African-Americans over 40 years of age are

5x more likely to have glaucoma than Caucasians
● Fam History of Glaucoma – familial history with a possible genetic link
● Age – aging increases the vulnerability of the optic nerve over time make
it less able to withstand various affronts such as elevated eye pressure.
Precipitating
● Diseases (Diabetes & Hypertension) -
○ Diabetes - a complication of diabetes (diabetic retinopathy), can
damage the blood vessels of the retina causing growth of
abnormal blood vessels and can block the eye’s natural drainage
system
○ Hypertension - increased BP leads to reduced ocular blood flow
due to thickening and stiffening of the blood vessels
● Eye trauma - may damage the eye’s drainage system. The damaged
drainage canal can build up excess scarring. The scarring blocks fluid
flow.
● Prolonged use of corticosteroids - increases risk of glaucoma by
raising IOP when administered exogenously. It causes changes in the
aqueous fluid outflow system resulting in increased eye pressure.
SYMPTOMATOLOGY Wide-Angle
(significant features/ ● Eye pain
manifestations) ● Halos around lights
● Gradual loss of peripheral vision
● Inability to detect color
● Difficulty adjusting to darkness
Narrow-Angle
● Sudden onset of severe pain in the eye
● Headache
● Nausea
● Vomiting
● Blurred vision
GENERAL
PATHOPHYSIOLOGY
(Simplified)

DIAGNOSTIC TESTS
● Tonometry - assess IOP
● Visual Field Testing
● Imaging - to determine optic nerve damage
MEDICAL Pharmacologic Management

MANAGEMENT Medications to Lower Pressure
a. Decrease PRODUCTION of aqueous humor
○ Beta-adrenergic receptor antagonists (e.g. metipranolol)
○ Carbonic anhydrase inhibitors (e.g. acetazolamide)
b. Increase OUTFLOW of aqueous humor

○ Prostaglandin analogs
c. Decrease PRODUCTION & Increase OUTFLOW of aqueous humor

○ Alpha-adrenergic agonists
d. Constriction of pupil
○ Miotics

MANAGEMENT ● Trabeculoplasty - opens trabecular meshwork; treats wide-angle
glaucoma. Uses a beam of light to treat drainage. making it easier for
fluid to flow out of the front part of the eye.
● Iridotomy - makes a hole in the iris; used to treat narrow-angle

glaucoma
● Destroys humor-producing cells (cyclophotocoagulation laser) -
decreases the production of aqueous humor
● Implants - shunt fluid out of anterior chamber; aqueous humor bypasses

the trabecular meshwork
● Iridectomy - a surgical incision is made through the cornea to remove a

portion of the iris to facilitate aqueous drainage (much less commonly
performed)

1. Monitor status of the eye dressing after surgery
Rationale: To assess for surgical complications (e.g. presence of
bleeding)
2. Position the client in a semi-fowler’s position while having the client lie on
the unaffected side
Rationale: To reduce IOP in the affected eye
3. Assess the client and medicate or assist to avoid vomiting, coughing,

sneezing or straining
Rationale: These activities increase IOP
4. Place an eye patch or eye shield in place

Rationale: The eye patch or shield helps prevent injury to the operative
site
5. Assess comfort and watch out for complaints such as pain or scratchy
sensation in eye
Rationale: To immediately report to physician and may indicate
hemorrhage or other ocular emergency
NURSING 1. Administer the ophthalmic agent indicated for glaucoma

MANAGEMENT (10) Rationale: To help decrease IOP
2. Monitor vital signs

Rationale: Osmotic agents may lead to side effects such as hypotension,
tachycardia, etc.
3. Monitor intake and output q8

Rationale: Medications like osmotic agents acts as a diuretic and fluid
balance needs to be assessed.
4. Monitor the level of eye pain every 30 mins.

Rationale: Level of eye pain indicates effectiveness of medication. Lesser
eye pain means IOP may be decreasing
5. Inform the client that miotics may cause blurred vision and difficulty in
adjusting to darkness due to pupillary constriction
Rationale: To avoid alarm and stress to the client and for the client to be
cautious in walking to dark rooms
6. Provide sufficient lighting for the patient to carry out activities

Rationale: Adequate lighting helps to prevent injury
7. Encourage conversation to determine the client’s concerns and answer

questions
Rationale: To assess client’s anxiety levels and provide needed
knowledge and support
8. Provide a safe environment by removing excess furniture from client’s

surroundings
Rationale: Prevent falls and protects client from injury
9. Suggest large-print books, talking books, audiotapes or radio as

preferred by client
Rationale: These items compensate for vision loss
10. Explain procedures and treatment clearly and concisely but avoid
overload
Rationale: Encourages compliance and keeps client informed of nursing
interventions
PRIORITY NURSING 1. Acute pain r/t closed-angle glaucoma

