Advanced Pathophysiology

LEGEND: Diagnostic Test

Klabisella pneumoniae infection with Pneumonia
Progression of COPD, Pulmonary Embolism, C/S reveals: Klabisella pneu- Nursing Diagnosis COPD
The client: MARCOS, YASNID of symptoms, client was Impaired physical mobility Pulmonary Edema to Respiratory Failure moniae : heavy growth
57 years old, male, married brought for consultation and Pharmacological int. Pulmonary Hypertension
30 years, born in the Philip- the subsequent admission S/S Pulmonary Embolism
Aspiration of Secretions Containing Microbes Failure of Immuno-defensive Invasion of the Activation of B Cells
pines, known smoker, no re- into the NCCU. mechanisms
cent history of travels Klabisella Lower Respiratory Tract Pulmonary Edema
(+) HPN II due having a chronic underlying disease
pneumoniae Release of Antibodies
CC: (+) reduced consiousness that impairs host defenses. (p559)
encapsulated gram negative aerobic
Right-sided weakness; inabil- (+) Mutism bacillus Antigen-Antibody Reaction
ity to speak; aspiration pneu- (+) immobility
Incidence greatest in elderly and pts. in
monia; Cerebro Vascular Dis- (-) N/V chronic care facilities. (p556)
CBC reveals:
ease; pontine area hyperten-
Dx related to Pneumonia: Antigen Antibody Complexes Initiation of Complement System
sive cardiovascular disease Pharmacological intervention: EXAM RESULT REFERENCE
CBC, CXR NAME Adhere to the Mucosal Lining (Non-Specific and Specific Immune System)
Piperacillin/tazobactam Combo-antibio 280 mg IVTT q12hr
History of illness: of the Lower Respiratory with promotion of inflammatory response
Tracheostomy inserted; O2 Inhibits bacterial cell wall synthesis by binding to one or more of the peni- RBC 4.44 4.5-6.0
10 years prior: regulated initially at 11LPM cillin binding proteins (PBPs); which in turn inhibits the final transpepti- HgB 125 120-170
dation step of peptidoglycan synthesis in bacterial cell walls, thus inhib-
A known hypertensive and is Hct 0.378 0.4-0.54
3 weeks prior: iting cell wall biosynthesis. Bacteria eventually lyse due to ongoing activity
compliant to to medications, of cell wall autolytic enzymes (autolysins and murein hydrolases) while WBC 14.8 5-10X10^9/l Increased Mucus Production Vasodilation (PGE2, PGD2 Nitric Oxide)
(+) HPN II
which were unrecalled. cell wall assembly is arrested. Tazobactam inhibits many beta-lactamases, (White blood cells, mostly
(+) reduced consiousness NEUTRO- 76.5 45-70%
including staphylococcal penicillinase and Richmond and Sykes types II, III, Increased Blood Flow
(+smoker (+) Mutism
PHILS neutrophils, also migrate into
IV, and V, including extended spectrum enzymes; it has only limited activi-
(+) HPN II (+) immobility ty against class I beta-lactamases other than class Ic types. the alveoli and fill the nor-
(+) Febrile mally air-filled spaces) Increased Plasma Hydrostatic Pressure
3 month prior:
(+) cough & colds Adventitious breath sounds
Client met with business as-
X-ray reveals: ;
sociate doing work. Business Ineffective airway clearance Accumulation of Mucus in airway Increased Capillary Permeability
broncho-
(-) N/V
associate observed client ex- pneumonia productive cough
CBC, CXR, C&S, Rapid shallow Hyperse- pattern (p556)
periencing diffuculty of Pharmacological intervention:
Breathing Index cretion of
speaking, prompting him to Herparin Anticoagulant 10,000u to mucus Transportation of
Escape of Plasma Exudate formation
call the clients wife. Upon her PEG & EGD insertion 50,000u q4-6h Phagocyting Cells
Proteins p602
arrival, the client was con- Heparin increases the inhibitory action of antithrom-
scious, but unable to speak bin III (AT III) on clotting factors XIIa, XIa, IXa, Xa and (proximal air- Body attempts structural
thrombin. This inhibits the conversion of prothrombin ways) in- to repair changes Edema Engulfing
and unable to move right side to thrombin and fibrinogen to fibrin.
