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1) Padiatric

Mrs.King 2,5 year-old Billy to the pediatricians officer because he has been irritable
and faversh since last night. Further history reveals that Billy also had a runny nose snd
cough for two day, and that has appatide and fluid intake have decreased since the fever
started .Billy is otherwise healthy,this is the first episodic illness. His physical examination
reveals slight, irritable , 2,5 year old girl ,pulling eat ears, temperature of 120 F , nasal
congestion with clear discharge ,tympanic membranes red and bulging bilaterally ,pharynx
slightly red without exudates. Chest clear ,abdomen soft without hepatosplenomegaly (HSM)
and no meningeal signs
The pediatrician diagnoses an upper respiratory infection (URL) an bilateral otitis (BOM)
and order amoxicillin 250 mg t.d.s for 10 day. You as the officer nurse, are to perform the
parentss teaching for Billys home care. During your discussion with Mrs. King ,she tells
you that she is concerned that Billy is jealous of his new baby sister when she holds the baby.
She is concerned about Billys development because he recently started to refuse using the
potty, a skill that is newly acquired Mrs. King is very attentive to both new baby and Billy
throught the interview, and she asks you for suggestions in how to help Billy cope to the
arrival. While doing so, she point out that her husband has been extra attentive to Billy since
his sister was born.


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8.

Subjective and objective Data


Billy 2,5 years-old
Runny nose and cough for two days
Got fever, so that appetite and fluid intake have dicrease
Temperature of 102 0F
Tympanic membranes red and bulging bilaterally
Upper respiratory infection (URI)
Bilateral otitis media (BOM)
Amoxicillin 250 mg

Etiology

Etiology of Upper respiratory infection


Upper respiratory infection is generally caused by the direct invasion of the inner lining
(mucosa or mucus membrane) of the upper airway by the culprit virus or bacteria. In order
for the pathogens (viruses and bacteria) to invade the mucus membrane of the upper airways,
they have to fight through several physical and immunologic barriers. Etiology of bilateral
otitis mediaOtitis media is middle ear infection caused by bacteria, fungi,and viruses that
cause inflammation of the mucosal lining.

Viral pathogens

RSV is a large RNA paramyxovirus that is most commonly associated with bronchiolitis
and pneumonia in very young persons, though it may cause acute respiratory disease in
persons of any age group.[ In northern climates, RSV is normally identified during annual
epidemics in the winter and early spring, but it should be considered in any neonate with
lethargy, irritability, or apnea, with or without otitis media. In older infants and children,
respiratory symptoms are usually more prominent, making diagnosis easier.
RSV was identified early as a pathogen that appeared to create long-term pulmonary
complications, primarily asthma, in as many as half of infants with bronchiolitis. RSV may
be particularly lethal for children with congenital heart disease, cystic fibrosis,
immunodeficiency, bronchopulmonary dysplasia, or prematurity of less than 37 weeks
gestational age.
RSV-specific intravenous (IV) immunoglobulin prophylaxis is recommended only for
high-risk children. When treating a child with concomitant pneumonia or other systemic
disease and otitis media, the practitioner must ensure appropriate diagnosis and management
of all aspects of the childs illness. Drainage of the ear by tympanocentesis or myringotomy
for culture and therapy may be necessary in some cases. Drainage is mandatory in neonates
who are suspected to be in a septic state or in children who are immunosuppressed.

Bacterial pathogens
Pathogenic bacteria are recovered from the middle ear effusion in at least half the children
with AOM, and bacterial DNA or cell wall debris is found in another quarter to a third of
specimens previously classified as sterile. Four bacterianamely, S pneumoniae, H
influenzae, Moraxella catarrhalis, andStreptococcus pyogenes are responsible for the
majority of episodes of AOM in persons older than 6 weeks. Other bacteria recovered and
implicated in AOM include Staphylococcus aureus, viridans streptococci, andPseudomonas
aeruginosa.
The emergence of resistance to antimicrobial agents is of increasing importance in the
management of AOM and other bacterial illnesses.[6] The various mechanisms used by
bacteria to confer this resistance will be delineated as the common pathologic agents linked to
AOM are described.

Streptococcus pneumoniae

S pneumoniae is the most common etiologic agent responsible for AOM and for invasive
bacterial infections in children of all age groups. [7] It is a gram-positive diplococcus with 90
identified serotypes (classified on the basis of the polysaccharide antigen), the frequency of
which varies between age groups and geography. On direct culture, various studies have
shown these bacteria to be responsible for 29-40% of isolates, but additionally pneumococcal
antigens are recovered from approximately a third of those cultures classified as sterile.
Pneumococcal infections are probably responsible for at least 50% of AOM episodes.
Serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F are responsible for most invasive pneumococcal
disease in America; in ear aspirates from patients with AOM, serotypes 19 (23%), 23
(12.5%), 6 (12%), 14 (10%), 3 (8.5%), and 18 (6%) are isolated most commonly. The
polyvalent pneumococcal vaccine confers immunity to approximately 85% of those serotypes
responsible for AOM.
S pneumoniae was once susceptible to almost all common antibiotics, including penicillin
G, erythromycin, and most sulfonamides. Alteration of the cell walls penicillin-binding
protein (the antimicrobial target) has led to the appearance of multidrug-resistant S
pneumoniae (MDRSP), which is resistant to beta-lactam compounds, macrolides, and
sulfonamides. Resistance rates as high as 40% have been reported for these 3 antimicrobial
groups. Serotypes 6B, 9V, 14, 19A, 19F, and 23F have the highest frequency of penicillin
resistance.
Ceftriaxone, cefotaxime, rifampin, and vancomycin still appear to have therapeutic
efficacy, as does immunization with polyvalent pneumococcal vaccine for prevention.
Unfortunately, polysaccharide antigens are not immunogenic early in life. To overcome this
problem, conjugated antigens, in which the polysaccharide antigen is attached to a protein
carrier, may be administered to induce production of antibodies to these polysaccharides.
Some conjugated antigens (eg, vaccinations for H influenzae type b [Hib]) are in widespread
use.
A heptavalent vaccine for S pneumoniae is now in widespread use and appears to have
made an impact on the number of cases of invasive pneumococcal disease. This vaccine
confers long-term immunity to 7 of the most common and invasive strains. Emerging

evidence suggests that other serotypes are beginning to be recovered more frequently in ear
and sinus infections. This might render the vaccine less useful in future years. In North
America, this vaccine has now been replaced by an updated 13-valent vaccine that contains
conjugated antigenic material for 6 of those additional serotypes of the pneumococcus.

Haemophilus influenzae

In middle ear aspirates from patients with AOM, H influenzae is the second most
frequently isolated bacterium and is responsible for approximately 20% of episodes in
preschool children. The frequency may be higher in otitis-prone children, older children, and
adults who have received the pneumococcal vaccine.
The bacterium is a small, pleomorphic, gram-negative coccobacillus. Those bacteria
encapsulated with a polysaccharide coating are classified into 6 distinct types (a-f);
nonencapsulated types are referred to as nontypeable and are responsible for the great
majority of AOM episodes. (The nonencapsulated strains have been subtyped biochemically
and antigenically, but, to date, this classification has limited clinical application.)
Traditionally, Hib has been found responsible for most invasive illnesses attributed to
these bacteria and for meningitis, epiglottitis, and septicemia. Hib accounts for only 10% of
all episodes of AOM in which H influenzae is recovered. In areas of the world where the
aforementioned Hib-conjugated vaccine is administered early in life, risks from this
potentially lethal strain have greatly diminished.
Antimicrobial resistance in Hib is conferred almost exclusively (95%) by the formation of
a single enzyme, triethylenemelamine 1 lactamase, which, in some series, is secreted by as
many as 40% of all nontypeable strains. This resistance is overcome relatively easily by using
blocking agents, extended-coverage cephalosporins, broad-spectrum macrolides, or
sulfonamides.
H influenzae may participate more widely in head and neck infections than was once
believed. One of the principal mechanisms is related to the ability of the bacterium to hide
and recover from antibiotic action by forming a mucous complex known as a biofilm.
Research has focused on enhancing penetration of or dissolving the protective biofilm.

Moraxella catarrhalis

In the mid-1970s, M catarrhalis was classified as nonpathogenic in middle ear infections,


even though under its previous name, Neisseria catarrhalis, it constituted approximately 10%
of all isolates from middle ear aspirates. At that time, M catarrhalis was almost universally
susceptible to ampicillin-type penicillins. After 20 years and 2 name changes (from N
catarrhalis toBranhamella catarrhalis to M catarrhalis), it is isolated in up to a quarter of
children with AOM, and resistance to the ampicillin-type beta-lactams is almost universal.
M catarrhalis is a gram-negative diplococcus and is considered part of the normal flora of
the human upper respiratory tract. Resistance is conferred by the secretion of multiple
isoenzymes of lactamase, which may be plasmid or chromosomal in origin and which may be
inducible (ie, present only in low levels until a substrate is provided). More than 1 isoenzyme
may be secreted by a single bacterium.
At present, almost all forms are blocked by clavulanic acid, and most are still susceptible
to sulfonamides, lactamase-stable cephalosporins, or broad-spectrum macrolides. M
catarrhalis is often found to coexist with other airway pathogens. The lactamases

(cephalosporinases) that M catarrhalis secretes may protect those other bacteria from
antimicrobial agents to which the second target pathogen might ordinarily be susceptible.