DIAGNOSIS (5) 2. Disturbed sensory perception (visual) r/t peripheral vision loss
3. Anxiety r/t sensory visual impairment
4. Deficient knowledge r/t information misinterpretation/lack of
exposure/lack of recall
5. Risk for Injury r/t visual impairment or knowledge deficit
PROGNOSIS Glaucoma isn’t curable however medications may help slow down the
progress of glaucoma and prevent vision loss.
REFERENCES

3rd Yr 2nd Sem Oral Rev

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1.

Schizophrenia is a chronic illness requiring long-term management

(galing sa notes ni maam apol)

PHASES OF SCHIZOPHRENIA ah yess

The pattern of development of schizophrenia may be viewed in four phases: the

Phase I: The Premorbid Phase

Phase II: The Prodromal Phase

During the prodromal phase the person experiences substantial functional

Recognition of the behaviors associated with the prodromal phase provides an

Phase III: Schizophrenia

C. Continuous signs of the disturbance persist for at least 6 months. This 6-

D. Schizoaffective disorder and depressive or bipolar disorder with psychotic

E. The disturbance is not attributable to the physiological effects of a substance

F. If there is a history of autism spectrum disorder or a communication disorder

Phase IV: Residual Phase

YW RAH KADAGHAN BA DIAY ANI

• Schizophreniform Disorder: The client exhibits an acute, reactive psychosis

• Shared psychotic disorder (folie à deux): Two people share a similar

• Schizotypal personality disorder: This involves odd, eccentric behaviors,

ANATOMY & Brain ra man ni diba? IYAKKK T-T

Areas of the Brain Affected

● Two major groups of dopamine receptors and their highest tissue

ETIOLOGY Predisposing Factors

SYMPTOMATOLOGY Schizophrenia is characterized by positive and negative symptoms that are

Positive or Hard Symptoms

Negative or Soft Symptoms

LABORATORY & Laboratory findings

● SCALE FOR THE ASSESSMENT OF NEGATIVE SYMPTOMS (SANS)

YW AMBOT UNSA NI WALA GI EXPLAIN SA BOOK TABANG

MEDICAL Cognitive behavioral therapy, behavioral skills training, supported

Coordinated specialty care (CSC) - general term used to describe recovery-

Antipsychotic medications- help reduce the intensity and frequency of

● Conventional (typical) antipsychotics- haloperidol

SURGICAL Surgical Procedures/s (if applicable)

Nursing Interventions (Post-op care)

NURSING 1. Initiate a nurse–patient relationship by using an accepting,

Galing ito kay maam apol (ADDITIONAL NOTES LANG HEHEHE)

Points to Consider When Working with Clients with Schizophrenia

1. Help them get treatment and encourage them to stay in treatment

PRIORITY NURSING 1. Impaired Verbal Communication r/t Altered Perceptions.

The North American Nursing Diagnosis Association’s (NANDA) nursing

*Mania - A distinct period of abnormally and persistently elevated, expansive, or irritable

*Hypomanic - A distinct period of abnormally and persistently elevated, expansive, or

Bipolar I – an individual who is experiencing a manic episode or has a history of

Bipolar II – recurrent depressive episodes with episodic occurrence of

Cyclothymic – chronic mood disturbance of at least 2-years’ duration involving

Substance/Medication-Induced Bipolar and Related Disorder – classified as

ANATOMY & White and Gray Matter

SYMPTOMATOLOGY Symptoms of mania may be observed on a continuum of three phases, each

Ito yung sa powerpoint ni maam apol:

1. Predisposing and Precipitating

LABORATORY & Laboratory findings

Mood Disorder Questionnaire (MDQ) - The Mood Disorder Questionnaire

MEDICAL 1. Individual Psychotherapy - Interpersonal and social rhythm therapy is

2. Group Therapy - Once an acute phase of the illness is passed, groups

3. Family Therapy - The ultimate objectives in working with families of

4. Cognitive Therapy - the individual is taught to control thought distortions

5. Electroconvulsive Therapy - done when the client does not tolerate or

2. Antimanic (e.g. lithium carbonate - DRUG OF CHOICE)

3. Anticonvulsants (e.g. valproic acid)

*depakote is valproic acid

SURGICAL Surgical Procedures/s (if applicable)

Nursing Interventions (Post-op care)