Inflammation devel-
creased num- inflammation From chronic of the Antigen
of body. Due to sudden onset op and spreads
bers of goblet inflammation
around the alveoli
Formation of Deep Vein Thrombosis into pleura and inter-
ongoing injury Narrowing of itiump47) Replication of
at popliteal vein Disrupted ventila- (lung paren- Pulmo- Airway
alveolar dead partially Thrombus -and-repair the Antigen
tion and gas ex- process caus- chyma) nary vas- (obstructive
within the Cells
space is obstructs a dislodges bronchitis) p602
es scar tissue Alveolar wall culature
increased pulmonary from leg change Consolidation of Lung
formation destruction
artery
Use of accessory muscles Cells become
Increased RR Infected
Substances are re- regional blood vessels pulmonary vascular Loss of alveolar attachments Thickening of the lining of Decreased
although continuing Substances are re-
leased from clot to leased from clot to and bronchioles to con- resistance also increases and decrease of in elastic the vessels and hypertro- Lung Inflation
to be ventilated,
receives little or no surrounding area surrounding area strict recoil phy of smooth muscles
Ineffective breath patterns Detection of the
blood flow
Infected Cells by the
increase in right ventric- Further Increase in pul- increased blood flow then ability to handle Pulmonary Rapid Shallow Breathing T Cells
work requirements of the
ular work to maintain monary arterial pressure increases the pulmonary whatever flow or volume of hypertension Index RSBI = 66.34 N= <105
Gas exchange is im- right ventricle may ex- artery pressure blood it receives is impaired p579
paired or absent ceed its capacity pulmonary flow TIDAL V 0.407 Effector T Cells De-
Ineffective gas exchange stroy the Antigen
Disrupted ventila-
Respiratory Failure decrease in arterial oxygen tension VE 11LPM
right ventricular failure tion and gas ex-
(PaO2) to less than 50 mm Hg
occurs change
(hypoxemia) and an increase in arterial- RR 27
Regulator T Cells
Ineffective gas exchange carbon dioxide tension (PaCO2) to great-
ABG reveal: resp acidosis
Strengthen the Activ-
decrease in cardiac out- er than 50 mm Hg(hypercapnia), with an TEMP 38.3 ity of thje Effector
Decrease lung compliance Capillary and interstitial arterial pH of less than 7.35 pH 7.20 7.35-7.45
put Cells
pressure increase further PaCO2 92 35-45 HR 80
PO2 76 80=100
fluid begins to leak into
decrease in systemic Ineffective gas exchange HCO3 22 22-28 Effector and Regula-
the interstitial space and Tight junctures of alveo-
BP 130/70
blood pressure alveoli tor Cells Synthesize
lar walls are disrupted and Release Cyto-
SPO2 95%
Pharmacological intervention: kines
Possible development of Paracetamol NSAID 500 mg OD q4hr PRN for fever
Increase microvascular
shock Fluid enters alveoli with Disrupted ventila- Decreases fever by a hypothalamic effect leading to sweating and vasodila-
pressure tion
large RBC and CHON tion and gas ex- Release of Pyrogens
Inhibits pyrogen effect on the hypothalamic-heat-regulating centers
molecules change (hypoxia Inhibits CNS prostaglandin synthesis with minimal effects on peripheral
Systemic high blood pressure causes an increase in Backup of blood into pul- worsens) prostaglandin synthesis
Does not cause ulceration of the GI tract and causes no anticoagulant
Increased temperature Altered Temperature
aortic blood pressure; left ventricle has difficulty open- monary vasculature Regulating Mechanism
action.
ing again this pressure (afterload); CO drops as it can- Hyperthermia Fever in the Hypothalamus
not escape the Left ventricle