Streptococcus pyogenes

Although S pyogenes (a gram-positive coccus that constitutes the group A streptococci


[GAS] in the Lancefield classification), is still the fourth most commonly isolated bacterial
pathogen from ears with AOM, it has shown a steady decline in frequency of recovery from
the ear and in virulence over the past half-century. Similarly, a substantial decline in the
major complications of streptococcal infection, rheumatic fever, glomerulonephritis, and
scarlet fever has occurred.
Spyogenes may be associated with streptococcal toxic shock syndrome, which may
include coagulopathy, soft tissue necrosis or fasciitis, desquamating rash, and liver or renal
involvement. It is primarily a pathogen of the pharynx, with more than 80 distinct M-protein
strains identified. Currently, with the improvement in primary care and the availability of
rapid identification tests, early aggressive treatment is normally instituted against this
bacterium, which has shown minimal ability to develop resistance to antimicrobial agents.
Acute necrotic otitis media was associated with scarlet fever in the early 1900s; however,
the condition was also associated with measles, pneumonia, and influenza. Generally, the
patient was extremely ill with the systemic component of the disease and presented with a
spontaneous perforation shortly after the onset of otalgia.
Early inspection of the ear would show the perforation to be moderate to large; within
days, significant evidence of tissue necrosis would be observed, perhaps including the entire
tympanic membrane, ossicles, the tympanic mucoperiosteum, or the bone of the mastoid air
cells. The patient would demonstrate a marked conductive hearing loss, although
sensorineural loss was not uncommon.
Pathologically, the ear showed a marked paucity of the normal vascular proliferation
associated with an inflammatory reaction. Instead, a complete loss of the vascularity normally
associated with vasculitis or toxin exposure occurred. Healing was never normal; tissue was
replaced by epithelial invasion or scar tissue formation.
In industrialized societies, acute necrotic otitis media is now primarily of historic interest.
The disease is still reported in aboriginal populations living in areas where modern medicine
has not yet penetrated.
In the preantibiotic era, S pyogenes also appeared to be the organism most commonly
recovered from patients with acute coalescent mastoiditis. In the 1990s, S
pyogenes relinquished this distinction to S pneumoniae, but it remains a prominent pathogen
when this disease is encountered in very young persons.

Other aerobes

Except in neonates and children with chronic disease, few other pathogens have been
demonstrated in aspirates from the middle ears of immunologically intact individuals.
S aureus is rarely recovered, except in Japan, where studies indicate a somewhat higher
incidence (up to 10%). Mycobacterium tuberculosis is most often associated with chronic
otitis media but should be considered when a patient presents with painless otorrhea as an
initial complaint and/or has multiple tympanic perforations. Any patient with a compromised

immune system may be at risk for this opportunistic infection. Chlamydia pneumoniais an
uncommon but significant pathogen in persons with AOM and responds only to macrolide
therapy.

Anaerobes

Anaerobic bacteria have been recovered from the middle ears of children with AOM, but
the data do not support a prominent role for these microorganisms in persons with otitis
media, at least in the acute form. They may, however, play a greater role in chronic
inflammation of the adenoid bed and biofilm formation. When recovered from ears of
children with AOM, the anaerobic pathogen most often is not the sole pathogen cultured.

Common bacterial pathogens in neonatal period

In the perinatal period, the Escherichia coli, Enterococcus species, and group B
streptococci are the etiologic agents most commonly responsible for sepsis and meningitis.
These agents are often recovered from the middle ear, though the total percentage is probably
less than 10% of neonates with AOM.
Spneumoniae remains the most common pathogen responsible for AOM in all age groups,
including neonates. The nonencapsulated H influenzae and nontypeable varieties may be
invasive in these infants and constitute the second most common pathogens recovered from
the ear.
Because bacteremia is common in all neonates with AOM, tympanocentesis should be
performed for both diagnosis and therapy in any infant with signs of AOM or generalized
sepsis and any middle ear effusion. This should be part of any septic workup in neonates.

Problems

Recurrent otitis
media may cause damage
to
the bone, the
facial
nerve and
the cochlea, causing hearing loss is permanent. Otitis media can be acute or chronic. The
acute form usually associated with infections of the upper respiratory tract whereas
persistent form known as chronic suppurative otitis media.

2. Medical Surgical
A. Diabetes Mellitus
Mrs. Jody, 78 years old, has history of insulin-dependent diabetes (IDDM). When you
wigh her during your weekly home visit, you note that she weigh 98 pounds. Which is 12
pounds less then she weighed at your last visit. You try to weigh her at the same time of day
each week-09.30. She usually has breakfast at 06.30 and takes her morning NPH insulin, 40
units at 07.30. Today she tells you that she has been urinating a lot and that she has had flu
for about three days, with nausea and just a little vomiting. She says she has not been
eating well but ads, Im keeping my blood sugar up by drinking orange juice.
On assessment, you note that she has soft, sunken eyeball and her tongue is dry and
furrowed. Her blood pressure is 140/86 (usual is 150/88), her pulse is 92, and respiration are
22. The temperature is 99.4F. Her finger stick blood glucose (FSBG) is 468 mg/dl (usual is
250-300). Mrs. Jody refuses to check finger stick blood glucose herself. When asked what she
did not call the nurse or the doctor when she became ill, she stated, I didnt think it was that
serious, I didnt have a high temperature.

Key word: blood pressure is 140/86 (usual is 150/88), her pulse is 92, and respiration are 22.
The temperature is 99.4F. Her finger stick blood glucose (FSBG) is 468 mg/dl (usual is 250-

300).
Problem: she has been urinating a lot and that she has had flu for about three days, with

nausea and just a little vomiting. She says she has not been eating well but ads.
Diabetes mellitus type 2
Diabetes mellitus type 2 formerly non-insulin-dependent diabetes mellitus (NIDDM)
or adult-onset diabetes is a metabolic disorder that is characterized by high blood glucose in
the context of insulin resistance and relative insulin deficiency. Diabetes is often initially
managed by increasing exercise and dietary modification. If the condition progresses,
medications may be needed. Often affecting the obese, diabetes requires patients to routinely
check their blood sugar.
Unlike type 1 diabetes, there is very little tendency toward ketoacidosis although it is not
unheard of. One effect that can occur is nonketonic hyperglycemia. Long-term complications

from high blood sugar can include increased risk of heart attacks, strokes, diabetic
retinopathy where eye sight is affected, and kidney failure. For extreme cases, circulation of
limbs is affected, potentially requiring amputation. Loss of hearing, eyesight, and cognitive
ability has also been linked to this condition.
1. Signs and symptoms
The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased
thirst), polyphagia (increased hunger), fatigue and weight loss. Type 2 diabetes has been
associated with an increased risk of cognitive dysfunction and dementia through disease
processes such as Alzheimer's disease and vascular dementia. Researchers have shown that
reduced glucose tolerance has deleterious effects on memory in the elderly, and concomitant
hippocampal atrophy.
2. Cause
Type 2 diabetes is due to a combination of lifestyle and genetic factors. Recently,
intrauterine growth restriction (IUGR) or prenatal undernutrition (macro- and micronutrient)
was identified as another probable factor A clue for this concept was the Dutch Hunger
Winter (19441945) during World War II, and the pioneering work of Professor Barker
3. Lifestyle
A number of lifestyle factors are known to be important to the development of type 2
diabetes. In one study, those who had high levels of physical activity, a healthy diet, did not
smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a
normal weight was included, the rate was 89% lower. In this study, a healthy diet was defined
as one high in fiber, with a high polyunsaturated to saturated fat ratio, and a lower mean
glycemic index. Obesity has been found to contribute to approximately 55% of cases of type
2 diabetes, and decreasing consumption of saturated fats and trans fatty acids while replacing
them with unsaturated fats may decrease the risk. The increased rate of childhood obesity
between the 1960s and 2000s is believed to have led to the increase in type 2 diabetes in
children and adolescents. Dietary fat intake is linked to diabetes risk.
A 2010 meta-analysis of eleven studies involving 310,819 participants and 15,043 cases
of type 2 diabetes found that "SSBs [sugar-sweetened beverages] may increase the risk of

metabolic syndrome and type 2 diabetes not only through obesity but also by increasing
dietary glycemic load, leading to insulin resistance, -cell dysfunction, and inflammation."
Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A
weak positive correlation has been found between the concentration in the urine of bisphenol
A, a constituent of some plastics, and the incidence of type 2 diabetes.
4. Medical conditions
There are many factors which can potentially give rise to, or exacerbate, type 2 diabetes.
These include obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and
with the condition often termed metabolic syndrome (it is also known as Syndrome X,
Reavan's syndrome, or CHAOS). Other causes include acromegaly, Cushing's syndrome,
thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer, and drugs. Additional
factors found to increase the risk of type 2 diabetes include aging, high-fat diets and a less
active lifestyle.
Subclinical Cushing's syndrome (cortisol excess) may be associated with type 1 diabetes.
The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%.
Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal
of these microadenomas.
Hypogonadism is often associated with cortisol excess, and testosterone deficiency is
also associated with type 2 diabetes, even if the exact mechanism by which testosterone
improves insulin sensitivity is still not known.

5. Genetics
There is also a strong inheritable genetic connection in type 2 diabetes: having relatives
(especially first degree) with type 2 increases risks of developing type 2 diabetes
substantially. Genetic risk for type 2 diabetes decreased as humans first began migrating
around the world, implying a strong environmental component has affected the genetic-basis
of type 2 diabetes. In addition, there is also a mutation to the Islet Amyloid Polypeptide gene
that results in an earlier onset, more severe, form of diabetes.

There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree
relatives with type 2 diabetes have a much higher risk of developing type 2 diabetes,
increasing with the number of those relatives. Concordance among monozygotic twins is
close to 100%, and about 25% of those with the disease have a family history of diabetes.
Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG,
FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[31]
[32] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the
islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7like 2)
regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.
[33] Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly
inherited.[34]
Monogenic forms, e.g., MODY, constitute 15 % of all cases.[35]
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and
Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative
disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes
mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.
Gene expression promoted by a diet of fat and glucose, as well as high levels of
inflammation related cytokines found in the obese, results in cells that "produce fewer and
smaller mitochondria than is normal," and are thus prone to insulin resistance.
6. Pathophysiology
Insulin resistance means that body cells do not respond appropriately when insulin is
present.
This is a more complex problem than type 1, but is sometimes easier to treat, especially
in the early years when insulin is often still being produced internally. Severe complications
can result from improperly managed type 2 diabetes, including renal failure, erectile
dysfunction, blindness, slow healing wounds (including surgical incisions), and arterial
disease, including coronary artery disease. The onset of type 2 diabetes has been most
common in middle age and later life, although it is being more frequently seen in adolescents
and young adults due to an increase in child obesity and inactivity. A type of diabetes called
MODY is increasingly seen in adolescents, but this is classified as a diabetes due to a specific
cause and not as type 2 diabetes.

In the 2008 Banting Lecture of the American Diabetes Association, DeFronzo


enumerates eight main pathophysiological factors in the type 2 diabetic organism
Diabetes mellitus with a known etiology, such as secondary to other diseases, known
gene defects, trauma or surgery, or the effects of drugs, is more appropriately called
secondary diabetes mellitus or diabetes due to a specific cause. Examples include diabetes
mellitus such as MODY or those caused by hemochromatosis, pancreatic insufficiencies, or
certain types of medications (e.g., long-term steroid use).
Recent studies of pancreatic beta cells have indicated a molecular connection between
diet, obesity that involves the role of fat in activating a pathway to type 2 diabetes. In this
mechanism, loss of beta cell glucose sensing contributes substantially to the early
manifestation of diabetes, and beta cell dysfunction is responsible for the onset and severity
of multiple systemic disease signs including impaired glucose tolerance, hyperglycemia,
hepatic steatosis and insulin resistance in muscle and adipose cells. Previous work published
in past decades by the laboratories of Roger Unger, Jerrold Olefsky, and Bernard Thorens
alluded to the possibility of the importance of beta cell function and glucose sensing in these
disease signs. This mechanism of beta cell dysfunction may be contributing substantially to
the current epidemic of type 2 diabetes.

7. Diagnosis
2006 WHO Diabetes criteria edit Condition
mmol/l(mg/dl)
1.
2.
3.
4.

Normal
Impaired fasting glycaemia
Impaired glucose tolerance
Diabetes mellitus

2 hour glucose Fasting glucose:


mmol/l(mg/dl)
1. <7.8 (<140) <6.1 (<110)
2. <7.8 (<140) 6.1(110) &
<7.0(<126)
3. 7.8 (140) <7.0 (<126)
4. 11.1 (200) 7.0 (126)

The World Health Organization definition of diabetes is for a single raised glucose
reading with symptoms, otherwise raised values on two occasions, of either: fasting plasma
glucose 7.0 mmol/l (126 mg/dl) or With a glucose tolerance test, two hours after the oral
dose a plasma glucose 11.1 mmol/l (200 mg/dl) If a 2-hour postload glucose level of at

least 11.1 mmol/L ( 200 mg/dL) is used as the reference standard, the fasting plasma glucose
> 7.0 mmol/L (126 mg/dL) diagnoses current diabetes with: sensitivity about 50% and
specificity greater than 95%.
A random capillary blood glucose > 6.7 mmol/L (120 mg/dL) diagnoses current diabetes
with: sensitivity = 75% and specificity = 88%
Glycated hemoglobin values that are elevated (over 5%), but not in the diabetic range
(not over 7.0%) are predictive of subsequent clinical diabetes in United States female health
professionals. In this study, 177 of 1061 patients with glycated hemoglobin value less than
6% became diabetic within 5 years compared to 282 of 26281 patients with a glycated
hemoglobin value of 6.0% or more. This equates to a glycated hemoglobin value of 6.0% or
more having:

8. Screening
No major organization recommends universal screening for diabetes as there is no
evidence that such a program would improve outcomes. Screening is recommended by the
United States Preventive Services Task Force in adults without symptoms whose blood
pressure is greater than 135/80 mmHg. For those whose blood pressure is less, the evidence is
insufficient to recommend for or against screening. The World Health Organization
recommends only testing those groups at high risk. Based on a survey conducted in 2011 on
70,000 average persons, the Hungarian Diabetes Society recommends the introduction of a
general screening of the adult population for Diabetes Type II.

9. Prevention
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and
regular exercise. Intensive lifestyle measures may reduce the risk by over half. Evidence for
the benefit of dietary changes alone however is limited. In those with impaired glucose
tolerance, diet and exercise and/or metformin or acarbose may decrease the risk of
developing diabetes. Lifestyle interventions are more effective than metformin.
10. Management

Management of type 2 diabetes focuses on lifestyle interventions, lowering other


cardiovascular risk factors, and maintaining blood glucose levels in the normal range. Selfmonitoring of blood glucose for people with newly diagnosed type 2 diabetes was
recommended by the National Health Services in 2008 however the benefit of self monitoring
in those not using multi-dose insulin is questionable. Managing other cardiovascular risk
factors including hypertension, high cholesterol, and microalbuminuria improves a person's
life expectancy. Intensive blood sugar lowering as opposed to standard blood sugar lowering
does not appear to change mortality
11. Lifestyle
Aerobic exercise is beneficial in diabetes with a greater amount of exercise yielding
better results. It leads to a decrease in HbA1C, improved insulin sensitivity, and a better V02
max. Resistance training is also useful and the combination of both types of exercise may be
most effective. A diabetic diet that promotes weight loss is important. While the best diet type
to achieve this is controversial a low glycemic index diet has been found to improve blood
sugar control. Culturally appropriate education may help people with type 2 diabetes control
their blood sugar levels, for up to six months at least.
12. Medications
Metformin 500mg tablets.
There are several classes of medications available. Metformin is generally
recommended as a first line treatment as there is good evidence that it decreases mortality.
Injections of insulin may either be added to oral medication or used alone. Other classes of
medications used to treat type 2 diabetes are sulfonylureas, nonsulfonylurea secretagogues,
alpha glucosidase inhibitors, and thiazolidinediones.
13. Insulin
When insulin is used, a long-acting formulation is usually added initially, while
continuing oral medications. Doses of insulin are increased to effect.
The initial insulin regimen is often chosen based on the patient's blood glucose profile.
Initially, adding nightly insulin to patients failing oral medications may be best. Nightly
insulin combines better with metformin than with sulfonylureas.When nightly insulin is
insufficient, choices include:

Premixed insulin with a fixed ratio of short and intermediate acting insulin; this tends
to be more effective than long acting insulin, but is associated with increased hypoglycemia.
Initial total daily dosage of biphasic insulin can be 10 units if the fasting plasma glucose
values are less than 180 mg/dl or 12 units when the fasting plasma glucose is above 180
mg/dl". A guide to titrating fixed ratio insulin is available.
Long acting insulins include insulin glargine and insulin detemir. A meta-analysis of
randomized controlled trials by the Cochrane Collaboration found "only a minor clinical
benefit of treatment with long-acting insulin analogues for patients with diabetes mellitus
type 2". More recently, a randomized controlled trial found that although long acting insulins
were less effective, they were associated with reduced hypoglycemic episodes.
14. Surgery
Gastric Bypass procedures are currently considered an elective procedure with no
universally accepted algorithm to decide who should have the surgery. In the diabetic patient,
certain types result in 99-100% prevention of insulin resistance and 80-90% clinical
resolution or remission of type 2 diabetes. In 1991, the NIH (National Institutes of Health)
Consensus Development Conference on Gastrointestinal Surgery for Obesity proposed that
the body mass index (BMI) threshold to consider surgery should drop from 40 to 35 in the
appropriate patient. More recently, the American Society for Bariatric Surgery (ASBS) and
the ASBS Foundation suggested that the BMI threshold be lowered to 30 in the presence of
severe co-morbidities. Debate has flourished about the role of gastric bypass surgery in type 2
diabetics since the publication of The Swedish Obese Subjects Study. The largest prospective
series showed a large decrease in the occurrence of type 2 diabetes in the post-gastric bypass
patient at both 2 years (odds ratio was 0.14) and at 10 years (odds ratio was 0.25).
15. Progression
The way type 2 diabetes is managed may change with age. Insulin production decreases
because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance
increases because of the loss of lean tissue and the accumulation of fat, particularly intraabdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively
declines with age, leading to a high prevalence of type 2 diabetes and postchallenge
hyperglycemia in the older population. Age-related glucose intolerance is often accompanied
by insulin resistance, but circulating insulin levels are similar to those of younger people.

Treatment goals for older patients with diabetes vary with the individual, and take into
account health status, as well as life expectancy, level of dependence, and willingness to
adhere to a treatment regimen.

2 B. TUBERCULOSIS (See Exemple)


Mr M 12 year old, admitted to dr soetomo hospital his chief complain is severe
cough(hardly at night)since two year ago very severe cough. she had been taken medicine
from public hospital,but she hasn't recovered from illness ,and she still suffering and hardly to
normal breathing .he has allergic with seafood and cool weather .respratory rate 30x/min
breathing bronchovesicular ,ronchi + on left right lobus of lung O2 adm mucus secretion
yelow viscous
KEY WORD

Mr M 12 year old
Complain is severe cough(hardly at night)since two year ago very severe

cough
He has allergic with seafood and cool weather
Respiratory rate 30x/min breathing bronchovesicular ,ronchi + on left right
lobus of lung O2 adm mucus secretion yelow viscous

PROBLEMS

Mr M suffered from tuberculosis because of the experienced symptoms similar


to symptoms of tuberculosis disease

TUBERCULOSIS

Defenition of Tubercolosis
Tuberculosis (TB) is a chronic, progressive infection with a period of latency

following initial infection. It occurs most commonly in the lungs. Pulmonary symptoms
include productive cough, chest pain, and dyspnea. Diagnosis is most often by sputum culture
and smear. Treatment is with multiple antimicrobial drugs.

Etiology Tubercolosis

TB properly refers only to disease caused by Mycobacterium tuberculosis. Similar disease


occasionally results from the closely related mycobacteria, M. bovis, M. africanum, and M.
microti.
TB results almost exclusively from inhalation of airborne particles (droplet nuclei)
containing M. tuberculosis. They disperse primarily through coughing, singing, and other
forced respiratory maneuvers by people who have active pulmonary TB and whose sputum
contains a significant number of organisms (typically enough to render the smear positive).
People with pulmonary cavitary lesions are especially infectious. Droplet nuclei containing
tubercle bacilli may remain suspended in room air currents for several hours, increasing the
chance of spread. However, once these droplets land on a surface, it is difficult to resuspend
the organisms (eg, by sweeping the floor, shaking out bed linens) as respirable particles.
Although such actions can resuspend dust particles containing tubercle bacilli, these particles
are far too large to reach the alveolar surfaces necessary to initiate infection. Fomites (eg,
contaminated surfaces, food, and personal respirators) do not appear to facilitate spread.
Although there is wide variability, patients with pulmonary TB infect about 7 close
contacts, on average, but most of those infected do not develop active disease. Transmission
is enhanced by frequent or prolonged exposure to a patient who is dispersing large numbers
of tubercle bacilli in overcrowded, enclosed, poorly ventilated spaces; thus, people living in
poverty or in institutions are at particular risk. Health care practitioners who have close
contact with active cases have increased risk. However, once effective treatment begins,
cough rapidly decreases, organisms are inactivated, and within weeks, TB is no longer
contagious.

Much less commonly, spread results from aerosolization of organisms after irrigation of
infected wounds, in mycobacteriology laboratories, or in autopsy rooms. TB of the tonsils,
lymph nodes, abdominal organs, bones, and joints was once commonly caused by ingestion
of milk or milk products (eg, cheese) contaminated with M. bovis, but this transmission route
has been largely eradicated in developed countries by slaughter of cows that test positive on a
tuberculin skin test and by pasteurization of milk. Tuberculosis due to M. bovis still occurs in
developing countries and in immigrants from developing countries where bovine tuberculosis
is endemic (eg, some Latin American countries).

Risk Factors Tuberculosis

HIV infection is the greatest single medical risk factor because cell-mediated immunity,
which is impaired by HIV, is essential for defense against TB; other immunosuppressive
illnesses (eg, diabetes) or therapies (eg, tumor necrosis factor [TNF] inhibitors,
corticosteroids) increase risk but less than HIV.
Age has traditionally been considered an independent risk factor because the elderly have
more years of potential exposure and are more likely to have impaired immunity. However, in
the US, the difference in the age-specific case rate is no longer as large, probably because the
incidence of infectious cases (and hence lifetime risk of significant exposure) has declined.

Pathophysiology

Tubercle bacilli initially cause a primary infection, which only rarely causes acute illness.
Most (about 95%) primary infections are asymptomatic and followed by a latent (dormant)
phase. However, a variable percentage of latent infections subsequently reactivate with
symptoms and signs of disease. Infection is usually not transmissible in the primary stage and
is never contagious in the latent stage.
Primary infection: Infection requires inhalation of particles small enough to traverse the
upper respiratory defenses and deposit deep in the lung, usually in the subpleural airspaces of
the lower lung. Large droplets tend to lodge in the more proximal airways and typically do
not result in infection. Infection usually begins from a single initial focus.
To initiate infection, tubercle bacilli must be ingested by alveolar macrophages. Tubercle
bacilli that are not killed by the macrophages actually replicate inside them, ultimately killing

the host macrophage (with the help of CD8 lymphocytes); inflammatory cells are attracted to
the area, causing a focal pneumonitis that evolves into the characteristic tubercles seen
histologically. In the early weeks of infection, some infected macrophages migrate to regional
lymph nodes (eg, hilar, mediastinal), where they access the bloodstream. Organisms may then
spread hematogenously to any part of the body, particularly the apical-posterior portion of the
lungs, epiphyses of the long bones, kidneys, vertebral bodies, and meninges.
In 95% of cases, after about 3 wk of uninhibited growth, the immune system suppresses
bacillary replication before symptoms or signs develop. Foci of infection in the lung or other
sites resolve into epithelioid cell granulomas, which may have caseous and necrotic centers.
Tubercle bacilli can survive in this material for years; the balance between the host's
resistance and microbial virulence determines whether the infection ultimately resolves
without treatment, remains dormant, or becomes active. Infectious foci may leave
fibronodular scars in the apices of one or both lungs (Simon foci), calcified scars from the
primary infection (Ghon foci), or calcified hilar lymph nodes. The tuberculin skin test (see
Mycobacteria: Skin testing) and the newer interferon- release assay become positive.
Less often, the primary focus immediately progresses, causing acute illness with
pneumonia (sometimes cavitary), pleural effusion, and marked mediastinal or hilar lymph
node enlargement (which, in children, may compress bronchi). Small pleural effusions are
predominantly lymphocytic, typically contain few organisms, and clear within a few weeks.
This sequence may be more common among young children and recently infected or
reinfected immunosuppressed patients. Extrapulmonary TB at any site can sometimes
manifest without evidence of lung involvement. TB lymphadenopathy is the most common
extrapulmonary presentation; however, meningitis is the most feared because of its high
mortality in the very young and very old.
Active disease: In about 10% of immunocompetent patients, latent infection develops into
active disease, although the percentage varies significantly by age and other risk factors. In
50 to 80% of those who develop active disease, TB reactivates within the first 2 yr, but it can
occur decades later. Any organ initially seeded may become a site of reactivation, but
reactivation occurs most often in the lung apices, presumably because of favorable local
conditions such as high O2 tension. Ghon foci and affected hilar lymph nodes are much less
likely to be sites of reactivation.

Conditions that facilitate activation include impaired immunity (particularly HIV


infection), certain immunosuppressants (eg, corticosteroids, infliximab ,other TNF
inhibitors), gastrectomy, jejunoileal bypass surgery, silicosis, renal insufficiency, stress,
diabetes, head or neck cancer, significant weight loss, adolescence, and advanced age
(particularly > 70 yr).
TB damages tissues through delayed-type hypersensitivity (DTHsee Allergic and
Other Hypersensitivity Disorders: Type IV), typically producing granulomatous necrosis with
a caseous histologic appearance. Lung lesions are characteristically but not invariably
cavitary, especially in immunosuppressed patients with impaired DTH. Pleural effusion is
less common than in progressive primary TB but may result from direct extension or
hematogenous spread. Rupture of a large tuberculous lesion into the pleural space may cause
empyema with or without bronchopleural fistula and sometimes causes pneumothorax. In the
prechemotherapy era, TB empyema sometimes complicated medically induced pneumothorax
therapy and was usually rapidly fatal, as was sudden massive hemoptysis due to erosion of a
pulmonary artery by an enlarging cavity.
The course varies greatly, depending on the virulence of the organism and the state of
host defenses. The course may be rapid among blacks, American Indians, and other
populations who have not had as many centuries of selective pressure to develop innate or
natural immunity as descendents of the European and American TB epidemics have had. The
course is often more indolent in the latter populations.
Acute respiratory distress syndrome (ARDS), which appears to be due to hypersensitivity
to TB antigens, develops rarely after diffuse hematogenous spread or rupture of a large cavity
with spillage into the lungs

Symptoms and Signs

In active pulmonary TB, even moderate or severe disease, patients may have no
symptoms, except not feeling well, anorexia, fatigue, and weight loss, which develop
gradually over several weeks, or they may have more specific symptoms. Cough is most
common. At first, it may be minimally productive of yellow or green sputum, usually on
rising, but cough may become more productive as the disease progresses. Hemoptysis occurs
only with cavitary TB (sometimes due to fungal growth in a cavity). Low-grade fever is

common but not invariable. Drenching night sweats are a classic symptom but are neither
common in nor specific for TB. Dyspnea may result from lung parenchymal damage,
spontaneous pneumothorax, or pleural TB with effusion.
With HIV coinfection, the clinical presentation is often atypical because DTH is
impaired; patients are more likely to have symptoms of extrapulmonary or disseminated
disease.
Diagnosis

Chest x-ray
Tuberculin skin test
Acid-fast stain and culture
When available, DNA-based testing

Pulmonary TB is often suspected based on chest x-rays taken while evaluating respiratory
symptoms (cough > 3 wk, hemoptysis, chest pain, dyspnea), an unexplained illness, FUO, or
a positive tuberculin skin test (see Mycobacteria: Skin testing).
Initial tests are chest x-ray, sputum examination, and tuberculin skin testing. If the chest
x-ray is highly characteristic (upper lobe lung cavitation) in patients with TB risk factors,
sputum examination is still required, but skin testing is often not done.

Chest x-ray
In adults, a multinodular infiltrate above or behind the clavicle (the most

characteristic location, most visible in an apical-lordotic view or with CT) suggests


reactivation of TB. Middle and lower lung infiltrates are nonspecific but should prompt
suspicion of primary TB in patients (usually young) whose symptoms or exposure history
suggests recent infection, particularly if there is pleural effusion. Calcified hilar nodes may be
present; they may result from primary TB infection but also may result from histoplasmosis
in areas where histoplasmosis is endemic (eg, the Ohio River Valley).

Sputum examination
Sputum is tested for the presence of acid-fast bacilli (AFB). Tubercle bacilli are

nominally gram-positive but take up Gram stain inconsistently; samples are best prepared

with Ziehl-Neelsen or Kinyoun stains for conventional light microscopy or fluorochrome


stains for fluorescent microscopy.
Drug susceptibility tests (DSTs) should be done on initial isolates from all patients to identify
an effective anti-TB regimen. These tests should be repeated if patients continue to produce
culture-positive sputum after 3 mo of treatment or if cultures become positive after a period
of negative cultures. Results of DSTs may take up to 8 wk if conventional bacteriologic
methods are used. However, several new molecular DSTs can detect drug resistance in a
sputum sample within hours.
Tests of other specimens

Transbronchial biopsies can be done on infiltrative lesions, and samples are submitted for
culture, histologic evaluation, and molecular testing. Gastric washings, which are culturepositive in a minority of samples, are no longer commonly used except in small children, who
usually cannot produce a good sputum specimen. Ideally, biopsied samples of other tissue
should be cultured fresh, but NAAT can be used for fixed tissues (eg, for biopsied lymph
node if histologic examination unexpectedly detects granulomatous changes). The latter use
of NAAT has not been approved but can be extremely useful, although positive and negative
predictive values have not been established.
Skin testing

Multiple-puncture devices (tine test) are no longer recommended. The tuberculin skin
test (TST; Mantoux or PPDpurified protein derivative) is usually done, although it is a test
of infection, latent or active, and is not diagnostic of active disease. The standard dose in the
US of 5 tuberculin units (TU) of PPD in 0.1 mL of solution is injected on the volar forearm. It
is critical to give the injection intradermally, not subcutaneously. A well-demarcated bleb or
wheal should result immediately. The diameter of induration (not erythema) transverse to the
long axis of the arm is measured 48 to 72 h after injection. Recommended cutoff points for a
positive reaction depend on the clinical setting:

Treatment of Tuberculosis

Most patients with uncomplicated TB and all patients with complicating illnesses (eg,
AIDS, hepatitis, diabetes), adverse drug reactions, or drug resistance should be referred to a

TB specialist. (See also the Joint Statement from the American Thoracic Society, Centers for
Disease Control and Prevention, and the Infectious Diseases Society of America: Treatment
of Tuberculosis.) However, most TB can be fully treated at home with instructions on how to
avoid spreading disease; these measures include
1. Staying at home
2. Avoiding visitors (previously exposed family members may stay)
3. Covering coughs with a tissue or hand
Surgical face masks for TB patients are stigmatizing and are generally not recommended for
cooperative patients. For drug-susceptible TB that is being treated effectively, precautions
must be continued for at least 2 wk in or outside the hospital. For patients with MDR-TB and
XDR-TB, response to treatment may be slower, and the consequences of transmission
greater; thus, precautions are continued longer, until there is clear evidence of treatment
response.

Hospitalization

The main indications for hospitalization are


1. Serious concomitant illness
2. Need for diagnostic procedures
3. Social issues (eg, homelessness)
4. Need for respiratory isolation, as for people living in congregate settings where
previously unexposed people would be regularly encountered
Initially, all hospitalized patients should be in respiratory isolation, ideally in a negativepressure room with 6 to 12 air changes/h. Anyone entering the room should wear a respirator
(not a surgical mask) that has been appropriately fitted and that meets National Institute for
Occupational Safety and Health certification (N-95 or greater). Because risk of exposing
other hospitalized patients is high, release from respiratory isolation usually requires 3
negative sputum smears over 2 days, including at least one early-morning negative specimen.

Public health considerations: To improve treatment adherence, ensure cure, and


limit transmission and the development of drug-resistant strains, public health
programs closely monitor treatment, even if patients are being treated by a private
physician. In most states, TB care (including skin testing, chest x-rays, and drugs) is
available free through public health clinics to reduce barriers to treatment.

Increasingly, optimal patient case management includes supervision by public health


personnel of the ingestion of every dose of drug, a strategy known as directly observed
therapy (DOT). DOT increases the likelihood that the full treatment course will be completed
from 61% to 86% (91% with enhanced DOT, in which incentives and enablers such as
transportation vouchers, child care, outreach workers, and meals are provided). DOT is
particularly important
1. For children and adolescents
2. For patients with HIV infection, psychiatric illness, or substance abuse
3. After treatment failure, relapse, or development of drug resistance
In some programs, selective self-administered treatment (SAT) is an option for patients
who are committed to treatment; ideally, fixed-dose combination drug preparations are used
to avoid the possibility of monotherapy, which can lead to drug resistance. Mechanical drug
monitors have been advocated to improve adherence with SAT.
Public health departments usually visit homes to evaluate potential barriers to treatment
(eg, extreme poverty, unstable housing, child care problems, alcoholism, mental illness) and
to check for other active cases and close contacts. Close contacts are people who share the
same breathing space for prolonged periods, typically household residents, but often include
people at work, school, and places of recreation. The precise duration and degree of contact
that constitutes risk vary because TB patients vary greatly in infectiousness. For patients who
are highly infectious as evidenced by multiple family members with disease or positive skin
tests, even relatively casual contacts (eg, passengers on the bus they ride) should be referred
for skin testing and evaluation for latent infection (see Mycobacteria: Screening); patients
who do not infect any household contacts are less likely to infect casual contacts.

2.C Heart failure


Mr W 56 year old.weigh 60 kg. admitted to ER with nocturne dyspnea (PND) since i
week go .medical history : AMI month ago T :36.8;rr 40xx/min ;P=92x/min ;bp/50 mmHg
;X-ray cardiomyogali.ECG show ST elevation and heart sound s3 and s4.medical
order;insert uinary catheter and IV line plus diuretic 2 amp IV

KEY WORDS :

Mr W 56 year old.weigh 60 kg
Nocturne dyspnea (PND)
T :36.8;rr 40xx/min ;P=92x/min ;bp/50 mmHg ;X-ray cardiomyogali
Heart sound s3 and s4
1. Heart failure

Heart failure is the pathophysiologic state in which the heart, via an abnormality of
cardiac function (detectable or not), fails to pump blood at a rate commensurate with the
requirements of the metabolizing tissues or is able to do so only with an elevated diastolic
filling pressure.
Heart failure (see the images below) may be caused by myocardial failure but may also
occur in the presence of near-normal cardiac function under conditions of high demand. Heart
failure always causes circulatory failure, but the converse is not necessarily the case, because
various noncardiac conditions (eg, hypovolemic shock, septic shock) can produce circulatory
failure in the presence of normal, modestly impaired, or even supranormal cardiac function.
To maintain the pumping function of the heart, compensatory mechanisms increase blood
volume, cardiac filling pressure, heart rate, and cardiac muscle mass. However, despite these
mechanisms, there is progressive decline in the ability of the heart to contract and relax,
resulting in worsening heart failure.
Signs and symptoms of heart failure include tachycardia and manifestations of venous
congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness is a cardinal
symptom of left ventricular (LV) failure that may manifest with progressively increasing
severity.
Heart failure can be classified according to a variety of factors (see Heart Failure Criteria
and Classification). The New York Heart Association (NYHA) classification for heart failure
comprises 4 classes, based on the relationship between symptoms and the amount of effort
required to provoke them, as follows[1] :

Class I patients have no limitation of physical activity

Class II patients have slight limitation of physical activity

Class III patients have marked limitation of physical activity

Class IV patients have symptoms even at rest and are unable to carry on any physical
activity without discomfort

The American College of Cardiology/American Heart Association (ACC/AHA) heart


failure guidelines complement the NYHA classification to reflect the progression of disease
and are divided into 4 stages, as follows[2, 3] :

Stage A patients are at high risk for heart failure but have no structural heart disease or
symptoms of heart failure

Stage B patients have structural heart disease but have no symptoms of heart failure

Stage C patients have structural heart disease and have symptoms of heart failure

Stage D patients have refractory heart failure requiring specialized interventions

Laboratory studies for heart failure should include a complete blood cell (CBC) count,
electrolytes, and renal function studies. Imaging studies such as chest radiography and 2dimensional echocardiography are recommended in the initial evaluation of patients with
known or suspected heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-Btype natriuretic peptide (NT-proBNP) levels can be useful in differentiating cardiac and
noncardiac causes of dyspnea. (See the Workup Section for more information.)
In acute heart failure, patient care consists of stabilizing the patient's clinical condition;
establishing the diagnosis, etiology, and precipitating factors; and initiating therapies to
provide rapid symptom relief and survival benefit. Surgical options for heart failure include
revascularization procedures, electrophysiologic intervention, cardiac resynchronization
therapy (CRT), implantable cardioverter-defibrillators (ICDs), valve replacement or repair,
ventricular restoration, heart transplantation, and ventricular assist devices (VADs). (See the
Treatment Section for more information.)
The goals of pharmacotherapy are to increase survival and to prevent complications.
Along with oxygen, medications assisting with symptom relief include diuretics, digoxin,
inotropes, and morphine. Drugs that can exacerbate heart failure should be avoided
(nonsteroidal anti-inflammatory drugs [NSAIDs], calcium channel blockers [CCBs], and
most antiarrhythmic drugs). (See the Medication Section for more information.)

Prevention Heart failure

The key to preventing heart failure is to reduce your risk factors. You can control or
eliminate many of the risk factors for heart disease high blood pressure and coronary

artery disease, for example by making lifestyle changes along with the help of any needed
medications.
Lifestyle changes you can make to help prevent heart failure include:

Not smoking

Controlling certain conditions, such as high blood pressure, high cholesterol and
diabetes

Staying physically active

Eating healthy foods

Maintaining a healthy weight

Reducing and managing stress

2. Paroxysmal nocturnal dyspnoea


Paroxysmal nocturnal dyspnea refers to attacks of severe shortness of breath and
coughing that generally occur at night, usually awakening the person from sleep, and may be
quite frightening. Though simple orthopnea may be relieved by sitting upright at the side of
the bed with legs dependent, in the patient with paroxysmal nocturnal dyspnea, coughing and
wheezing often persist even in this position.

Causes

Paroxysmal nocturnal dyspnea may be caused in part by the depression of the


respiratory center during sleep, which may reduce arterial oxygen tension, particularly in
patients with interstitial lung disease and reduced pulmonary compliance. Also, in the
horizontal position there is redistribution of blood volume from the lower extremities and
splanchnic beds to the lungs. In normal individuals this has little effect, but in patients in
whom the additional volume cannot be pumped out by the left ventricle because of disease,
there is a significant reduction in vital capacity and pulmonary compliance with resultant
shortness of breath. Additionally, in patients with congestive heart failure the pulmonary
circulation may already be overloaded because the failing left ventricle is suddenly unable to
match the output of a more normally functioning right ventricle; causing pulmonary
congestion. It is, also, important to note that left-sided heart failure can lead to right-sided
heart failure. Pulmonary congestion decreases when the patient assumes a more erect
position, and this is accompanied by an improvement in symptoms.
3. Paroxysmal Nocturnal Dyspnea and Heart Failure
Paroxysmal Nocturnal Dyspnea, for example, is just one of the symptoms of left-side
heart failure. During the day, a person with left-side heart failure accumulates fluid in his
legs. At night when he lies down, the hearts failure to maintain proper blood pressure allows
the fluid to accumulate in the lungs, specifically, in the air sacs. As the lungs fill up, oxygen

levels drop down. The heart now functions on overdrive. Unable to match the capacity of the
right side of the heart, the left side triggers a pulmonary distress.

3).MATERNITY
Mrs Ernie is a 28 year-old woman,gravida 3 ,para 2 .who presents to the clinic today
for her initial prenatal examination. she state that her last menstrual period (LMP) is 9/15/98
.she has not received prenatal care before today because lack of transportation. however,she
does verbalize the importance of early prenatal care to ensure the well-being of her new born
she states that things have gone well so far.she eats fast food and drink soda frequently. she
lives with husband and two son in -law, who are very supportive .her husband works full time
at a fast food chain store. he is is looking for another job that pay more money. she states that
it hard to make financial ends meet at time. she stay at home with children.
The past medical history is unremarkable exept for two pregnancies ,which were both
term gestation,delivered vaginally. during the last pregnancy, she was diagnosed pregnancy
induced hypertension and gestational diabetes and was induced at 38 weeks gestation. she
states that she gained 60 pound and that her son weighed 9 pound 2 ounces
KEY WORD

Mrs .Ernie is a 28 year-old


Last Menstrual 9/15/98
Eats Fast Food and Drink Soda Frequently
hypertension and gestational diabetes and was induced at 38 weeks gestation
on weighed 9 pound 2 ounces

ANSWER
Hypertension (HTN)
Chronic hypertension is defined as blood pressure exceeding 140/90 mm Hg before
pregnancy or before 20 weeks' gestation. When hypertension is first identified during a
woman's pregnancy and she is at less than 20 weeks' gestation, blood pressure elevations
usually represent chronic hypertension.
In contrast, new onset of elevated blood pressure readings after 20 weeks' gestation
mandates the consideration and exclusion of preeclampsia. Preeclampsia occurs in up to 5%
of all pregnancies, in 10% of first pregnancies, and in 20-25% of women with a history of
chronic hypertension. Hypertensive disorders in pregnancy may cause maternal and fetal
morbidity, and they remain a leading source of maternal mortality.

Hypertension in Pregnancy

During pregnancy, hypertension can affect blood flow to the kidneys, liver, brain,
placenta, and other organs. Possible types of hypertension include preeclampsia, eclampsia,
and gestational pregnancy. Treatment options involve bed rest, more frequent prenatal visits,

and early delivery (after 36 weeks). Even though high blood pressure and related disorders
can be serious, most women with high blood pressure during pregnancy (and those who
develop preeclampsia) have successful pregnancies.

Types of Pregnancy-Related Hypertension

Types of hypertension in pregnancy include:

Chronic hypertension

Eclampsia or preeclampsia

Chronic hypertension with preeclampsia

Late hypertension (also referred to as gestational hypertension).

Preeclampsia

Preeclampsia, a condition that can occur during pregnancy, results


from a narrowing of the blood vessels. Because of this narrowing, women
with this condition can have decreased blood flow to the kidneys, brain,
liver, retina, and placenta. Symptoms include high blood pressure,
swelling of the hands and face, and protein in the urine. The only definite
cure is delivering the fetus. However, if the condition occurs early in a
pregnancy, treatment will involve careful monitoring of the mother and
the fetus until the fetus can be delivered.

Gestational Hypertension

Gestational hypertension is high blood pressure that develops after the twentieth week of
pregnancy. The causes of this condition are unknown, but it is clear that the condition affects
blood flow to organs such as the kidneys, placenta, brain, and liver. There is no way of
preventing this type of hypertension, but regular prenatal care will usually catch it early,
reducing the chances of complications.

What Causes It?

High blood pressure research scientists do not yet know the cause or causes of
hypertension in pregnancy; however, they do know that it can affect blood flow to organs
such as the:

Kidneys

Placenta

Liver

Retina

Brain.

Prevent Pregnancy Hypertension


1. Know your blood pressure level before getting pregnant. Make an appointment for
a checkup with your primary care doctor or ob-gyn and make a note of your blood
pressure. You can also stop by a health fair for a free evaluation, or check you
blood pressure at a pharmacy that has a self-service machine.
2. Kick the salt habit. High salt, or sodium, intake can raise blood pressure. If you
typically sprinkle salt on every dish, now is the time to break the habit. Most
adults should keep salt intake to 1 teaspoon per day that includes what comes
out of the shaker as well as the hidden sodium in processed foods.
3. Get off the couch. Get up and get moving before you conceive. If youre already
pregnant, ask your doctor about starting a regular exercise program. Sedentary
women are likely to gain weight, which can increase the risk of hypertension
during pregnancy, as well as before and after. Try to start your pregnancy at a
healthy body weight.
4. Pay attention to medication. Make sure you aren't taking medication that can raise
blood pressure levels check with your doctor to see what's safe. You may not
realize that popping a decongestant, such as pseudoephedrine (Sudafed and
others), for something minor like a stuffy nose can cause an increase in blood
pressure. Think twice about using any medication unless your doctor approves. If

you already have high blood pressure, talk to your doctor about medication use
before and during pregnancy. It is very important to have your blood pressure
under control and stable before becoming pregnant, as those nine months are not
the best time to try new or additional medication. Work with your doctor to make
sure that you are taking a medication that will be safe to continue during
pregnancy.
5. Get regular prenatal checkups. If your blood pressure starts to rise during
pregnancy, you want to catch it early. Make sure to keep all appointments and
consider buying a home blood pressure monitor to check your blood pressure
more frequently.

4. Familly
The Corn family has returned to the clinic for help in dealing with dan recent
diagnosis and treatment for type diabetes militus. Dan is a 17 year old senior high shcool who
is not following the diet-exercise-insulin protocol prescribed for diabetes diagnosis 4 month
ago. The physician refers the Corn family to the nurse to help the family discuss how to
addres the identified problem of dan's refusal to follow the protocol. Because the diet and
foot preparation affect the whole family, sister jenny attends the family session as well
KEY WORD

Dan is a 17 year old senior high school


The diet-exercise-insulin

PROBLEM

Dan is a 17 year old senior high shcool who is not following the diet-exercise-insulin
protocol prescribed for diabetes diagnosis 4 month ago.
Dan refusal to follow the protocol
Dan have diabetes type 1 which is already underway
Dan have type 1 diabetes because it has suffered for 4 month

DIABETES MILITUS

Definition Diabetes Militus

Diabetes mellitus, often simply referred to as diabetes, is a group of metabolic


diseases in which a person has high blood sugar, either because the body does not produce
enough insulin, or because cells do not respond to the insulin that is produced. This high
blood

sugar

produces

the

classical

symptoms

of polyuria (frequent

urination), polydipsia (increased thirst) and polyphagia (increased hunger).


There are three main types of diabetes:

Type 1 diabetes: results from the body's failure to produce insulin, and presently
requires the person to inject insulin. (Also referred to as insulin-dependent diabetes
mellitus, IDDM for short, and juvenile diabetes.)

Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use
insulin properly, sometimes combined with an absolute insulin deficiency. (Formerly
referred to as non-insulin-dependent diabetes mellitus, NIDDM for short, and adultonset diabetes.)

Gestational diabetes: is when pregnant women, who have never had diabetes before,
have a high blood glucose level during pregnancy. It may precede development of type 2
DM.

Classification
Most cases of diabetes mellitus fall into three broad categories: type 1, type 2,
and gestational diabetes. A few other types are described. The term diabetes, without
qualification, usually refers to diabetes mellitus. The rare disease diabetes insipidus has
similar symptoms as diabetes mellitus, but without disturbances in the sugar metabolism
(insipidus meaning "without taste" in Latin).
Comparison of type 1 and 2 diabetes

Feature

Onset

Type 1 diabetes

Type 2 diabetes

Sudden

Gradual

Age at onset

Any age
(mostly young)

Mostly in adults

Body habitus

Thin or normal

Often obese

Ketoacidosis

Common

Rare

Autoantibodies

Usually present

Absent

Endogenous insulin

Low or absent

Normal, decreased
or increased

Concordance
in identical twins

Prevalence

50%[4]

90%[4]

Less prevalent

More prevalent
- 90 to 95% of
U.S. diabetics

The term "type 1 diabetes" has replaced several former terms, including childhood-onset
diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the
term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes,
obesity-related diabetes, and non-insulin-dependent diabetes mellitus (NIDDM). Beyond
these two types, there is no agreed-upon standard nomenclature. Various sources have defined
"type 3 diabetes" as: gestational diabetes, insulin-resistant type 1 diabetes (or "double
diabetes"), type 2 diabetes which has progressed to require injected insulin, and latent
autoimmune diabetes of adults (or LADA or "type 1.5" diabetes).

a) Type 1 diabetes
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of
the islets of Langerhans in the pancreas leading to insulin deficiency. This type of diabetes
can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is
of the immune-mediated nature, where beta cell loss is a T-cell mediated autoimmune attack.
There is no known preventive measure against type 1 diabetes, which causes approximately
10% of diabetes mellitus cases in North America and Europe. Most affected people are
otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness
to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect
children or adults but was traditionally termed "juvenile diabetes" because it represents a
majority of the diabetes cases in children.
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was
traditionally used to describe to dramatic and recurrent swings in glucose levels, often
occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no
biologic basis and should not be used.There are many different reasons for type 1 diabetes to
be accompanied by irregular and unpredictable hyperglycemias, frequently with ketosis, and
sometimes serious hypoglycemias, including an impaired counterregulatory response to
hypoglycemia, occult infection, gastroparesis (which leads to erratic absorption of dietary
carbohydrates), and endocrinopathies (eg, Addison's disease). These phenomena are believed
to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.

PREVENTION

a) Immunosuppressive drugs
b) Diet
c) Insulin therapy
d) Pancreas transplantation
e) Islet cell transplantation

Conclusion
That can be done by families is to make a corn diet exercise Dan

insulin

schedules in accordance with the DAN want to diabetes mellitus experienced Dan not
damage vital organs that can treat the state of health.

5. Elderly
Joshepin Carmino is a 66-year-old woman who lives alone in a small urban apartment.
She lives on a fixed income from her decreased husbands Social Security. She has come
to the clinic for her routine check up. During the initial interview, you notice that she does
not always answer your question appropriately and she talks very softly when she offers
information spontaneously. When you check her hearing with the whisper test, she asks
you to repeat several times, and finally tells you, with annoyance in her voice, that you
just have to speak up if you expect people to hear you! when you do the Rinne test, the
result show BC > AC. When questioning her about problems, she denies having any
hearing loss. She says she has never had audiometry and she cant afford it now. She also
tells you that she doesnt talk to friends on the telephone anymore, because they dont talk
loud enough.

KEYWORD

Woman a 66-year-old
Rinne test the result show BC > AC.

PROBLEM
Josep Carmino elderly have the disease because of the results shows the results
of BC>AC,

and he did

not hear what

we're

talking by

asking us

to repeat our

conversation many times.

Disease That Often Affects the Ederly are As Follows


1) Less moving: physical impairment, mental, and environmental factors can cause the
less mobile elderly. The most common cause is a disorder of the bones, joints and
muscles, nerve disorders, and diseases of the heart and blood vessels.
2) Instability: causes of falls in the elderly can be either intrinsic factors (things related
to the state of the patient's body), either because of the aging process, disease or
extrinsic factors (things that come from outside the body) such as certain medications
and environmental factors.
3) Depression: change in social status, increased disease and reduced social
independence as well as changes due to aging process to be one trigger depression in
the elderly.However, once symptoms of depression often accompanies patients with

diseases of physical disorders, which can not be known or thought of, because the
symptoms of depression that appears often considered as a part of the normal aging
process or are not typical.
4) Impaired sensory perception, communication, healing, and skin: aging due to all the
senses prosesd reduced function, as well as disorders of the brain, nerves and muscles
used for speaking could menyebabkn disruption of communications, while the skin
becomes

more

dry,

brittle

and

easily

damaged

by

trauma the

minima

Intellectual impairment: a collection of clinical symptoms that include impaired


intellectual function and memory are severe enough to cause the disruption of
activities of daily livingThis incidence increases rapidly from age 60 to 85 years or
more, which is less than 5% of older adults aged 60-74 years had dementia (severe
dementia), while at the age of 85 years after these events increased nearly 50%. One
of the things that can cause depression so it needs interlektual is distinguished from
other intellectual impairment.

Communicating with persons with Alzheimers Disease or related


disorders

1. Always approach the person from the front, or within his/her line of vision no
surprise appearances;
2. Speak in a normal tone of voice and greet the person as you would anyone else;
3. Face the person as you talk to him/her;
4. Minimize hand movements that approach the other person;
5. Avoid a setting with a lot of sensory stimulation, like a big room where many people
may be sitting or talking, a high-traffic area or a very noisy place;
6. Maintain eye contact and smile. A frown will convey negative feeling s to a person;
7. Be respectful of the persons personal space and observant of his/her reaction as you
move closer. Maintain a distance of one to one and a half feet initially;

8. If a person is a pacer, walk with him/her, in step with him/her while you talk;
9. Use distraction if a situation looks like it may get out of hand. A couple of examples
are: if the person is about to hit someone of if he/she is trying to leave the
home/facility.
10. Use a low-pitched, slow speaking voice which older adults hear best;
11. Ask only one question at a time. More than one question will increase confusion;
12. Repeat key words if the person does not understand the first time around;
13. Nod and smile only if what the person said is understood.

6) Community

-History

The area known as Evansboro was first settled by French explorers and established as a
military outspost. Soon afterward the area was settled by other French immigrant because of
its rich farmland. It was a busy trading post in the 1800s because of its location on the St.
Croix River.

Demographics

The total population of evansboro, as of the 1990 census, is 9.156. of the total residents,
the female/male ratio is 1.1;1. There are 1.767 persons who are 65 year of age or older, and
2.287 are 18 year or younger. Raciel distribution data reveal that 64.2% of the residents are

African American, 34.5% are cwhite, 0.8% are Native American, and 0.5% belong to other
recial group. The majotary of Evansboros residents are married (71,6%). 23.1% are single,
and the reminder are cither separated, divorced, or widowed. The leading couses of death are
cardiovascular disease and lung cancer. A number of religious denominations are represented
in Evansboro, those with the greatest percentage of member include Southern Baptist, African
Methodist Episcopal, and United Methodist.

Physcial

Evansboro is bordered on the west by the St. Croix River and as result is threatened by
farmland. It lies within the flood plain of the river and as result is threatened by flooding
periodically. The last time that homes were affected by flood water was 3 years ago.
Evansboro is located in Washington Country, State Highway 25 boarders the eastern limit of
the town and intersects with U.S Highway 62 along the northern border of Evansboro. The
average temperature during the month of January is 60.3 F and during the month of July, 95.1
F

a)
b)
c)
d)
e)
f)
g)

Health and Social Sevices


Economics
Safety and Transportation
Education
Recreation
Politics and Government
Communication

KEY WORD
1. Evansboro
2. The leading couses of death are cardiovascular disease and lung cancer
3. Suhu rata-rata selama bulan Januari adalah 60,3 F dan selama
bulan Juli,95,1 F

PROBLEMS

Why in countries evansboro cancer, lung and heart into major diseases deadly to the state is
there to do with of race, the existing air temperature evansboro country

1. Coronary heart disease


Coronary heart disease is a type of attack that many of Indonesia's population. This
condition occurs due

to narrowing / blockage in the

coronary artery walls due

to fatty

deposits and cholesterol suplaian causing blood to the heart becomes impaired. Changes
in lifestyle, diet, and stress can also lead to the occurrence of coronary heart disease.

What Causes Coronary Heart Disease?

The cause of coronary heart disease is due to excessive buildup of fatty substances in the
lining of artery walls of coronary arteries, which are influenced by anunhealthy diet.Addicted
to smoking, hypertension, high cholesterol can also be a cause of coronary heartdisease.

Symptoms of Coronary Heart Disease


Symptoms of coronary heart disease such as:

Pain in the chest, more specifically in the chest pain that spreads to the middle to the left
arm or neck, even to the back. This chest pain is pain typical of coronary heart disease.This
pain arises only when doing physical activity and will decrease when resting. Accompanying
symptoms such as sweating and the onset of nausea.

These factors trigger a heart attack are among others:


-

smoke

Consuming foods high in cholesterol.

Less motion.

Lazy to exercise.

Stress.

Lack of rest.

Heart attack is a condition when the damage suffered

by the heart muscle (myocardium) isreduced due to sudden blood supply to part of the
body.

Prevention of coronary heart disease


- Avoid fatty foods
- Use the idle time for sports
- Do not smoke or consume alcohol
- Do not have too many thoughts / stress.

2. Lung cancer
Lung cancer is the growth of cancer cells that are not controlled in the lung tissue. The
pathogenesis of lung cancer has not really understood. Looks like bronchial mucosal cells
metaplastik changes in response to chronic exposure of the particles are inhaled and injure
lungs. In response to cellular injury, inflammatory reactions and processes will evolve.
Mucosal basal cell proliferation and would have differentiated into mucus-secreting goblet

cells. Looks like metaplastik activity occurs due to change of columnar epithelium lining the
epithelium skuamus, which is accompanied by cellular atipia and increased mitotic activity
that develop into mucosal dysplasia. Span of time this process has not been established, only
approximately estimated between 10 to 20 years.
Cell origin of lung cancer is still unexplained. During these two theories
evolved,leuripotential cell theory by Auerbach, who explains the deviations occur in the
process of stem cell differentiation into other cells. The theory of small cells by Yesner,
which explains the small cell neoplasms transforming and evolving into cancer cells

But note that genetic mutations occur in p73, [2] p53 and PRB, in addition to the role
of c-MYB oncogene, c-myca, mycc c-, c-raf, L-myc, N-myc, K-sense, c-fura , N-ras, H-ra, cerbB1, c-fms, c-Fes, c-RLF, c-erbB1, c-ErbB2, c-sis, BCL1. [3]According to WHO, lung
cancer is the leading cause of death in the group of cancer in both men and girls.

1. Skuamus cell carcinoma


Called squamous cell carcinoma in English or SCC, a type of cancer is common in the
main bronchus in the channel. Generally there is a development of keratin and keratin pearls.
2. Lung adenocarcinoma
Adenocarcinoma of the lung were recorded around 30% - 45% and will likely
continue to increase. Cases of adenocarcinoma of the lung usually occurs in the lungs and
organs are more common in women than in men, with a trend in the area of early metastasis
in lymph nodes and brain around. Patients with lung adenocarcinoma usually have a history
of chronic interstitial lung disease, such as scleroderma, rheumatoid disease, sarcoidosis,
interstitial pneumonitis, tuberculosis, recurrent pulmonary infection or lung disease
accompanied by necrosis. This causes adenocarcinoma often called scar carcinoma.
3. Adenocarcinoma bronkioalveolar

A subtype of lung adenocarcinoma with an incidence rate of about 2% - 4% of the


total incidence of lung cancer, often associated with several lung diseases that result in
pulmonary fibrosis, such as pneumonia, idiopathic pulmonary fibrosis, granulomata,
asbestosis, alveolitis with fibrosis, scleroderma, and disease Hodgkin's lymphoma. Place of
occurrence of cancer is still a debate, but it may have been reduced between populations
Clara cells or type II pneumosit which propagate along the alveolar septa.
4. Large cell carcinoma
This cancer has an incidence rate of around 9%. The tumor has a characteristic large
cells with large cell nucleus. Grandular differentiation has not been found or skuamus
5. The main cause
Sub-types of non-small cell lung cancer in smokers and never-smokers histological
sub-type Frequency of non-small cell lung cancers (%) Never-smokers Smokers Squamous
cell lung carcinoma

Adenocarcinoma Adenocarcinoma (Not Otherwise Specified)

Bronchioloalveolar carcinoma 4 10 Carcinoid 7 16 Other 8 6 Smoking is a major cause of


about 90% of cases of lung cancer in men and about 70% in women. The more cigarettes
smoked, the greater the risk for lung cancer.
Only a small proportion of lung cancers (about 10% -15% in men and 5% in women)
caused by or inhaled substances encountered in the workplace. Working with asbestos,
radiation, arsenic, chromate, nickel, chloromethyl ethers, mustard gas and coke oven
emissions can cause lung cancer, although usually only occurs in workers who also smoke.
The role of air pollution as a cause of lung cancer is still unclear. Some cases occur because
of exposure by radon gas in the household.
Sometimes lung cancer (particularly adenocarcinoma and alveolar cell carcinoma)
occurred in people who already have lung scarring due to other lung diseases, like
tuberculosis and fibrosis .

6. Symptoms of lung cancer


The most common symptoms encountered in patients with lung cancer are Persistent
cough or become great.Bloody sputum, change colors and more.Shortness of breath and

shallow.Headache, sore or cracked bone with no apparent cause.Chronic Fatigue Selara loss
eating or weight loss for no apparent reason.Hoarseness husky Swelling in the face or
neckSymptoms of lung cancer are generally not too obvious, so that most lung cancer
patients who seek medical help has been in an advanced stage. Kasusk-case early stage / early
often found accidentally when someone makes a routine health check.

7. Diagnosis and treatment


Some procedures that can facilitate the diagnosis of lung cancer include X-ray,
Thoracic CT Scan, Fine Needle Biopsies, Bronchoscopy, and USG Abdomen.
Treatment of lung cancer can be done in ways such as Surgery by removing any part of one
lung - sometimes in excess of the discovery of the tumor and remove all the lymph nodes
affected by cancer.
Radiotherapy or radiation with high intensity X-rays to kill cancer cells.
Chemotherapy Taking the drugs orally with certain side effects which aims to prolong the
suffering of life expectancy